Halverson v. Secretary of Health and Human Services ( 2020 )

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 15-227V
(Filed: February 4, 2020)
* * * * * * * * * * * * * * *
BERNARD HALVERSON, EXECUTOR * To Be Published
of the ESTATE of SUSAN *
HALVERSON, deceased, *
* High-Dose Influenza (“Fluzone”);
Petitioner, * Vaccine; Cardiac Arrest; Death;
* Significant Aggravation
v. *
*
SECRETARY OF HEALTH *
AND HUMAN SERVICES, *
*
Respondent. *
*
* * * * * * * * * * * * * * *
Jerry Lindheim, Esq., Locks Law Firm, Philadelphia, PA, for petitioner.
Lisa Watts, Esq., U.S. Dept. of Justice, Washington, D.C., for respondent.
RULING ON ENTITLEMENT1
Roth, Special Master:
On March 4, 2015, Bernard Halverson (“Mr. Halverson” or “petitioner”) filed a petition
for compensation under the National Vaccine Injury Compensation Program, 42 U.S.C. § 300aa-
10, et seq.2 (“Vaccine Act” or “Program”) as executor of the estate of his late wife, Susan
Halverson (“Mrs. Halverson”). Petitioner alleges that Mrs. Halverson received a high-dose
1
This Ruling has been designated “to be published,” which means I am directing it to be posted on the
Court of Federal Claims’s website, in accordance with the E-Government Act of 2002, Pub. L. No. 107-
347, 116 Stat. 2899, 2913 (codified as amended at 44 U.S.C. § 3501 note (2006)). This means the Ruling
will available to anyone with access to the internet. However, the parties may object to the Ruling’s
inclusion of certain kinds of confidential information. Specifically, under Vaccine Rule 18(b), each party
has fourteen days within which to request redaction “of any information furnished by that party: (1) that is
a trade secret or commercial or financial in substance and is privileged or confidential; or (2) that includes
medical files or similar files, the disclosure of which would constitute a clearly unwarranted invasion of
privacy.” Vaccine Rule 18(b). Otherwise, the whole Ruling will be available to the public. Id.
2
National Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660, 100 Stat. 3755 (1986). Hereinafter,
for ease of citation, all “§” references to the Vaccine Act will be to the pertinent subparagraph of 42 U.S.C.
§ 300aa (2012).
seasonal influenza vaccine (“Fluzone”) on January 9, 2014, which caused cardiac arrest and her
subsequent death on January 13, 2014. See Petition (“Pet.”), ECF No. 1. Alternatively, petitioner
claims that the flu vaccine significantly aggravated Mrs. Halverson’s ischemic heart disease,
leading to her death.
As explained fully and in detail below, petitioner has established that the high-dose flu
vaccine received by Mrs. Halverson was a substantial factor in her cardiac arrest and subsequent
death.
I. Procedural History
The petition was filed on March 4, 2015. ECF No. 1. On April 2, 2015, petitioner filed
Mrs. Halverson’s death certificate and medical records, as well as proof that he had been appointed
the executor of her estate, as Petitioner’s Exhibits (“Pet. Ex.”) 1-9.3 ECF No. 7. These exhibits
were later stricken from the record as incorrectly filed. See Non-PDF Order, issued Aug. 25, 2016.
The initial status conference was held on May 7, 2015. Petitioner was ordered to file
additional medical records. Scheduling Order, ECF No. 8.
On July 16, 2015, respondent filed his Rule 4(c) Report (“Resp. Rpt.”), stating that this
case was not appropriate for compensation. Resp. Rpt., ECF No. 13. More specifically, respondent
noted that Mrs. Halverson’s cardiologist had previously discussed her risk of sudden cardiac death
related to ventricular tachycardia, which resulted in Mrs. Halverson having an automatic
implantable cardioverter defibrillator (“AICD”) placed. Id. at 3. Respondent submitted that Mrs.
Halverson’s death was the result of her longstanding heart disease which was marked by worsening
cardiac function over the previous year, and required placement of the AICD. Id. at 7.
Following a status conference on November 12, 2015,4 petitioner was ordered to file expert
reports. Scheduling Order, ECF No. 27. Petitioner filed expert reports from Dr. Robert Stark and
Dr. Gourang Patel on January 28, 2016. Pet. Ex. 10-11, ECF No. 30.
On June 14, 2016, respondent filed an expert report from Dr. Joseph Murphy. Resp. Ex.
A-B, ECF No. 33. Respondent filed an addendum to Dr. Murphy’s report on June 16, 2016. Resp.
Ex. C, ECF No. 34.
Petitioner filed two additional reports from Dr. Stark on July 5 and 8, 2016. Pet. Ex. 19,
ECF No. 35, 38;5 Pet. Ex. 20, ECF No. 37.
Respondent filed an expert report from Dr. Noel Rose on July 6, 2016 and supporting
medical literature on July 11, 2016. Resp. Ex. D-E, ECF No. 36; Resp. Ex. F-N, ECF No. 39.
3
Petitioner submitted an affidavit that stated nothing more than he had not filed a civil action in this
matter. See Pet. Ex. 5.
4
This case was reassigned to me on October 19, 2015. ECF No. 21.
5
Dr. Stark’s report, Pet. Ex. 19, was filed twice and occurs on the docket at ECF Nos. 35 and 38.
2
Petitioner filed medical literature on July 12, 2016, as Pet. Ex. B-L. ECF No. 40. These
exhibits were later stricken due to improper filing. See Non-PDF Order, issued Aug. 25, 2016.
A status conference was held on July 14, 2016. Scheduling Order, ECF No. 41. During the
conference, it was “clarified that petitioner’s experts claim that [Mrs. Halverson’s] death was not
necessarily caused by the vaccine, but rather that the vaccine significantly aggravated petitioner’s
pre-morbidities and contributed to petitioner’s eventual death.” Id. at 1. Respondent requested the
opportunity for supplemental reports to “flesh out” his response to petitioner’s significant
aggravation claim. Id. Respondent was ordered to file supplemental expert reports by September
12, 2016. Id. at 2.
Respondent filed a second report from Dr. Murphy and supporting medical literature on
August 3, 2016. Resp. Ex. O-U, ECF No. 42.
Petitioner filed a Motion to Strike Pet. Ex. 1-14 and his supporting medical literature, which
was filed as “Medical Exhibits A-L,” due to improper filing. See Motion to Strike, ECF No. 43.
This Motion was granted. Non-PDF Order, issued Aug. 25, 2016. Petitioner properly filed Pet. Ex.
1-16 on September 7, 2016. See Pet. Ex. 1-9, ECF No. 44; Pet. Ex. 10-16, ECF No. 45.
Respondent filed an additional expert report from Dr. Rose on September 9, 2016. Resp.
Ex. V, ECF No. 46.
Petitioner filed supplemental expert reports from Dr. Stark and Dr. Patel on September 13,
2016. Pet. Ex. 17-23, ECF No. 47.
A Rule 5 status conference was held on December 21, 2016. Scheduling Order, ECF No.
48. I summarized the medical records as follows:
…Ms. [sic] Halverson, then 65 years old, had a complicated medical history which
included but was not limited to congestive heart failure, insulin dependent diabetes, renal
failure, hypertension and left ventricular systolic dysfunction. Mrs. Halverson’s health
declined in 2013 due to her heart problems, and in September of 2013 she underwent
implantation of a biventricular cardioverter defibrillator (ICD) to avoid the risk of sudden
cardiac death. Mrs. Halverson was noted to be doing well in the months that followed the
implantation of the defibrillator. On January 9, 2014, Mrs. Halverson presented to her
doctor with complaints of congestion, ears feeling clogged, loose cough, and scratchy
throat….She was administered the Fluzone high dose vaccine intramuscularly. In the days
that followed, Mrs. Halverson was noted to be weaker, with cough and congestion,
decreased food and water intake, and shortness of breath. On January 13, 2014, Mrs.
Halverson went to get dressed so that her husband could take her to the emergency room.
She apparently went into cardiac arrest. According to her husband, the internal
defibrillator’s warning system did not sound. Attempts to resuscitate her were unsuccessful
and Mrs. Halverson passed away at that time.
Id. at 1. Following that recitation, I noted that no blood work was performed on Mrs. Halverson in
the course of her emergency treatment, and no autopsy was performed after her death. Id. The
3
parties were encouraged to settle this matter, but were unable to reach a resolution. Id.; Joint Status
Report, ECF No. 49.
An entitlement hearing was initially scheduled for November 5 and 6, 2018, to be held in
Washington, D.C. Prehearing Order, ECF No. 51. It was later rescheduled to November 6 and 7,
2018. Scheduling Order, ECF No. 58.
The parties elected not to file post-hearing briefs. See Transcript (“Tr.”) 313-14.
This matter is ripe for decision.
II. Overview of Heart Function
The heart is made up of four chambers. Heart, DORLAND’S ILLUSTRATED MEDICAL
DICTIONARY 825 (32nd ed. 2012) [hereinafter “DORLAND’S”]. The upper two chambers are called
the atria and the lower two chambers are called the ventricles. Id. The heart functions as a two-part
pump. MARY M. CANOBBIO, CARDIOVASCULAR DISORDERS 4 (William G. Brottmiller ed., 1st ed.
1990) [hereinafter “CANOBBIO”]. The sinoatrial (“SA”) node conducts an electrical impulse which
causes both atria to contract, forcing blood from the atria into the ventricles. Id. at 6, 15. The
atrioventricular (“AV”) node, located in the floor of the right atrium, receives the electrical impulse
and spreads it to the ventricles. Id. at 15. The ventricles then contract, pushing blood out to the
body. Id. at 6. The chambers of the heart only contract if stimulated by electrical activity. GAIL
WALRAVEN, BASIC ARRHYTHMIAS 2 (3rd ed. 1992) [hereinafter “WALRAVEN”].
If another conduction site in the heart discharges electrical impulses at a faster-than-normal
rate, it can override the SA node and take over the pacemaking function for the heart. WALRAVEN
at 8. The process of another conduction site taking over as pacemaker is called “irritability.” Id.
Increased irritability to either the atria or the ventricles can result in increased electrical impulses.
This can cause “fibrillation,” where the chamber “quivers ineffectively” rather than contracting
fully. Id. at 100. Atrial fibrillation (“Afib”) causes the ventricular rhythm to be “grossly irregular,”
but Afib can be managed via medication. Id. at 100-01; CANOBBIO at 67. In contrast, ventricular
fibrillation (“Vfib”) is a lethal arrhythmia because the heart rhythm becomes chaotic and
ineffective. WALRAVEN at 191.
Afib occurring alone can be unrecognizable or very symptomatic. HURST’S THE HEART
824 (Valentin Furster et al. eds., 10th ed. 2001) [hereinafter “HURST’S”]. However, when Afib
occurs in conjunction with other cardiac conditions, such as mitral or aortic stenosis, restrictive
cardiomyopathies, or advanced left ventricular dysfunction, Afib may cause severe hemodynamic
deterioration. Id. Afib can be caused by mitral or aortic stenosis or regurgitation, hypertension,
coronary heart disease, cardiomyopathy, atrial septal defect, or pericarditis; it can also occur
secondary to left or right ventricular overload. Id. at 826. People with Afib are five times more
likely to have a stroke than people who do not have Afib. Id. at 828. Chronic recurrent atrial
fibrillation may require an automatic implantable cardioverter defibrillator (“AICD”). Id. at 828.
Vfib occurs most commonly in the setting of acute ischemic events, like myocardial
infarction, or in advanced chronic ischemic heart disease. HURST’S at 852. It is the cause of death
4
in 25 to 50 percent of all cardiac fatalities. Id. Vfib may also develop during ischemia caused by
coronary artery spasm or atrial fibrillation with rapid ventricular responses. Id. A particularly high-
risk setting for Vfib is acute myocardial infarction with right or left bundle-branch block. Id. Vfib
is a life-threatening condition that requires emergency defibrillation. Id. at 853.
Chronic Vfib requires implantation of an AICD. HURST’S at 854. An AICD is implanted
in the chest and connected to the heart via electrodes. Id. at 950. The AICD detects abnormal heart
rhythms, such as Vfib, and defibrillates the heart via an electric shock within 10 to 15 seconds of
detecting Vfib. Id. at 947. AICDs are very effective in terminating ventricular tachydysrhythmias;
in a large-scale study over five years, approximately 98% of episodes of Vfib were detected and
successfully terminated. Id. at 1037. However, the overall mortality in patients with AICDs
remains high at approximately 22% because most AICD recipients already have heart failure. Id.
at 954; Resp. Ex. S at 42.6 The AICD may help the patient survive an episode of Vfib, but the
patient may still die due to other cardiac problems. HURST’S at 954.
Factors that contribute to Afib and Vfib are smoking, excessive caffeine, obesity, high
blood pressure, diabetes, high alcohol intake, hyperthyroidism, coronary heart disease, and heart
failure. See CANOBBIO at 72; Resp. Ex. V, Tab 6 at 1, 4.7
Myocardial infarction, commonly referred to as heart attack, and cardiac arrest are very
different. In a heart attack, a blocked artery prevents blood from reaching sections of the heart; if
it is not opened quickly, the part of the heart normally nourished by that artery begins to die. See
CONOBBIO at 81. Symptoms can include chest pain, shortness of breath, dizziness, nausea and
vomiting, weakness, gastrointestinal distress, and/or low-grade fever. Id. at 85-86. Symptoms can
be immediate or start slowly and persist for hours, days, or weeks before a heart attack. HURST’S
at 1278-79.
Cardiac arrest is the sudden cessation of the pumping function of the heart; it signifies
either ventricular fibrillation or ventricular standstill. Cardiac arrest, DORLAND’S at 133. It is
characterized by abrupt loss of consciousness that uniformly leads to death without immediate
intervention. HURST’S at 1030. Cardiac arrest can occur as a result of the electrophysiologic effects
of acute ischemia, acute changes in mechanoelectrical feedback, or changes in autonomic
innervation of the heart. Id. at 1022-23. Approximately 70% of patients who have cardiac arrest
suffer from Vfib; many also have coronary artery disease or other underlying structural heart
disease. Id.
There are increased risks of cerebrovascular and cardiovascular events following upper
respiratory tract infections like influenza. Resp. Ex. K at 8-10.8 Potential adverse events include
6
Steve E. Phurrough et al., Decision Memo for Implantable Defibrillators (CAG-00157R3), CMS.GOV (Jan.
27, 2005) (printed July 25, 2016), filed as “Resp. Ex. S.”
7
Darae Ko et al., Atrial Fibrillation in Women: Epidemiology, Pathophysiology, Presentation, and
Prognosis, 13 NAT. REV. CARDIOL. 321-32 (2016), filed as “Resp. Ex. V, Tab 6.”
8
Kristin L. Nichol et al., Influenza Vaccination and Reduction in Hospitalizations for Cardiac Disease and
Stroke among the Elderly, 348 N. ENGL. J. MED. 14: 1322-32 (2003), filed as “Resp. Ex. K.”
5
alterations in circulating clotting factors, platelet aggregation and lysis, concentrations of
inflammatory-response proteins, and alterations in cytokine concentrations. Id. These changes
might enhance thrombotic tendencies, impair vasodilation, or cause endothelial injury. Id.
Influenza vaccines are recommended for persons over the age of 65 and for anyone with a high-
risk medical condition in order to reduce the risk of hospitalization for cardiac and cerebrovascular
causes. Id. at 10. However, subspecialists are less likely than generalists to recommend influenza
vaccination to their high-risk patients, and only half of cardiology practices in the U.S. stock
influenza vaccine compared to 70% of primary care practices. Id.; Resp. Ex. L at 4.9
III. Medical History
A. Mrs. Halverson’s Health Prior to Receiving Fluzone
Mrs. Halverson was born on December 14, 1948. Pet. Ex. 3 at 2. Her father suffered from
diabetes and heart disease before passing away at age 65, while her mother had heart disease and
hypertensive disorder and passed away at age 62. Id. At the time of her death, Mrs. Halverson and
her husband, the petitioner, had been married for almost 44 years. Tr. 8.
Mrs. Halverson had a complicated medical history. At the time of her death, her chronic
conditions included insulin-dependent diabetes, stage IV chronic kidney disease, hypertension,
hyperlipidemia, hypothyroidism, anemia, obesity, left bundle branch block,10 ventricular
tachycardia, ischemic heart disease, occasional palpitations, and congestive heart failure with left
ventricular diastolic dysfunction (NYHA class II).11 See Pet. Ex. 3 at 2-7; Pet. Ex. 4 at 7, 11; Pet.
Ex. 7 at 1, 5.
Mrs. Halverson’s past surgical history included a vitrectomy in 1986, a 1987 repair of an
atrial septal defect (“ASD”) that had existed since childhood, orthopedic surgeries on her left palm
in 1994 and on both shoulders in 1996, and cataract surgeries in 2003 and 2004. Pet. Ex. 3 at 2. In
2000, she developed complete heart block and underwent placement of a permanent pacemaker;
she required a second procedure in 2001 due to lead dislodgement and later had multiple generator
changes. Pet. Ex. 7 at 41, 104. Mrs. Halverson was a smoker for 25 years but quit in or around
2004. Pet. Ex. 3 at 3.
9
Matthew M. Davis et al., Influenza Vaccination as Secondary Prevention for Cardiovascular Disease, 48
J. AM. COLL. CARDIOL. 7: 1498-1502 (2006), filed as “Resp. Ex. L.”
10
“Left bundle branch” refers to the left branch of the bundle of His, “a small band of atypical cardiac
muscle fibers” which “propagates the atrial contract rhythm to the ventricles.” Bundle of His, DORLAND’S
at 260 The left bundle branch transmits the atrial contraction rhythm from the AV node to the left ventricle.
The interruption of the left bundle branch can cause heart block. Bundle branch, id. at 248.
11
“NYHA class II” refers to the New York Heart Association classification, a functional and therapeutic
classification for prescription of physical activity for cardiac patients. A person who falls into Class II has
a slight limitation of activity, with symptoms on moderate or normal exertion. New York Heart Association
(NHYA) c., DORLAND’S at 369.
6
In 2008, Mrs. Halverson was assessed for ventricular systolic dysfunction due to a high
rate of ventricular episodes. Pet. Ex. 7 at 28. She had experienced frequent episodes of palpitations
without chest pain or lightheadedness but sometimes accompanied by shortness of breath. Id. Her
cardiologist, Dr. Arluck, concluded that she had idiopathic ventricular tachycardia in the absence
of left ventricular systolic dysfunction or severe ischemic heart disease that did not warrant
suppression for prevention of sudden cardiac death at that time. Id. at 28-29.
In 2009, Mrs. Halverson’s pacemaker check showed runs of non-sustained ventricular
tachycardia (“NSVT”).12 Pet. Ex. 6 at 35-36; Pet. Ex. 7 at 26-27. Dr. Arluck noted a concern for
high estimated right ventricular systolic pressure but did not suggest immediate action to address
it. Id.
On April 9, 2010, Mrs. Halverson presented to Dr. Arluck emergently. Pet. Ex. 4 at 53-54;
Pet. Ex. 6 at 29-30; Pet. Ex. 7 at 20-21. Three days before, she had called Dr. Arluck, complaining
of extreme lightheadedness ongoing for four or five days. Id. He instructed her to “hold Captopril,”
and her dizziness resolved. Id. It was noted that Mrs. Halverson had a “fairly brittle cardiovascular
system,” and with a bit of excess fluid she would have symptoms of congestion. Id. She also had
diabetic proteinuria. Id.
Blood work throughout 2010 and onward showed high glucose, BUN, and creatinine, with
low eGFR, sodium, and chloride. Pet. Ex. 4 at 20-22, 33-36, 41-42, 46, 48, 51-52, 57; Pet. Ex. 6
at 44-49; Pet. Ex. 8 at 157- Pet. Ex. 8 at 16, 17, 51, 60, 61. She also had high B-Type natriuretic
peptide (“BNP”). Pet. Ex. 4 at 51. At times, she had low TSH and high hemoglobin A1C. Pet. Ex.
4 at 33, 34, 42, 48; Pet. Ex. 6 at 45, 47, 49; Pet. Ex. 7 at 158, 160.
By May 11, 2011, Dr. Villorani noted that Mrs. Halverson’s kidney function had declined
and changed her diagnosis to stage IV chronic kidney disease. Pet. Ex. 4 at 37-38; Pet. Ex. 8 at 91-
92. She also had uncontrolled anemia. Id. She was referred for pre-dialysis education. Id. By
November of 2011, she was referred for dialysis training. Pet. Ex. 4 at 32.
In April of 2012, Mrs. Halverson underwent pacemaker explant and replacement. Pet. Ex.
4 at 27.
Mrs. Halverson routinely presented for her follow-up visits. See generally Pet. Ex. 3; Pet.
Ex. 4; Pet. Ex. 6; Pet. Ex. 7.
On April 26, 2013, Mrs. Halverson presented to Dr. Arluck emergently with a four-week
history of dyspnea on minimal exertion, non-productive cough, orthopnea, nocturnal dyspnea,
chest aching, and two weeks of edema with increased abdominal girth. Pet. Ex. 6 at 5; Pet. Ex. 7
1. She reported snoring and waking up exhausted. Pet. Ex. 6 at 7; Pet. Ex. 7 at 3. Her active medical
problems included type I diabetes, hypertension, hyperlipidemia, congestive heart failure, renal
injury secondary to diabetes, orthostatic hypotension, shortness of breath, paroxysmal ventricular
tachycardia, and hypothyroidism. Id. She was noted to have decompensated congestive heart
12
Non-sustained ventricular tachycardia, or NSVT, is an abnormally rapid ventricular rhythm that
terminates spontaneously within 30 seconds and does not result in the heart’s failure to function.
Nonsustained ventricular tachycardia, DORLAND’S at 1867; ventricular tachycardia, id. at 1868.
7
failure. Id. Dr. Arluck ordered several tests, including an echocardiogram, chest x-ray, basic
metabolic panel (“BMP”), BNP, and a nuclear stress test. Id. Bloodwork from this appointment
showed high glucose, BUN, creatinine, and BNP, and low eGFR, sodium, and chloride. Pet. Ex. 6
at 43.
An echocardiogram was performed on May 14, 2013 and showed the left ventricle had
moderately to severely depressed systolic function and an estimated ejection fraction 13 of 25 to
35%. Pet. Ex. 4 at 7; Pet. Ex. 6 at 78; Pet. Ex. 7 at 87, 150. Mrs. Halverson had abnormal left
ventricular diastolic function with a restrictive pattern, suggesting elevated left ventricle diastolic
pressure. Id. Her right ventricle had normal systolic function but a pressure overload pattern. Pet.
Ex. 4 at 8; Pet. Ex. 6 at 79; Pet. Ex. 7 at 88, 151. She had mild tricuspid regurgitation and abnormal
septal motion, with right ventricular pacing, right bundle branch block, or right ventricular volume
overload. Id.
On May 17, 2013, Mrs. Halverson underwent Regadenoson Cardiolite Perfusion Imaging
with Gating. Pet. Ex. 4 at 5-6; Pet. Ex. 6 at 82-83; Pet. Ex. 7 at 94-95, 148-49. She did not have
ECG changes or pain with stress, but premature ventricular contractions were observed with
exercise. Id. She did not have any ischemia. Id. Her left ventricular systolic function appeared to
be moderately to severely depressed, and she had prominent right ventricular uptake. Id. It was
noted that accuracy of the measured ejection fraction is diminished in patients with ventricular
paced rhythm. Id.
Blood work was performed on May 22, 2013, and showed low WBC, RBC, hemoglobin,
hematocrit, MCHC, eGFR, sodium, and chloride, and high glucose, BUN, creatinine, and BNP.
Pet. Ex. 8 at 13-14.
At her May 28, 2013 visit with Dr. Arluck, Mrs. Halverson was noted to have
decompensated congestive heart failure with continued weakness, fatigue, and dyspnea. Pet. Ex. 6
at 9; Pet. Ex. 7 at 5. The potential for sudden cardiac death related to NSVT and decreased ejection
fraction was discussed. Pet. Ex. 6 at 11-12; Pet. Ex. 7 at 7-8. Dr. Arluck noted that she was a
candidate for an AICD and recommended a consultation with Dr. Bullinga regarding the
replacement of her pacemaker. Id. She was instructed to continue with a healthy diet and
appropriate activity, to continue prescribed medications, and to monitor her renal function and
electrolytes closely. Id.
In July of 2013, Mrs. Halverson continued to experience fatigue, dizziness, increased
urination, numbness of feet, and shortness of breath when walking and lying down. Pet. Ex. 3 at
15. She was not seeing an eye doctor yearly and was not taking her blood pressure medications as
directed because of side effects; furosemide was decreased due to lightheadedness and low blood
pressure readings. Id. Blood work performed at that time showed low WBC, platelets, eGFR,
13
The ejection fraction is a measurement of the percentage of blood leaving the ventricle each time the
heart contracts. It is usually only measured in the left ventricle. An ejection fraction of 55% or higher is
considered normal; 50% or lower is considered reduced though experts vary and consider 50% borderline.
Rekha Mankad, Ejection fraction: What does it measure?, MAYO CLINIC (July 2, 2019),
https://www.mayoclinic.org/ejection-fraction/expert-answers/faq-20058286
8
sodium, and chloride, and high glucose, BUN, creatinine, BNP, and hemoglobin A1C. Pet. Ex. 6
at 41-42; Pet. Ex. 7 at 161-62; Pet. Ex. 8 at 11-12.
On July 30, 2013, Mrs. Halverson returned to Dr. Arluck for follow-up of congestive heart
failure and left ventricular systolic dysfunction. Pet. Ex. 6 at 14; Pet. Ex. 7 at 9. She reported that
she had an appointment with Dr. Bullinga scheduled for August 7 for consideration of an AICD.
Id. She had lost 24 pounds since presenting with congestive heart failure. Pet. Ex. 6 at 17; Pet. Ex.
7 at 12. She would need a repeat assessment of her left ventricular systolic function, most likely
by echocardiogram. Id. Bloodwork, including a hepatic function panel, lipid panel, creatine kinase,
and hemoglobin A1C, was ordered. Pet. Ex. 6 at 18; Pet. Ex. 7 at 12. Her creatine kinase and A1C
were high and her HDL cholesterol was low. Pet. Ex. 4 at 17.
On September 13, 2013, Mrs. Halverson presented to her nephrologist and reported that
she had passed out at home. Pet. Ex. 8 at 2. It was determined to be related to an adjustment of her
water medication. Id.
On September 17, 2013, Mrs. Halverson presented to Dr. Sparagna for follow-up. Pet. Ex.
3 at 8. She reported occasional shortness of breath and was scheduled to have a defibrillator placed
“next week.” Id. at 11.
On September 30, 2013, Mrs. Halverson presented to Dr. Bullinga at Penn Presbyterian
Medical Center for implantation of a permanent biventricular AICD. Pet. Ex. 6 at 24, 84; Pet. Ex.
7 at 100. She was noted to have had an exacerbation of congestive heart failure in May of 2013, a
left ventricle ejection fraction of 25%, shortness of breath upon walking half a block, and NSVT
into the 180s. Id. Her expected survival was greater than one year. Pet. Ex. 7 at 104. Blood work
performed on October 22, 2013 showed low hemoglobin, hematocrit, MCH, MCHC, platelets,
sodium, chloride, and eGFR, and high glucose, BUN, creatinine, BNP, and urine protein. Pet. Ex.
6 at 39-40; Pet. Ex. 7 at 163-64.
Petitioner testified that, after the implantation of the AICD, Mrs. Halverson’s health
improved. “She was doing a lot better. She had a lot more energy and…she was even thinking
more positively about her health. She was more active…. She wanted to go out more and go out
to restaurants…where she was mostly staying at home before. She didn’t have the energy to do
it.” Tr. 42. She was also able to walk more. Tr. 42.
On November 8, 2013, Mrs. Halverson returned to Dr. Arluck for follow-up. Her
pacemaker had been replaced with a biventricular AICD and she no longer had nocturnal dyspnea.
Pet. Ex. 6 at 19; Pet. Ex. 7 at 14. She complained of shortness of breath when walking but attributed
it to her unsteady gait and difficulty walking. Id. She did not climb steps. Id. She reported being
given furosemide in the hospital, but got light headed, so she was only taking it when her weight
was above 125 pounds. Id. She had severe chronic renal failure. Id. An electrocardiogram was
performed; Mrs. Halverson was noted to have atrial and biventricular racing. Pet. Ex 4 at 4. She
had not had any AICD discharges. Pet. Ex. 6 at 19.
On November 15, 2013, a cardiovascular disease risk profile was performed. Pet. Ex. 4 at
14-16. Her hemoglobin A1C and creatine kinase were high, and her HDL cholesterol was low. Id.
9
at 14-15; see also Pet. Ex. 3 at 5 (indicating that these lab results were discussed at a primary care
appointment on January 9, 2014).
On December 12, 2013, Mrs. Halverson had an echocardiogram, which showed an
estimated left ventricle ejection fraction of 45 to 55%. Pet. Ex. 4 at 2; Pet. Ex. 6 at 89; Pet. Ex. 7
at 96. Her left ventricular systolic function was most likely depressed but had markedly improved
since the last study. Id. She had stage III abnormal diastolic function compatible with elevated left
ventricular filling pressure. Pet. Ex. 4 at 2-3; Pet. Ex. 6 at 89-90; Pet. Ex. 7 at 96-97. She also had
mild tricuspid regurgitation. Pet. Ex. 4 at 3; Pet. Ex. 6 at 90; Pet. Ex. 7 at 97.
Petitioner accompanied Mrs. Halverson to this appointment with Dr. Arluck on December
12, 2013. Tr. 19, 45. According to petitioner, Dr. Arluck “tweaked” the AICD and said that it
needed a little adjustment, but that Mrs. Halverson was “doing fine.” Tr. 45. Petitioner stated that
Dr. Arluck “was one of the best pacemaker doctors in the country for that defibrillator pacemaker”
and had written 11 books on the subject. Tr. 45-46. Petitioner testified that, at this time, Mrs.
Halverson was upbeat and strong. Tr. 9, 46.
Petitioner recounted that on January 7 and 8, Mrs. Halverson “started to get a cough and
started sneezing with congestion,” which he described as a “slight cold.” Tr. 8, 47. Petitioner did
not recall having similar symptoms. Tr. 24. “I don’t think so, but if I did, it wasn’t very severe, to
me.” Tr. 24. Petitioner did not recall Mrs. Halverson being fatigued or having shortness of breath.
Tr. 25-26. He recalled that they were talking about taking a trip. Tr. 26.
On January 9, 2014, Mrs. Halverson presented to Dr. Sparagna for a sick visit for nasal
congestion, a loose but non-productive cough, “clogged” ears, and a scratchy throat for three days.
Pet. Ex. 3 at 5. She also complained of numbness in her feet, fatigue, and occasional shortness of
breath. Id. She reported difficulty hearing but no ear pain. Id. She walked with a cane for balance.
Id. Upon exam, her heart rate was “regularly irregular” but she did not have difficulty breathing or
shortness of breath. Id. She was noted to have hyperlipidemia, hypertension, type II diabetes,
complete atrioventricular block, chronic ischemic heart disease, and an upper respiratory infection.
Id. at 5, 7. Dr. Sparagna recommended Mucinex, saline nasal spray, and Tylenol or Advil. Id. at 7.
She was administered Fluzone on that day. Id. at 2.
Petitioner recalled Mrs. Halverson receiving a flu shot during the appointment with Dr.
Sparagna on January 9, 2014 and a prescription for her nasal congestion. Tr. 9, 10. Petitioner noted
that Mrs. Halverson had diabetic neuropathy in her feet and “wasn’t sure of herself walking up and
down steps…or on uneven pavement, so she used the cane for balance” but “[s]he very rarely used
the cane in the house.” Tr. 25-26. He recalled after the doctor’s appointment going together to Rite
Aid to fill the prescription. Tr. 26. Mrs. Halverson did not have any difficulty walking around the
drug store. Tr. 26.
According to the medical records, Mrs. Halverson received a tetanus-diphtheria vaccine in
2004; a diphtheria-tetanus-acellular pertussis vaccine on April 27, 2011; a pneumococcal vaccine
on October 15, 2011; and a seasonal influenza preservative-free vaccine on October 9, 2012,
without event. Pet. Ex. 3 at 9. January 9, 2014 was the first time Mrs. Halverson received Fluzone,
the high-dose flu vaccine.
10
B. Mrs. Halverson’s Health After Receiving the Fluzone
According to petitioner, Mrs. Halverson experienced “rapid degeneration” following the
Fluzone vaccination. Tr. 11. About an hour after they ate dinner the night of the vaccination, Mrs.
Halverson began vomiting and “continued to vomit every couple of hours.” Tr. 11. She barely
slept “because she kept throwing up, and she had a tremendous cough because of it…” Tr. 11.
Petitioner recalled Mrs. Halverson coughing throughout the night and into the next
morning, January 10. Tr. 11. She had dry heaves. Tr. 28. She also started to lose her voice and her
hearing. Tr. 12. She told him that her arms were numb and tingling. Tr. 12. She described it “like
when your foot goes to sleep.” Tr. 19. Tr. She had less than half of her normal energy. Tr. 12. She
had to use a cane in the house when she normally only used it when she left the house. Tr. 12. He
had to make sure that she could walk to the bathroom. Tr. 12-13.
According to petitioner, over the next several days, Mrs. Halverson continued to
deteriorate. By Monday, January 13, she was “sitting there in a zombie-like state on the couch.”
Tr. 14, 18. She asked petitioner to lower a window shade that was about two feet away from the
couch, where she was sitting. Tr. 14. Petitioner told her that if she could not lower the window
shade in ten minutes, he would call an ambulance to take her to the hospital. Tr. 14. It took her the
full ten minutes to stand up from the chair and lower the shade. Tr. 14-15. Petitioner asked her to
go to the hospital or the doctor, but she resisted. Tr. 15. Finally, around 7:00 pm that night, she
agreed that he could take her to the hospital. Tr. 15. She needed to go to the bathroom, but she
could not walk, so petitioner carried her to the bathroom. Tr. 15-16. While she was in the bathroom,
petitioner called Mrs. Halverson’s sister, Linda, to ask her advice. Linda agreed that Mrs.
Halverson needed to go to the hospital. Tr. 16. Petitioner recalled that, while he was on the phone,
his wife called to him and then collapsed. He called 911. He was a volunteer fireman and trained
in CPR, so he began performing CPR on Mrs. Halverson. The paramedics arrived and performed
CPR and “shocked” her. Tr. 16; Pet. Ex. 9 at 20-21. According to petitioner, the paramedics were
there for over an hour. Tr. 16. “[T]hey said they didn’t revive her…but they cannot (sic) pronounce
her dead, so they took her to the hospital.” Tr. 16.
Mrs. Halverson arrived at Shore Medical Center in cardiorespiratory arrest. Pet. Ex. 9 at
16. Petitioner reported to hospital personnel that Mrs. Halverson had been ill for the “past few
days” with an upper respiratory infection, malaise, weakness, decreased intake, cough, shortness
of breath, nausea, vomiting, “retching,” and congestion; she had an internal defibrillator. Id. at 16-
17. She had “finally” agreed to go to the hospital and went to change her clothes first. Id. He called
911 and found her in the bathroom slumped over on the toilet. Id. He laid her on the floor and
started CPR. Id. He reported that she had complained of shortness of breath before she collapsed.
Id.
The hospital notes show that BLS (Basic Life Support) arrived and shocked Mrs. Halverson
twice with an AED (automated external defibrillator), then medics arrived and shocked her an
additional two times, while CPR continued with attempted failed intubation. Pet. Ex. 9 at 16. BVM
(bag valve mask) was used to oxygenate. Id. During transport, she was shocked twice by medics
and given IV epinephrine. Id. Upon arrival at the hospital, Mrs. Halverson had pacer spikes without
a pulse; pacer spikes ceased with magnet placement. Id. Mrs. Halverson was intubated. Id. There
11
was no response to medical therapy. Id. at 17. Mrs. Halverson was shocked multiple times in the
emergency room without success. Id. She was pronounced deceased at 11:14 pm. Id.
The immediate cause of death was cardiac arrest due to ischemic heart disease. Pet. Ex. 2
at 1. Other significant conditions contributing to death were diabetes myelitis, hyperlipidemia,
arrhythmia and hypertension. Id. An autopsy was not performed. Id.
A note by Dr. Sparagna dated January 14, 2014, stated that he spoke with petitioner, who
informed him that Mrs. Halverson had been ill and unable to breathe well for a few hours
“yesterday.” Pet. Ex. 4 at 62. Dr. Sparagna noted that petitioner told him, “Her defibrillator
warning system did not go off. She suddenly fell to the floor, dead.” Id.
At hearing, petitioner recalled that, after Mrs. Halverson’s death, Dr. Sparagna called him
and asked what happened. Tr. 40. Petitioner testified that he did not tell Dr. Sparagna that Mrs.
Halverson’s defibrillator warning system did not go off or make any statements about Mrs.
Halverson’s pacemaker and did not know whether or not her pacemaker fired. Tr. 17, 40-41.
Petitioner stated that he did not know how the AICD worked and he would not know what it would
look like if it did not go off. Tr. 41. He testified that he never saw the AICD “shock” Mrs.
Halverson. Tr. 34.
IV. The Experts
A. Petitioner’s Experts
1. Robert Stark, M.D.
Dr. Stark received his M.D. from Harvard Medical School, where he graduated with
honors. Pet. Ex. 21 at 1. While at Harvard, he carried out a four-year research project in the
Genetics Unit which focused on metabolic disorders and mutations in human cells in culture. Pet.
Ex. 20 at 2. He then served as a clinical associate, a cardiology fellow, and the chief resident at the
National Heart, Lung, and Blood Institute at the National Institutes of Health (“NIH”). Pet. Ex. 21
at 1. At the NIH, Dr. Stark carried out parallel biochemical and cellular studies investigating
cholesterol metabolism and biochemical risk factors for heart attack. Pet. Ex. 20 at 2. He is board
certified in internal medicine and cardiovascular disease. Pet. Ex. 21 at 2. Dr. Stark was a clinical
cardiologist and internist at Greenwich Hospital, where he chaired the Cardiopulmonary
Resuscitation Committee. Id. at 3; Pet. Ex. 20 at 2. He currently teaches preventive cardiology at
the New York Medical College; he estimated that he spends five to ten percent of his time teaching.
Tr. 76. He also has a private clinical practice. Tr. 104.
2. Gourang Patel, Pharm.D
Dr. Patel is a clinical pharmacist in the areas of pharmacy and pharmacology/toxicology at
RUSH University Medical Center (RUSH), where he also has teaching appointments in several
departments, including Pharmacy, Pharmacology, Anesthesiology, and Pulmonary and Critical
Medicine. Pet. Ex. 22 at 1. He works with a clinical care team which includes the attending
physician, resident, intern, and nurse to put together the patient’s drug therapy plan, focusing on
12
maximizing benefits to the patient and minimizing side effects. Tr. 64. Dr. Patel is familiar with
flu vaccine preparations and the pharmacology/toxicology of the flu vaccine, including its effect
on the cardiovascular system and subsequent sequelae. Pet. Ex. 22 at 1.
B. Respondent’s Experts
1. Joseph Murphy, M.D.
Dr. Joseph Murphy received his medical degree from University College Cork in Ireland.
Resp. Ex. B at 2. He completed a year-long research fellowship in cellular cardiology at Harvard
Medical School, followed by additional fellowships in clinical cardiology and invasive cardiology
at the Mayo Clinic. Id. Dr. Murphy has been in full-time clinical practice as an attending
cardiologist at the Mayo Clinic since 1990. Id.; Tr. 146. He is board certified in internal medicine,
cardiology, transplant cardiology, and advanced heart failure. Resp. Ex. B at 3; Tr. 146. Dr.
Murphy’s interests include critical care cardiology, pulmonary hypertension, and valvular heart
disease. Resp. Ex. A at 2. Dr. Murphy estimated that 50 percent of his patients have advanced heart
failure due to a variety of conditions. Tr. 148. He sends two or three patients per week to have
AICDs placed. Tr. 148. He published an article on vaccine-associated myocarditis after treating
Army members who had cardiac complications following receipt of a smallpox vaccine. Tr. 150-
51.
2. Noel Rose, M.D., Ph.D.
Dr. Rose is a Professor Emeritus at Johns Hopkins University, with appointments in the
departments of Pathology and Medicine, Microbiology and Immunology, and Environmental
Health Sciences. Resp. Ex. D at 1; Resp. Ex. E at 1. He was the founding director of the Johns
Hopkins Center for Autoimmune Disease Research and is the former director of the Division of
Immunology in the Department of Pathology and former Chairman in the Department of
Immunology and Infectious Diseases. Id. He is presently a senior lecturer in the Department of
Pathology at Brigham and Women’s Hospital. Id. Dr. Rose is board certified in clinical pathology,
microbiology, and laboratory immunology. Tr. 237-38. His practice does not involve treating
patients. Tr. 243. Dr. Rose’s published works include the Manual of Clinical Immunology, a
textbook of immunology applied to medical practice. Tr. 234. He is also a co-editor of the textbook
The Autoimmune Disease. Tr. 234-35.
V. Legal Framework
The Vaccine Act provides two avenues for petitioners to receive compensation. First, a
petitioner may demonstrate a “Table” injury—i.e., an injury listed on the Vaccine Injury Table
that occurred within the provided time period. § 11(c)(1)(C)(i). “In such a case, causation is
presumed.” Capizzano v. Sec’y of Health & Human Servs., 440 F.3d 1317, 1320 (Fed. Cir. 2006);
see § 13(a)(1)(B). Second, where the alleged injury is not listed on the Vaccine Injury Table, a
petitioner may demonstrate an “off-Table” injury, which requires that the petitioner “prove by a
preponderance of the evidence that the vaccine at issue caused the injury.” Capizzano, 440 F.3d at
1320; see § 11(c)(1)(C)(ii). Initially, a petitioner must provide evidence that he or she suffered, or
continues to suffer, from a definitive injury. Broekelschen v. Sec’y of Health & Human Servs., 618
13
F.3d 1339, 1346 (Fed. Cir. 2010). A petitioner need not show that the vaccination was the sole
cause, or even the predominant cause, of the alleged injury; showing that the vaccination was a
“substantial factor” and a “but for” cause of the injury is sufficient for recovery. See Pafford v.
Sec’y of Health & Human Servs., 451 F.3d 1352, 1355 (Fed. Cir. 2006); Shyface v. Sec’y of Health
& Human Servs., 165 F.3d 1344, 1352 (Fed. Cir. 1999).14
To prove causation for an “off-Table” injury, petitioners must satisfy the three-pronged test
established in Althen v. Sec’y of Health & Human Servs., 418 F.3d 1274 (Fed. Cir. 2005). Althen
requires that petitioners show by preponderant evidence that a vaccination petitioner received
caused his or her injury “by providing: (1) a medical theory causally connecting the vaccination
and the injury; (2) a logical sequence of cause and effect showing that the vaccination was the
reason for the injury; and (3) a showing of a proximate temporal relationship between vaccination
and injury.” Id. at 1278. Together, these prongs must show “that the vaccine was ‘not only a but-
for cause of the injury but also a substantial factor in bringing about the injury.’” Stone v. Sec’y of
Health & Human Servs., 676 F.3d 1373, 1379 (Fed. Cir. 2012) (quoting Shyface, 165 F.3d at 1352-
53). Causation is determined on a case-by-case basis, with “no hard and fast per se scientific or
medical rules.” Knudsen v. Sec’y of Health & Human Servs., 35 F.3d 543, 548 (Fed. Cir. 1994).
Petitioners are not required to identify “specific biological mechanisms” to establish causation,
nor are they required to present “epidemiologic studies, rechallenge, the presence of pathological
markers or genetic disposition, or general acceptance in the scientific or medical communities.”
Capizzano, 440 F.3d at 1325 (quoting Althen, 418 F.3d at 1280). “[C]lose calls regarding causation
are resolved in favor of injured claimants.” Althen, 418 F.3d at 1280.
Each of the Althen prongs requires a different showing. Under the first Althen prong,
petitioner must provide a “reputable medical theory” demonstrating that the vaccine received can
cause the type of injury alleged. Pafford, 451 F.3d at 1355-56 (citation omitted). To satisfy this
prong, petitioner’s “theory of causation must be supported by a ‘reputable medical or scientific
explanation.’” Andreu ex rel. Andreu v. Sec’y of Health & Human Servs., 569 F.3d 1367, 1379
(Fed. Cir. 2009) (quoting Althen, 418 F.3d at 1278). This theory need only be “legally probable,
not medically or scientifically certain.” Id. at 1380 (emphasis omitted) (quoting Knudsen, 35 F.3d
at 548). Nevertheless, “petitioners [must] proffer trustworthy testimony from experts who can find
support for their theories in medical literature.” LaLonde v. Secretary of Health & Human Servs.,
746 F.3d 1334, 1341 (Fed. Cir. 2014).
The second Althen prong requires proof of a “logical sequence of cause and effect.”
Capizzano, 440 F.3d at 1326 (quoting Althen, 418 F.3d at 1278). Even if the vaccination can cause
the injury, petitioner must show “that it did so in [this] particular case.” Hodges v. Sec’y of Health
& Human Servs., 9 F.3d 958, 962 n.4 (Fed. Cir. 1993) (citation omitted). “A reputable medical or
scientific explanation must support this logical sequence of cause and effect,” id. at 961 (citation
omitted), and “treating physicians are likely to be in the best position to determine whether a
logical sequence of cause and effect show[s] that the vaccination was the reason for the injury,”
14
The Vaccine Act also requires petitioners to show by preponderant evidence the vaccinee suffered from
the “residual effects or complications” of the alleged vaccine-related injury for more than six months, died
from the alleged vaccine-related injury, or required inpatient hospitalization and surgical intervention as a
result of the alleged vaccine-related injury. § 11(c)(1)(D). It is undisputed that this requirement is satisfied
in this case.
14
Paluck v. Sec’y of Health & Human Servs., 786 F.3d 1373, 1385 (Fed. Cir. 2015) (quoting Andreu,
569 F.3d at 1375).
The third Althen prong requires that petitioner establish a “proximate temporal
relationship” between the vaccination and the alleged injury. Althen, 418 F.3d at 1281. This
“requires preponderant proof that the onset of symptoms occurred within a timeframe for which,
given the medical understanding of the disorder’s etiology, it is medically acceptable to infer
causation-in-fact.” De Bazan v. Sec’y of Health & Human Servs., 539 F.3d 1347, 1352 (Fed. Cir.
2008). Typically, “a petitioner’s failure to satisfy the proximate temporal relationship prong is due
to the fact that onset was too late after the administration of a vaccine for the vaccine to be the
cause.” Id. However, “cases in which onset is too soon” also fail this prong; “in either case, the
temporal relationship is not such that it is medically acceptable to conclude that the vaccination
and the injury are causally linked.” Id.; see also Locane v. Sec’y of Health & Human Servs., 685
F.3d 1375, 1381 (Fed. Cir. 2012) (“[If] the illness was present before the vaccine was administered,
logically, the vaccine could not have caused the illness.”).
A petitioner may also be eligible for compensation if the vaccinee had a preexisting
condition which was significantly aggravated by a vaccine. See § 11(c)(1)(C). In considering a
significant aggravation claim for an on-Table injury, the Federal Circuit placed the most
significance on whether petitioner’s symptoms began within the time period proscribed.
Whitecotton v. Sec’y of Health & Human Servs., 81 F.3d 1099, 1107 (Fed. Cir. 1996) (“Instead of
asking whether the person's symptoms would have occurred absent the vaccine, our test hoves
close to the statutory mandate, and relieves a petitioner of the burden of proving causation if she
can show that the first symptom or manifestation of the significant aggravation of her condition
occurred within the table time period provided in the statute.”).
For a significant aggravation claim for an off-Table injury, the petitioner’s burden is
expanded to six elements, requiring petitioner to show, by preponderant evidence, proof of
(1) the person’s condition prior to administration of the vaccine, (2) the person’s
current condition (or the condition following the vaccination if that is also
pertinent), (3) whether the person’s current condition constitutes a “significant
aggravation” of the person’s condition prior to vaccination, (4) a medical theory
causally connecting such a significantly worsened condition to the vaccination, (5)
a logical sequence of cause and effect showing that the vaccination was the reason
for the significant aggravation, and (6) a showing of a proximate temporal
relationship between the vaccination and the significant aggravation.
Loving ex rel. Loving v. Sec’y of Health & Human Servs., 86 Fed. Cl. 135, 144 (2009). The fourth,
fifth, and sixth factors are derived from Althen prongs one, two, and three, respectively. Id. The
Federal Circuit has agreed with this approach. See W.C. v. Sec’y of Health & Human Servs., 704
F.3d 1352, 1357 (Fed. Cir. 2013) (“We hold that the Loving case provides the correct framework
for evaluating off-table significant aggravation claims.”)
However, the third Loving factor, determining whether the person suffered a “significant
aggravation” of his or her condition, leads to the question of what constitutes a significant
15
aggravation. Based on the legislative history and the language of the statute, it appears that
Congress intended for a “significant aggravation” of a condition to present rather dramatically. See
H.R. Rep. 908, 99th Cong.2d Sess. 1, reprinted in 1986 USCCAN 6287, 6356 (“This [significant
aggravation] provision does not include compensation for conditions which might legitimately be
described as preexisting (e.g., a child with monthly seizures who, after vaccination, has seizures
every three and a half weeks), but is meant to encompass serious deterioration (e.g., a child with
monthly seizures who, after vaccination, has seizures on a daily basis” (emphasis added)); see also
42 U.S.C. § 300aa-33(4) (“The term “significant aggravation” means any change for the worse in
a preexisting condition which results in markedly greater disability, pain, or illness accompanied
by substantial deterioration of health” (emphases added)).
Once a petitioner has established that his or her condition worsened post-vaccination, the
special master must determine “whether the change for the worse in [petitioner’s] clinical
presentation was aggravation or a natural progression” of the preexisting condition. Hennessey,
2009 WL 1709053 at *42. In doing so, special masters have relied on evidence supporting the
“typical” clinical course of the petitioner’s condition. See, e.g., Locane, 685 F.3d at 1381-82
(Special master’s determination that petitioner’s Crohn’s disease was not significantly aggravated
by her hepatitis B vaccinations where her disease flare-ups after her first and third vaccinations
were typical of frequent flares in adolescents’ expected course of Crohn’s disease was reasonable);
Faoro v. Sec'y of Health & Human Servs., No. 10-704V, 2016 WL 675491, at *27 (Fed. Cl. Spec.
Mstr. Jan. 29, 2016), mot. for review denied, 128 Fed. Cl. 61 (Fed. Cl. Apr. 11, 2016) (finding that
“the vaccinations would not have changed her clinical course and thus, the vaccinations did not
significantly aggravate her preexisting condition”).
The process for making factual determinations in Vaccine Program cases begins with
analyzing the medical records, which are required to be filed with the petition. § 11(c)(2). Medical
records created contemporaneously with the events they describe are presumed to be accurate and
“complete” such that they present all relevant information on a patient’s health problems. Cucuras
v. Sec’y of Health & Human Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993). In making
contemporaneous reports, “accuracy has an extra premium” given that the “proper treatment
hang[s] in the balance.” Id. Contemporaneous medical records that are clear, consistent, and
complete warrant substantial weight “as trustworthy evidence.” Id. Indeed, “where later testimony
conflicts with earlier contemporaneous documents, courts generally give the contemporaneous
documentation more weight.” Campbell ex rel. Campbell v. Sec’y of Health & Human Servs., 69
Fed. Cl. 775, 779 (2006); see United States v. U.S. Gypsum Co., 333 U.S. 364, 396 (1948). But
petitioners can support their claim with oral testimony if it is credible and consistent with the
medical records. See, e.g., Stevenson ex rel. Stevenson v. Sec’y of Health & Human Servs., No. 90-
2127V, 1994 WL 808592, at *7 (Fed. Cl. Spec. Mstr. June 27, 1994) (crediting the testimony of a
fact witness whose “memory was sound” and “recollections were consistent with the other factual
evidence”). In short, “the record as a whole” must be considered. § 13(a).
Furthermore, establishing a sound and reliable medical theory connecting the vaccine to
the injury often requires a petitioner to present expert testimony in support of his or her claim.
Lampe v. Sec’y of Health & Human Servs., 219 F.3d 1357, 1361 (Fed. Cir. 2000). The Supreme
Court’s opinion in Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579 (1993), requires
that courts determine the reliability of an expert opinion before it may be considered as evidence.
16
“In short, the requirement that an expert’s testimony pertain to ‘scientific knowledge’ establishes
a standard of evidentiary reliability.” Id. at 590 (citation omitted). Thus, for Vaccine Act claims, a
“special master is entitled to require some indicia of reliability to support the assertion of the expert
witness.” Moberly ex rel. Moberly v. Sec’y of Health & Human Servs., 592 F.3d 1315, 1324 (Fed.
Cir. 2010). The Daubert factors are used in the weighing of the reliability of scientific evidence
proffered. Davis v. Sec’y of Health & Human Servs., 94 Fed. Cl. 53, 66-67 (2010) (“uniquely in
this Circuit, the Daubert factors have been employed also as an acceptable evidentiary-gauging
tool with respect to persuasiveness of expert testimony already admitted”). Where both sides offer
expert testimony, a special master’s decision may be “based on the credibility of the experts and
the relative persuasiveness of their competing theories.” Broekelschen v. Sec’y of Health & Human
Servs., 618 F.3d 1339, 1347 (Fed. Cir. 2010) (citing Lampe, 219 F.3d at 1362). And nothing
requires the acceptance of an expert’s conclusion “connected to existing data only by the ipse dixit
of the expert,” especially if “there is simply too great an analytical gap between the data and the
opinion proffered.” Snyder ex rel. Snyder v. Sec’y of Health & Human Servs., 88 Fed. Cl. 706, 743
(2009) (quoting Gen. Elec. Co. v. Joiner, 522 U.S. 136, 146 (1997)).
Finally, although this decision discusses much but not all of the literature in detail, the
undersigned reviewed and considered all of the medical records and literature submitted in this
matter. See Moriarty ex rel. Moriarty v. Sec’y of Health & Human Servs., 844 F.3d 1322, 1328
(Fed. Cir. 2016) (“We generally presume that a special master considered the relevant record
evidence even though [s]he does not explicitly reference such evidence in h[er] decision.”);
Simanski v. Sec’y of Health & Human Servs., 115 Fed. Cl. 407, 436 (2014) (“[A] Special Master
is ‘not required to discuss every piece of evidence or testimony in her decision.’” (citation
omitted)), aff’d, 601 F. App’x 982 (Fed. Cir. 2015).
VI. Discussion
Because petitioner does not allege an injury listed on the Vaccine Injury Table, his claim
is classified as “off-Table.” As noted above, for petitioner to prevail on an “off-Table” claim, he
must show by preponderant evidence that the influenza vaccine at issue either caused Mrs.
Halverson’s cardiac arrest and subsequent death or significantly aggravated her preexisting
ischemic heart disease. Capizzano, 440 F.3d at 1320. Doing so shifts the burden to respondent to
show that Mrs. Halverson’s injuries and death were caused by factors unrelated to the vaccination.
Deribeaux, 717 F.3d at 1367.
Due to the requirement to prove causation, one special master has recommended evaluating
“the last three Loving factors first.” Hennessey v. Sec'y of Health & Human Servs., No. 01–190V,
2009 WL 1709053, at *42 (Fed. Cl. Spec. Mstr. May 29, 2009), motion for review denied, 41 Fed.
Cl. 126 (2010).
A. Althen Prong 1/Loving Factor 4: Reputable Medical Theory
Petitioner’s experts opined that Fluzone can cause a systemic inflammatory response,
sometimes referred to as “systemic inflammatory response syndrome,” or “SIRS.” Dr. Stark
explained that SIRS can cause a variety of cardiac complications, including sudden cardiac death
and myocardial infarction. See Pet. Ex. 18 at 3.
17
1. Fluzone can cause a systemic inflammatory response
According to Dr. Stark, Fluzone15 is an immunologically enhanced alternative to the
conventional flu vaccine and confers greater protection against infection than the conventional
vaccine. Pet. Ex. 18 at 1. He emphasized that Fluzone is “a highly immunogenic flu vaccine that
triggers an enhanced antibody response and systemic inflammation.” Pet. Ex. 19 at 3. “This
vaccine is deliberately enhanced to form more antibodies, [and] more immune response . . .”. Tr.
91. As a result, Fluzone induces a greater immune response than the regular flu vaccine. Pet. Ex.
18 at 4. Dr. Patel added that Fluzone contains three strains of three different types of viruses. Tr.
52. Both Dr. Stark and Dr. Patel added that Fluzone contains four times more antigen than the
regular seasonal flu vaccine. Tr. 53; Pet. Ex. 18 at 4. According to Dr. Patel, if a person who had
symptoms of an upper respiratory infection (“URI”) received Fluzone, the effects of the vaccine
would be magnified, because the immune system would already be activated by the URI. Tr. 58.
Respondent’s experts agreed that Fluzone is a powerful vaccine. Dr. Murphy stated that
the influenza A vaccine “excites a strong immune reaction as it is designed to do, with spillover
effects on many biological systems and functions that can be clearly demonstrated on laboratory
testing.” Resp. Ex. A at 23. Dr. Rose explained that flu vaccines contain a purified protein called
hemagglutinin, which causes agglutination, or clumping, of red blood cells. Tr. 255; Resp. Ex. D
at 2. Fluzone contains four times the usual amount of hemagglutinin found in the standard seasonal
flu vaccine. Resp. Ex. D at 2; Tr. 257. Dr. Rose noted that, in a study of 30,000 patients who
randomly receive either the high-dose or standard-dose flu vaccine, “[a]ntibody levels to the
influenza hemagglutinin were significantly higher in the high dose group.” Resp. Ex. D at 3; Resp.
Ex. D, Tab 3.16
Petitioner’s experts opined that patients are more likely to develop adverse events in
response to Fluzone than the standard-dose flu vaccine. Dr. Stark stated that the CDC has reported
a higher rate of adverse events in Fluzone recipients when compared with patients receiving the
conventional flu vaccine. Pet. Ex. 17 at 2; Pet. Ex. 18 at 4.17 According to Dr. Stark, cardiac
disorders and infections are the most frequent types of serious adverse events reported. Pet. Ex. 18
at 4. Dr. Patel noted that a higher rate of generalized weakness is reported by patients who receive
Fluzone than patients who receive a regular flu vaccination. Pet. Ex. 22 at 2.
Both of petitioner’s experts cited statistics on adverse events following Fluzone. Dr. Stark
noted that about 30% of patients develop an immune/hypersensitivity reaction at the injection site
within three days of immunization, while 8 to 10% of patients develop systemic reactions,
15
Dr. Murphy explained that elderly patients have diminished immune responses when compared to
younger patients. Resp. Ex. O at 3. Fluzone, a more potent vaccine, is given to combat this effect. Id.
16
Carlos A. Diaz Granados, et al., Efficacy of High-Dose versus Standard-Dose Influenza Vaccine in Older
Adults, 371 N. ENGL. J. MED. 7: 635-45 (2014), filed as “Pet. Ex. 11,” “Pet. Ex. 30,” and “Resp. Ex. D, Tab
3.”
17
As a reference for this statement, Dr. Stark cited “Centers for Disease Control “Fluzone-High Dose
Influenza Vaccine” 8/19/15.” See Pet. Ex. 18 at 5. This reference was not filed as an exhibit.
18
including myalgias, malaise, fever, and headache in response to the vaccine. Pet. Ex. 18 at 2. Dr.
Stark also referenced literature showing that the flu vaccine can cause the production of
inflammatory substances measurable in the blood stream, such as cytokines, including tumor
necrosis factor (“TNF”), and migration-inhibitory factor (“MIF”). Pet. Ex. 20 at 2; Resp. Ex. D,
Tab 13.18 “It is well recognized that inflammatory products lead to increased platelet aggregation
and blood clotting.” Pet. Ex. 20 at 2. According to Dr. Patel, up to 30% of patients develop an
immune phenomenon which can trigger a host of responses, including increased coagulation and
systemic/local vessel spasm, collectively referred to as systemic inflammatory response syndrome
(“SIRS”). Pet. Ex. 22 at 2. According to Dr. Patel, SIRS presents as “a whole body malaise,
deterioration and fatigue…” and usually has an identifiable trigger. Tr. 72.
2. A systemic inflammatory response affects cardiac function
Dr. Stark explained that the systemic inflammatory response triggered by Fluzone can
cause an increase in platelet aggregation, which can lead to coronary obstruction or heart attack
and result in cardiac arrest. The inflammatory response can also increase cardiac autonomic
function, which can lead to cardiac arrythmias.
Drs. Stark and Patel opined that Fluzone can trigger a systemic inflammatory response
which increases platelet aggregation, thereby increasing blood clotting. See Pet. Ex. 18 at 2; Pet.
Ex. 19 at 3; Pet. Ex. 22 at 4. Dr. Patel added that a systemic inflammatory reaction will also cause
increased blood pressure and heart rate; the increased clotting and systemic and local vessel spasms
caused by SIRS can lead to a significant imbalance in oxygen demand and supply to the heart. Pet.
Ex. 22 at 2, 4. The lack of oxygen ultimately leads to myocardial ischemia and myocardial
infarction, which can trigger cardiac arrest. Id.
According to Dr. Stark, inflammation, allergic reaction, or infection can cause white blood
cells to generate substances which cause platelets to become stickier; the platelets become more
likely to clump and cause blockages. Tr. 90. Platelet activation has a prothrombotic effect that
increases the risk of coronary obstruction and myocardial infarction in patients with underlying
coronary artery disease. Pet. Ex. 18 at 2-3. A systemic inflammatory response can also trigger
cardiac autonomic dysfunction by increasing heart rate and elevating contractility. Id. at 2; Pet.
Ex. 19 at 2. Cardiac autonomic dysfunction predisposes individuals to potentially fatal ventricular
arrhythmias, particularly if the coronary arteries are already compromised. Pet. Ex. 18 at 2-3. Dr.
Stark explained that an increased immune response can affect the balance between two nerves that
regulate the heartbeat. Tr. 91-92. “The vagus nerve makes the heart beat slower, and relax a little
bit, [and] the sympathetic nerve makes the heart beat faster and harder.” Tr. 92. “When you get an
immunization, and you induce an immune response, the balance between vagal stimuli slowing
the heart and sympathetic stimuli speeding up the heart, that balance is thrown off and that’s not
good for you if your heart is already impaired in any way.” Tr. 92.
To support his theory, Dr. Stark offered the Lanza paper, which found, “Together with an
inflammatory reaction, influenza A vaccine induced platelet activation and sympathovagal
imbalance…suggesting a pathophysiological link between inflammation and cardiac autonomic
18
Lisa M. Christian et al., Proinflammatory cytokine responses correspond with subjective side effects after
influenza virus vaccination, 33 VACCINE 3360-66 (2015), filed as “Resp. Ex. D, Tab 13.”
19
regulation. The vaccine-related platelet activation and cardiac autonomic dysfunction may
transiently increase the risk of cardiovascular events.” Pet. Ex. 10 at 1; Pet. Ex. 28 at 1.19 This was
a smaller study and the authors did not conclude that there is a direct causal relationship between
inflammatory stimulus and platelet activation. However, the study did find a correlation between
influenza vaccination and cardiac autonomic imbalance which warranted further investigation.
Similarly, a study by Willerson and Ridker found that “[e]pidemiological and clinical studies have
shown strong and consistent relationships between markers of inflammation and risk of future
cardiovascular events.” Pet. Ex. 33 at 1.20
Dr. Patel explained that platelets have a role in the immune system, engulfing antigens in
the body, whether the antigens are bacteria or vaccines. Tr. 58. When a vaccine is introduced to
the body, the platelets aggregate around the antigen, causing clumping. Tr. 58. Dr. Patel offered
four studies analyzing adverse cardiac events following flu vaccine. A 2012 study by Moro found
that, between July 2010 and December 2010, the Vaccine Adverse Event Reporting System
(“VAERS”) received 606 reports of people 65 years and older who experienced adverse events
after receiving a high-dose influenza vaccine. Pet. Ex. 12 at 1.21 Of 51 reports considered serious
events, nine (18%) were cardiac events; all nine patients had preexisting cardiac conditions. Id. at
3. In contrast, cardiac events were only 5% of serious events occurring after a standard-dose
influenza vaccine. Id. The authors concluded that adverse event reporting for cardiac events may
be “unexpectedly higher” after receipt of the high-dose flu vaccine than the standard-dose flu
vaccine. Id. at 5.
In 2013, Moro issued another study of patients who received an intradermal flu vaccine;
three out of the nine serious events were cardiac events. See Pet. Ex. 14 at 2-3.22 The only fatal
event was an 88-year-old woman who had sudden cardiac death 16 days after vaccination. Id. at
3.
Additionally, Haber studied adults 18 to 49 years old who received the standard-dose
trivalent flu vaccine between 2005 and 2013; of 107 serious events, 14 patients (13.6%)
experienced cardiac adverse events, including myocardial infarction and arrhythmias. Pet. Ex. 13
19
Gaetano A. Lanza et al., Inflammation-related effects of adjuvant influenza A vaccination on platelet
activation and cardiac autonomic function, 269 J. INTERN. MED. 118-25 (2011), filed as “Pet. Ex. 10” and
“Pet. Ex. 28.”
20
James T. Willerson and Paul M. Ridker, Inflammation as a Cardiovascular Risk Factor, 109
CIRCULATION 21: 2-10 (2004), filed as “Pet. Ex. 33.”
21
Pedro L. Moro et al., Postlicensure Safety Surveillance for High-Dose Trivalent Inactivated Influenza
Vaccine in the Vaccine Adverse Event Reporting System, 1 July 2010-31 December 2010, 54 CLIN. INFECT.
DIS. 11: 1608-14 (2012), filed as “Pet. Ex. 12,” “Pet. Ex. 25,” and “Pet. Ex. 29.”
22
Pedro L. Moro et al., Adverse events after Fluzone Intradermal vaccine reported to the Vaccine Adverse
Event Reporting System (VAERS), 2011-2013, 31 VACCINE 4984-87 (2013), filed as “Pet. Ex. 14.”
20
at 1, 3.23 In six of the 14 adverse events, smallpox vaccine was given concurrently with the flu
vaccine. Id. at 4. Another Haber study which examined adverse events following the quadrivalent
flu vaccine found nine serious events, two of which were cardiovascular and included myocardial
infarction. Pet. Ex. 15 at 3.
Dr. Rose criticized Dr. Patel’s reliance on the Moro and Haber studies due to their use of
data from VAERS. Drs. Stark, Patel, and Rose agreed that VAERS is a passive reporting system
and that VAERS data cannot be used to establish a causal relationship between a vaccine and a
certain adverse event. Pet. Ex. 20 at 1; Tr. 68, 287.
Ultimately, however, Dr. Rose seemed to agree that systemic inflammation can affect
cardiac autonomic function. See Resp. Ex. V at 3 (“A recent review…discusses our current
understanding of the role of inflammation in the pathogenesis of atrial fibrillation, a common
manifestation of systemic inflammation on the heart.”) He also cited several studies that confirmed
an association between inflammation and atrial fibrillation. Id.; see Resp. Ex. V, Tab 1;24 Resp.
Ex. V, Tab 2;25 Resp. Ex. V, Tab 3;26 Resp. Ex. V, Tab 4;27 Resp. Ex. V, Tab 5.28 Still, he cautioned
that “[t]here is no data to suggest that inflammation is the sole or even major risk factor for atrial
fibrillation.” Resp. Ex. V at 3.
3. Respondent submits that literature does not support petitioner’s theory
Dr. Rose and Dr. Murphy submitted a variety of articles in support of their assertions that
(1) Fluzone does not cause SIRS; (2) Fluzone does not cause adverse cardiovascular events; and
(3) Fluzone protects against adverse cardiovascular events.
According to Dr. Rose, “A clinical definition of SIRS is still under discussion but still
requires a broad array of multi-organ dysfunctions.” Resp. Ex. D at 6, citing Irene Cortes-Puch
and Christiane S. Hartog, Change Is Not Necessarily Progress: Revision of the Sepsis Definition
23
Penina Haber et al., Post-licensure surveillance of trivalent live attenuated influenza vaccine in adults,
United States, Vaccine Adverse Event Reporting System (VAERS), July 2005-June 2013, 32 VACCINE 6499-
6504 (2014), filed as “Pet. Ex. 13.”
24
Yu-Feng Hu et al., Inflammation and the pathogenesis of atrial fibrillation, 12 NAT. REV. CARDIOL. 230-
243 (2015), filed as “Resp. Ex. V, Tab 1.”
25
Anna Borowiec et al., Prospective assessment of cytokine IL-15 activity in patients with refractory atrial
fibrillation episodes, 74 CYTOKINE 1: 164-70 (2015), filed as “Resp. Ex. V, Tab 2.”
26
Renate B. Schnabel et al., Relations of Biomarkers of Distinct Pathophysiological Pathways and Atrial
Fibrillation Incidence in the Community, 121 CIRCULATION 2: 200-07 (2010), filed as “Resp. Ex. V, Tab
3.”
27
Dwayne S.G. Conway et al., Prognostic significance of raised plasma levels of interleukin-6 and C-
reactive protein in atrial fibrillation, 148 AM. HEART J 3: 462-66 (2004), filed as “Resp. Ex. V, Tab 4.”
28
David Conen et al., A multimarker approach to assess the influence of inflammation on the incidence of
atrial fibrillation in women, 31 EUR. HEART J. 1730-36 (2010), filed as “Resp. Ex. V, Tab 5.”
21
Should Be Based on New Scientific Insights, 194 AM. J. RESPIR. CRIT. CARE MED. 16-18 (2016).29
However, he did note that the clinical symptoms associated with SIRS include fever, malaise,
change in heart rate, headache, inordinate fatigue and exhaustion, muscle aches and pains, and
chills. Tr. 263.
Although Dr. Rose agreed that the Sanofi-Pasteur30 literature states that the most common
systemic adverse events associated with Fluzone were myalgia, malaise, and headache, he did not
believe that Fluzone was capable of causing a systemic inflammatory response. Tr. 297. “A
stimulus such as a vaccine comprising purified peptides with no added adjuvant is highly unlikely
to give rise to an uncontrolled, continuing inflammatory response unless the host has some genetic
abnormality or previous experience that would prepare her for such a pathologic reaction.” Resp.
Ex. D at 6. He stated that, regardless of whether one uses the term “out of control inflammatory
syndrome or “enhanced inflammatory response,” there is no objective evidence that Fluzone
induces greater systemic inflammation than the standard flu vaccine. Resp. Ex. V at 2. “Although
there is evidence from clinical trials that the high dose vaccine induces higher levels of circulating
antibody. (sic) There are no published investigations of humans documenting and quantitating an
enhanced, generalized inflammatory response.” Id.
Dr. Rose submitted that the best support for petitioner’s theory that Fluzone can cause SIRS
would be serial studies of blood samples taken periodically after vaccination; however, these
studies are rarely performed in humans. Resp. Ex. D at 5; see also Resp. Ex. D, Tab 13; Resp. Ex.
D, Tab 14;31 Resp. Ex. D, Tab 15;32 Resp. Ex. D, Tab 16.33 Dr. Rose referenced several studies
which have performed these tests, noting that the inconsistent results between studies illustrates
the technical and logistical difficulty in assessing cytokine levels in human blood. Resp. Ex. D at
5.
Dr. Rose opined that a causal connection between Fluzone and an adverse cardiovascular
event would require a “statistical association between high dose Fluzone and the initiation or
enhancement of cardiovascular disease…” Resp. Ex. D at 6. The literature does not support such
an association. He offered several studies in support of this opinion. A 2014 study funded by
Sanofi-Pasteur evaluated the effectiveness of a high-dose trivalent influenza vaccine in adults 65
29
This article was not filed into the record.
30
Sanofi-Pasteur is the manufacturer of Fluzone. 372 Fluzone High-Dose, SANOFI-PASTEUR (Revised July
2017), filed as “Pet. Ex. 31.”)
31
Helder I. Nakaya et al., Systems biology of vaccination for seasonal influenza in humans, 12 NAT
IMMUNOL 8: 786-96 (2011), filed as “Resp. Ex. D, Tab 14.”
32
Petru Liuba et al., Residual adverse changes in arterial endothelial function and LDL oxidation after a
mild systemic inflammation induced by influenza vaccination, 39 ANN. MED. 5: 392-99 (2007), filed as
“Resp. Ex. D, Tab 15.”
33
Michael Y. Tsai et al., Effect of influenza vaccine on markers of inflammation and lipid profile, 145 J.
LAB. CLIN. MED. 6: 323-27 (2005), filed as “Resp. Ex. D, Tab 16.”
22
years of age and older. Resp. Ex. D, Tab 3 at 1-2.34 It found that the high-dose trivalent flu vaccine
“induced significantly higher antibody responses” than the standard-dose flu vaccine. Id. at 1.
However, the study found that the number of deaths following the high-dose vaccine and standard-
dose vaccine was “essentially identical,” and the deaths were classified as unrelated to the vaccine.
Resp. Ex. D at 3; see also Resp. Ex. D, Tab 3 at 6 (stating that 83 of 15,990 participants in the
high-dose group died, as did 84 of 15,993 participants in the standard-dose group).
Dr. Rose also referred to several studies analyzing data from VAERS. Another Moro study
analyzed adverse events following the trivalent standard-dose flu vaccine from 2013 to 2015; of
309 reported adverse events, only five were cardiac events. Resp. Ex. D, Tab 6 at 3.35 The authors
of the study “did not identify any concerning pattern” of adverse events. Id. at 1. Similarly, a Haber
study also analyzed adverse events from 2013 to 2015 but examined the quadrivalent standard-
dose flu vaccine. Resp. Ex. D, Tab 7 at 1.36 Haber found that, of 127 serious reports of adverse
events, there were 12 deaths reported following this flu vaccine from a variety of causes, including
ventricular tachycardia leading to cardiac arrest/cardiogenic shock, dilated cardiomyopathy,
inferior wall myocardial infarction, and heart failure. Id. at 4. There were an additional four reports
of cardiac adverse events. Id. Nonetheless, Haber “did not identify any safety concerns” for the flu
vaccine. Id. at 5.
Additionally, Dr. Rose offered studies which conducted active surveillance, rather than
passive surveillance, of potential adverse effects of the flu vaccine. A Sanofi-Pasteur funded study
examining the effects of Fluzone administered to adults 65 years of age and older showed that 116
out of 319 recipients experienced systemic effects of the vaccine, but only 16 recipients
experienced a serious adverse event. Resp. Ex. D, Resp. at 7.37 According to Dr. Rose, the serious
adverse events consisted of vomiting or severe cough, and none suggested cardiac disease. Resp.
Ex. D at 4. Dr Rose also cited to the 2012 IOM report, which concluded, “The evidence is
inadequate to accept or reject a causal relationship between influenza vaccine and myocardial
infarction.” Resp. Ex. D, Tab 5 at 5.38 The IOM report recognized that, “[w]hile rare, influenza
infection has been associated with myocardial infarction…” it ultimately assessed the evidence of
such an association as “lacking.” Id. at 4. The IOM committee placed great weight on a 2004 study
34
See supra n.16.
35
Pedro L. Moro et al., Surveillance of adverse events after the first trivalent inactivated influenza vaccine
produced in mammalian cell culture (Flucelvax®) reported to the Vaccine Adverse Event Reporting System
(VAERS), United States, 2013-2015, 33 VACCINE 6684-88 (2015), filed as “Resp. Ex. D, Tab 6.”
36
Penina Haber et al., Post-licensure surveillance of quadrivalent inactivated influenza (IIV4) vaccine in
the United States, Vaccine Adverse Event Reporting System (VAERS), July 1, 2013-May 31, 2015, 34
VACCINE 2507-12 (2016), filed as “Resp. Ex. D, Tab 7.”
37
Peter Tsang et al., Immunogenicity and safety of Fluzone intradermal and high-dose influenza vaccines
in older adults ≥65 years of age: A randomized, controlled, phase II trial, 32 VACCINE 2507-17 (2014),
filed as “Resp. Ex. D, Tab 8.”
38
Kathleen Stratton et al., eds., ADVERSE EFFECTS OF VACCINES: EVIDENCE AND CAUSALITY, pp. 387-89
(2012) [“2012 IOM Report”], filed as “Resp. Ex. D, Tab 5.”
23
by Smeeth, which was submitted by respondent’s experts as Resp. Ex. M.39 Smeeth reported that
there was no increased risk of myocardial infarction within one month following influenza
vaccination. Resp. Ex. D, Tab 5 at 4; see also Resp. Ex. M at 1. The IOM committee placed “a
moderate degree of confidence in the epidemiologic evidence based on” the Smeeth study. Id.
Neither the Smeeth study nor the IOM report addressed Fluzone.
Dr. Stark agreed with Dr. Rose there is no epidemiologic evidence suggesting that Fluzone
has a poorer safety record or increased adverse reactions in recipients compared to the standard-
dose flu vaccine but suggested that this was because no one has looked for such a correlation. Pet.
Ex. 17 at 1.
Both of respondent’s experts opined that medical literature does not support the view that
Fluzone can induce or aggravate existing cardiovascular disease. Resp. Ex. D at 4; Resp. Ex. O at
9. To the contrary, both Dr. Rose and Dr. Murphy submitted literature indicating that the flu
vaccine protects recipients from adverse cardiovascular events. However, none of these studies
administered Fluzone to a subject who was already ill.
As an example, Dr. Rose offered a study published by the Cochrane Library which
evaluated “8 trials of influenza vaccination compared with placebo or no vaccination in 12,029
individuals.” Resp. Ex. D at 4, referencing Resp. Ex. D, Tab 10.40 According to Dr. Rose, this
study “found that cardiovascular mortality was significantly reduced by influenza vaccination as
were cardiovascular events.” Id. Dr. Rose explained that instances of acute myocardial infarction
increase during flu season; some studies show that the risk of myocardial infarction or stroke is
more than four times higher after a respiratory tract infection, with the highest risk within three
days. Id.
Another paper submitted by Dr. Rose analyzed case control studies on flu vaccine, flu
infection, and acute myocardial infarction, and found that flu infection significantly raised the risk
of disability and death in patients with ischemic heart disease. Resp. Ex. D at 5, referencing Resp.
Ex. D, Tab 12.41 The article suggested that flu infection can lead to myocardial infarction “via
acute coronary occlusion through thrombosis of a pre-existing, subcritical atherosclerotic plaque...
Infection causes tachycardia, hypoxia, release of inflammatory cytokines and a thrombophilic
state,” any of which can contribute to a myocardial infarction. Resp. Ex. D, Tab 12 at 1.
The Udell article offered by Dr. Rose reported that a study of adults over 65 years old who
received the high-dose flu vaccine were 24% less likely to develop the flu and also had a “reduced
risk of pneumonia, all-cause hospitalization, and cardiopulmonary events with no increase in
39
Liam Smeeth et al., Risk of Myocardial Infarction and Stroke after Acute Infection or Vaccination, 351
N. ENGL. J. MED. 25: 2611-18 (2004), filed as “Resp. Ex. M.”
40
Christine Clar et al., Influenza vaccines for preventing cardiovascular disease (Review), 5 COCHRANE
DATABASE SYST. REV. 1-55 (2015), filed as “Resp. Ex. D, Tab 10.”
41
Michelle Barnes et al., Acute myocardial infarction and influenza: a meta-analysis of case-control
studies, 101 HEART 1738-47 (2015), filed as “Resp. Ex. D, Tab 12.”
24
serious adverse events compared with standard-dose vaccine.” Resp. Ex. D, Tab 9 at 3.42 Dr. Rose
concluded, “In brief, there is no direct positive evidence for either an epidemiological association
or a plausible mechanism to link Fluzone High Dose to the fatal heart failure in Mrs. Halverson.”
Resp. Ex. D at 7.
Dr. Murphy emphasized that the American Heart Association and American College of
Cardiology (“AHA/ACC”) recommends the flu vaccine for all cardiac patients. Tr. 160; Resp. Ex.
A at 2, 7. He recommends that his own patients with advanced heart failure receive the flu vaccine.
Tr. 160. He explained, “patients with heart disease are generally very fragile, and are at very high
risk if they get the flu, that it will decompensate, get arrhythmias, get heart failure, and the
overwhelming evidence is that they benefit significantly from it.” Tr. 160-61. In Dr. Murphy’s
opinion, “there is no good evidence that the flu vaccine is harmful to [patients with heart failure].”
Tr. 161.
Dr. Murphy stated that flu vaccine, like any vaccine, is intended to excite an immune
response. Resp. Ex. O at 3. The elderly have diminished immune responses when compared to
younger patients, so a more potent vaccine is given to combat this effect. Id. The overall consensus
is that influenza vaccine is beneficial in the elderly when compared to the risk of actual influenza.
Id. at 4. In a 2006 paper, the AHA/ACC recommended the flu vaccine as secondary prevention for
patients with coronary and other atherosclerotic disease. Resp. Ex. A at 7; Resp. Ex. L.43 Notably
Dr. Stark pointed out that this recommendation was made three years before Fluzone was
introduced, and therefore did not consider the potential consequences of a more potent vaccine.
Pet. Ex. 19 at 2.
Dr. Murphy submitted several other articles to support his opinion that Fluzone protects
against cardiac events. A 2003 paper from the New England Journal of Medicine found that flu
vaccination was associated with a reduction in hospitalizations for heart disease, cerebrovascular
disease, pneumonia, and influenza, which supports the benefits of flu vaccines for the elderly.
Resp. Ex. A at 6; Resp. Ex. K.44 The Naghavi study found that patients with coronary heart disease
and a history of myocardial infarction who received the flu vaccine were 67% less likely to have
a subsequent myocardial infarction. Resp. Ex. Q at 3.45 Similarly, the Grau study found that
patients with a history of stroke or transient ischemic attack who received the flu vaccine were less
likely to have a subsequent stroke. Resp. Ex. R at 2-3, 6.46 A fourth study found that, while “acute
42
Jacob A. Udell et al., Does influenza vaccination influence cardiovascular complications?, 13 EXPERT
REV. CARDIOVASC. THER. 6: 593-96 (2015), filed as “Resp. Ex. D, Tab 9.”
43
See supra n.9.
44
See supra n.8.
45
Morteza Naghavi et al., Association of Influenza Vaccination and Reduced Risk of Recurrent Myocardial
Infarction, 102 CIRCULATION 3039-45 (2000), filed as “Resp. Ex. Q.”
46
Armin J. Grau et al., Influenza Vaccination Is Associated With a Reduced Risk of Stroke, 36 STROKE
1501-06 (2005), filed as “Resp. Ex. R.”
25
infections are associated with a transient increase in the risk of vascular events. . . influenza,
tetanus, and pneumonia vaccinations do not produce a detectable increase in the risk of vascular
events.” Resp. Ex. M at 1.47 None of the studies discussed by Dr. Murphy examined the effects of
Fluzone on patients already suffering from an upper respiratory infection at the time of vaccination.
When asked about incidences of myocardial infarction after receipt of Fluzone as noted in
the package insert,48 Dr. Murphy agreed that there have been incidences of myocardial infarction
after the administration of Fluzone but stated that these are “serendipitous events” which occur
due to the high number of heart attacks that occur every year in the U.S. Tr. 162. He agreed that
the relationship between Fluzone and myocardial infarction is “[n]ot necessarily causal, but it
could be.” Tr. 162.
4. Althen Prong 1/Loving Fact 4: Discussion
Dr. Stark and Dr. Patel opined that Fluzone, which contains four times more antigen than
the regular flu vaccine, can cause a susceptible individual to develop a systemic inflammatory
response. This response triggers platelet aggregation and increased blood clotting, which can cause
myocardial infarction leading to cardiac arrest. They supported these opinions with medical
literature. Dr. Stark offered the Lanza study finding that flu vaccine-related platelet activation and
cardiac autonomic dysfunction can increase the risk of cardiovascular events. See Pet. Ex. 10 at 1.
In turn, Dr. Patel submitted four studies showing that some patients had adverse cardiac events,
including myocardial infarction and cardiac arrest, following receipt of a flu vaccine. See Pet. Ex.
12; Pet. Ex. 14; Pet. Ex. 13; Pet. Ex. 15.
Dr. Rose and Dr. Murphy offered a bevy of literature to support their position that Fluzone
cannot induce or aggravate existing cardiovascular disease, but rather is protective against adverse
cardiovascular events. Dr. Rose criticized the studies offered by Dr. Patel for using data from
VAERS; however, Dr. Rose also cited to studies which relied on VAERS data to support his point
that Fluzone does not cause adverse cardiac events.
Neither Dr. Rose nor Dr. Murphy pointed to any deficits in petitioner’s theory. Conversely,
Dr. Rose noted that a protein in the flu vaccine, hemagglutinin, increases clumping of red blood
cells, and is four times higher in Fluzone than the regular flu vaccine. At hearing, he agreed that it
was possible for incidences of myocardial infarction to be associated with Fluzone. Tr. 288-89.
Despite these concessions, Dr. Rose maintained that there was no “statistical association,”
“epidemiological association,” or “plausible mechanism” to provide a causal connection between
Fluzone and adverse cardiac events.
However, “epidemiologic studies” are specifically not required in the Vaccine Program.
Capizzano, 440 F.3d at 1325. The standard of proof is only “preponderance of evidence,” in order
“to allow the finding of causation in a field bereft of complete and direct proof of how vaccines
affect the human body.” Althen, 418 F.3d at 1280. To require petitioner to present a statistical
association between a vaccine and a claimed injury would impermissibly raise the standard of
47
See supra n.39.
48
See supra n.30.
26
proof. And petitioner’s experts have supported their theory with medical literature, thus providing
the “indicia of reliability” to support their assertions. Moberly, 592 F.3d at 1324. Accordingly, I
find that petitioner’s experts have proffered a sound, reliable medical theory that Fluzone can cause
a systemic inflammatory response and increase clotting of red blood cells.
Petitioner has satisfied Althen prong 1/Loving factor 4.
B. Althen Prong 2/Loving Factor 5: Logical Sequence of Cause and Effect
Dr. Stark testified that Mrs. Halverson developed a systemic inflammatory response, which
caused platelets to form or cause a blockage in the coronary arteries. Tr. 101. This caused her to
suffer an acute coronary event, a heart attack, resulting in cardiac arrest. Tr. 101. He explained that
she suffered from a ventricular arrhythmia caused by a shortage of blood flow to her heart muscle
because her coronary artery was blocked by platelets. Tr. 130.
According to Dr. Stark, there was both a pathological and temporal link to implicate the
high dose flu vaccine in Mrs. Halverson’s sudden death. Pet. Ex. 18 at 4. Fluzone induced systemic
inflammation in Mrs. Halverson, which significantly increased her risk for arrhythmia, myocardial
infarction, and sudden cardiac death, given her preexisting co-morbidities of diabetes,
hypertension, hyperlipidemia, coronary artery disease, and congestive heart failure. Pet. Ex. 17 at
2; Pet. Ex. 19 at 2. He ultimately concluded that the Fluzone vaccine administered to Mrs.
Halverson on January 9, 2014, caused a systemic inflammatory response which caused platelets to
form, affecting blood flow to the heart. Tr. 101. This significantly aggravated her atrial fibrillation
and secondarily worsened her underlying congestive heart failure and was a substantial factor in
causing her ultimate cardiac arrest from which she could not be resuscitated. Pet. Ex. 18 at 1.
Dr. Patel similarly concluded that the Fluzone vaccine administered to Mrs. Halverson on
January 9, 2014 was a significant contributing factor in causing an adverse cardiac event and her
death on January 13, 2014. Pet. Ex. 22 at 3. “I believe it caused a hyper-response of the
inflammation and immune system, which caused the platelets to aggregate together and cause
subsequent cardiac events.” Tr. 59. Dr. Patel agreed that Mrs. Halverson’s URI symptoms
indicated that she was already immunocompromised when she was administered the vaccine. Tr.
59.
1. Fluzone caused Mrs. Halverson to develop a systemic inflammatory response
According to Dr. Patel, following receipt of Fluzone, Mrs. Halverson developed symptoms
consistent with the criteria for SIRS. Dr. Patel noted that she developed increased heart rate,
increased respiratory rate or shortness of breath, and increased white cell count, adding that, if a
person had an upper respiratory infection and then received Fluzone, the vaccine would have a
magnified effect, “because the patient’s immune system is already activated from an underlying
condition.” Tr. 58, 65-66. The effect would be synergistic. Tr. 58. Dr. Stark agreed that there was
a synergistic effect between Fluzone and Mrs. Halverson’s ongoing URI which worsened her
cardiac condition. Tr. 101-02. He noted that she complained of shortness of breath post-
vaccination and explained that an inflammatory response can affect breathing, causing shortness
of breath. Tr. 134. It can also cause a person to feel weak. Tr. 134.
27
Dr. Patel could only speculate about Mrs. Halverson’s symptoms, because there was no
evidence in the record reflecting that Mrs. Halverson actually did experience increased heart rate,
respiratory rate, and/or white cell count following her receipt of Fluzone. Tr. 65-66. Dr. Patel
conceded that diagnosing patients is not within the boundaries of his pharmacist licensure, and he
would defer to a medical doctor for diagnostic purposes. Tr. 67.
Petitioner reported to the paramedics and emergency room physicians that, in the days that
followed her receipt of Fluzone, Mrs. Halverson grew weaker, had lethargy, malaise, and shortness
of breath, and could not get up off of the couch. He also reported these symptoms to Dr. Sparagna
after she passed. See Pet. Ex. 9 at 16-17; Pet. Ex. 4 at 62; Tr. 12-15.
Dr. Rose offered a Sanofi-Pasteur study showing recipients of the flu vaccine experiencing
vomiting and severe cough. Resp. Ex. D, Tab 8 at 7.49 Petitioner testified to Mrs. Halverson
vomiting and coughing all night after receipt of Fluzone.
2. Mrs. Halverson’s systemic inflammatory response affected her cardiac function
Dr. Stark opined, “. . . on January 9, 2014, the date of the vaccination, Mrs. Halverson’s
cardiac condition was stable, and the examination did not reveal signs of an imminent adverse
event. Specifically, Mrs. Halverson did not have a displaced apical impulse, and she had normal
heart auscultation, including normal S1 and S2, without murmurs, rubs, or gallops. Her heartbeat
was regularly irregular.” Pet. Ex. 18 at 3. He explained, “A person can have an atrial arrhythmia,
which [Mrs. Halverson] did, occasionally, and can live and can thrive…A person can live with
[atrial fibrillation], a person can do all his or her usual activities, it’s very, very seldom fatal.” Tr.
129-31. In addition to her atrial fibrillation, she also had insulin-dependent diabetes with chronic
renal insufficiency, high cholesterol, obesity, and hypertension, as well as left bundle branch block
and intermittent ventricular tachycardia. Pet. Ex. 20 at 2. “Together, these risk factors put Mrs.
Halverson at extreme high risk for any external factor that could destabilize her heart rhythm,
impair her heart function, or make her blood and platelets more prone to clotting.” Id. Dr. Patel
agreed, stating “[t]he elevated/altered cardiovascular parameters in a patient with diabetes and
cardiovascular disease leads to catastrophic consequences and results in abnormal demand/supply
of blood flow to the heart.” Pet. Ex. 22 at 4.
Dr. Stark opined that Mrs. Halverson’s underlying risk factors made her “far more
vulnerable to the synergistic effect of platelet activation and autonomic dysfunction.” Pet. Ex. 17
at 1. When asked what ultimately caused her cardiac arrest and death, Dr. Stark responded, “It was
an acute coronary event causing a heart attack which caused her heart to stop…[d]ue to
inflammation causing platelets to complete a blockage of her coronary artery, and the
inflammation was due to a preceding flu immunization.” Tr. 101. He referred to the arm pain and
numbness that Mrs. Halverson complained of post-vaccination, explaining, “. . . females who are
having heart attacks, often get arm numbness and don’t get chest pain. [Mrs. Halverson] fits the
pattern.…it is more likely than not that [Mrs. Halverson] was experiencing the beginning of a heart
attack, at least before she collapsed.” Tr. 97.
49
See supra n.37.
28
Dr. Stark submitted medical literature indicating that in susceptible individuals,
particularly diabetics, the flu vaccine can induce platelet activation, adrenergic predominance, and
inflammatory reactions. Pet. Ex. 18 at 3; see also Pet. Ex. 10 (Study concluding “that influenza A
vaccination in patients with type II diabetes induces, together with the expected inflammatory
reaction, an increase in platelet activation and a cardiac sympathovagal imbalance”).50 He
explained that, due to her co-morbidities, which included diabetes, hypertension, hyperlipidemia,
atrial fibrillation, congestive heart failure, and coronary artery disease with permanent defibrillator
and reduced ejection fraction, Mrs. Halverson was extremely susceptible to “any external factor
that could destabilize her heart rhythm, impair her heart function, or make her blood and platelets
more prone to clotting.” Id.; Pet. Ex. 20 at 2. “The pathophysiological link between the
inflammatory and the cardiac autonomic responses to the vaccine are manifested by an increased
risk of cardiovascular events and significant changes in heart rate variables.” Id. at 3-4. Dr. Stark
concluded that the “systemic inflammatory effects” from Fluzone exacerbated Mrs. Halverson’s
cardiac conditions and contributed to or caused her cardiac arrest. Pet. Ex. 17 at 2; Pet. Ex. 20 at
2.
3. Respondent submits that there is no evidence that Fluzone caused Mrs. Halverson to
develop a systemic inflammatory response and/or a worsened cardiac condition
Dr. Rose agreed that, on the date of her vaccination, Mrs. Halverson was in relatively good
health, although she complained of upper respiratory symptoms for three days. Resp. Ex. D at 3.
In his opinion, there is nothing to suggest that Mrs. Halverson had hyperinflammation or any signs
of chronically dysregulated inflammasomes. Id. at 8. According to Dr. Rose, the best support for
petitioner’s expert’s suggestion of heightened chronic inflammation generated from Fluzone
would be serial blood samples taken periodically after vaccination. Id. at 6. This was not done here
and is rarely done on humans. Id. In Dr. Murphy’s opinion, however, measurement of serum
markers would not likely be helpful since patients with heart failure, renal failure, or diabetes may
have elevated cytokine levels absent influenza vaccine. Resp. Ex. O at 4.
In lieu of Dr. Stark’s theory that Fluzone caused out-of-control inflammation in Mrs.
Halverson, resulting in platelet aggregation and adverse effects to cardiac autonomic function, Dr.
Rose offered macrophage activation syndrome, a clinical condition marked by activation and
expansion of the macrophages and other innate immune cells, as an example of a systemic cytokine
response. Resp. Ex. D at 7. He stated, “These are systemic diseases involv[ing] multiple organs
caused by dysregulated production of many pro-inflammatory cytokines.” Id. In response, Dr.
Stark stated that Dr. Rose mischaracterized his opinion. On the contrary, his opinion invoked “the
well-recognized, enhanced inflammatory response that is characteristic following Fluzone
immunization,” but “in a highly susceptible individual, would be more than sufficient to trigger
cardiac arrhythmia, congestive heart failure or cardiac arrest.” Pet. Ex. 20 at 2.
Dr. Rose agreed that Mrs. Halverson’s condition became worse after Fluzone. Tr. 301. He
agreed that vomiting and severe cough were known adverse effects of Fluzone. Tr. 302. He stated
that he could not rule out the possibility that her malaise, vomiting, catatonia, and other symptoms
were due to Fluzone. Tr. 301. He noted the possibility that Fluzone could cause an enhanced
50
See supra n.19.
29
systemic response in a person with an ongoing upper respiratory infection and agreed that an upper
respiratory infection can induce an inflammatory response. Tr. 294, 309. Dr. Rose agreed that Mrs.
Halverson’s symptoms following receipt of the Fluzone vaccine “could be the result of an
inflammatory reaction” but stated that it would not be the result of an immune response, which
would take more time. Tr. 266. When asked if Mrs. Halverson developed SIRS, Dr. Rose
responded that she had some changes that were associated with SIRS but not others, and it
depended on the criteria used for SIRS. Tr. 277. In his opinion, he did not believe she suffered
from SIRS. Tr. 278. Dr. Rose concluded that there is no evidence that a systemic event like SIRS
caused heart failure in Mrs. Halverson. Resp. Ex. D at 7.
Dr. Murphy opined that, prior to her receipt of Fluzone, Mrs. Halverson “had really bad
heart disease. She had a cardiomyopathy, which means the [heart] muscle wasn’t squeezing well.”
Tr. 180. However, he also agreed that despite her health conditions, she was “doing pretty well.”
Tr. 180. He further agreed that Mrs. Halverson was “feeling a little bit crummy after the flu
vaccine”, and that she was sick and had symptoms that would be compatible with an upper
respiratory tract infection. Tr. 199, 217. “Based on the record it probably was an upper respiratory
infection, but…it could have been a heart failure exacerbation that wasn’t fully recognized.” Tr.
217. He stated, “[I]t would seem that she obviously was ill…she probably had some kind of an
upper respiratory infection, but I can’t exclude that it’s something a bit more.” Tr. 218. He also
suggested that she may have had pneumonia. Tr. 181.
Despite the foregoing, Dr. Murphy concluded that there is “no convincing clinical
evidence” to support that Mrs. Halverson had an inflammatory response following Fluzone. Resp.
Ex. O at 3. When asked about Mrs. Halverson’s symptoms of malaise, fatigue, vomiting, and
catatonia in the days after receiving Fluzone, Dr. Murphy responded that those symptoms could
be explained by a progression in her renal dysfunction, uncontrolled diabetes, or worsening heart
failure. She did not meet the definition of SIRS. Tr. 198. He noted that Mrs. Halverson reported
increasing shortness of breath prior to the administration of the Fluzone vaccine, and attributed it
to a respiratory tract infection, an exacerbation of her heart failure, or a combination of both. Resp.
Ex. A at 4. In Dr. Murphy’s opinion, it was possible, but not probable, that the Fluzone vaccine
given to Mrs. Halverson adversely affected her health. Tr. 201. “So my answer would be, there is
a possibility, but I think it’s improbable that the flu vaccine had anything to do with her eventual
and tragic death.” Tr. 201.
According to Dr. Murphy, Mrs. Halverson was a biologically fragile patient, so a specific
cause of sudden deterioration is often multifactorial and difficult to determine. Resp. Ex. O at 3.
She probably had coronary atherosclerosis, but due to her renal function, a coronary angiogram
could not be performed, so while this diagnosis was suspected, it could not be proven. Id. Dr.
Murphy opined that, due to a lack of testing, there was no evidence of inflammation in Mrs.
Halverson’s heart.
…the possibility of idiosyncratic individual harm in a specific patient cannot be
completely excluded. Short of an antemortem endocardial biopsy or postmortem
histological examination of Mrs. Halverson’s heart (which to the best of my
knowledge did not occur), there is no scientific method based on my review of her
30
clinical notes to reliably detect cellular inflammation in the heart muscle or
inflammation in a coronary artery atherosclerotic plaque.
Resp. Ex. O at 3-4.
Dr. Murphy pointed to Dr. Stark’s recognition of Mrs. Halverson’s frailties, submitting that
he was inconsistent when he referred to her being clinically stable and not at high risk for clinical
deterioration. Resp. Ex. O at 2, citing Pet. Ex. 20 at 2. Dr. Murphy took issue with Dr. Stark’s
statement that Mrs. Halverson’s medical problems were successfully treated for 65 years. Id. at 7.
Dr. Murphy stated that patients with congestive heart failure have a five-year survival rate of about
50% unless a structural defect is identified and remedied. Id. He pointed out that her cardiologist
noted her to have a “very brittle” cardiovascular system. Id.; see also Pet. Ex. 4 at 83. She also had
chronic renal failure, which is associated with a significantly increased risk of mortality. Id.
Dr. Murphy admitted that, if he had been treating Mrs. Halverson, he would have done a
chest x-ray when her symptoms did not improve following her appointment on January 9, 2014.
Tr. 192-93. If she had been his patient, he would have told her to come back a week after the
January 9, 2014 visit before giving her the flu vaccine. Tr. 194-95. Dr. Murphy explained, “I would
feel more comfortable that this upper respiratory tract infection had blown over before I would
give her the vaccine.” Tr. 195. “I would prefer to vaccinate somebody in the whole of their health
rather than vaccinating them when they have a concurrent infection going on.” Tr. 195. “I’m not
aware of data which says giving a flu vaccine to somebody with an upper respiratory tract infection
is dangerous,” but he agreed that studies of Fluzone have excluded patients with upper respiratory
infections from participating. He agreed that traditionally, a child will not be vaccinated if he or
she is ill. Tr. 196.
When asked if Mrs. Halverson’s condition/death could have been a combination of her
diabetes, her heart, other comorbidities, and the Fluzone vaccination, Dr. Murphy concluded, “I
cannot separate out any one of those as specifically causal.” Tr. 199-200.
5. Althen Prong 2/Loving Factor 5: Discussion
Petitioner testified that, in the days following her receipt of Fluzone, Mrs. Halverson
suffered from severe cough, vomiting, shortness of breath, fatigue, weakness, and malaise. Tr. 11-
16. Petitioner’s testimony is corroborated by the medical records and the emergency room records,
which reflect that petitioner reported that Mrs. Halverson had been suffering from an upper
respiratory infection, malaise, weakness, decreased intake, cough, shortness of breath, nausea,
vomiting, and congestion for the past few days. Pet. Ex. 9 at 16-17.
According to Drs. Patel, Stark, and Rose, a systemic inflammatory response is evidenced
by fever, chills, muscles aches and pains, headache, fatigue, malaise, increased heart rate, and
increased respiratory rate. Tr. 72, 114-15, 133-34, 263. The symptoms that Mrs. Halverson
developed in the days following her receipt of Fluzone fit squarely within the clinical symptoms
associated with SIRS.
31
All of the experts in this matter agreed that Mrs. Halverson had a fragile cardiovascular
system, and that she had a URI at the time she received Fluzone. Pet. Ex. 17 at 1; Pet. Ex. 18 at 3;
Pet. Ex. 20 at 2; Pet. Ex. 22 at 4; Resp. Ex. A at 3, 4, 22; Resp. Ex. O at 9; Resp. Ex. D at 3; Tr.
58, 101-02. Drs. Patel and Stark testified that the combination of Fluzone and the URI, in the
setting of Mrs. Halverson’s increased susceptibility to cardiac events, caused her cardiac arrest.
Dr. Murphy conceded that he could not separate out her diabetes, cardiac issues, other
comorbidities and the Fluzone vaccination as specifically causal. Tr. 199-200.
This case resembles Shyface v. Sec’y of Health & Human Services, in which Cheyenne
Shyface was vaccinated with whole-cell DPT at the time he was beginning an E. coli infection.
Both the DPT and the E. coli infection could and did cause a fever, which rose to 110 degrees,
resulting in Cheyenne’s death four days later. 165 F.3d at 1345. Respondent defended the case
and argued that the E. coli infection was the cause of his fever and death. Cheyenne’s treating
physician testified that both the vaccine and the infection were equally responsible for his fever
and death. The Federal Circuit held that each of the two factors, the vaccine and the infection, was
a substantial factor in causing the baby’s very high fever and death and but for the vaccination, the
baby would not have had the high fever and would not have died. Id. at 1353.
I find here that Mrs. Halverson’s upper respiratory infection, her co-morbidities, and
Fluzone were all substantial factors contributing to her death. But for Fluzone, Mrs. Halverson
would not have died. Accordingly, petitioner has satisfied Althen prong 2/Loving factor 5.
C. Althen Prong 3/Loving Factor 6: Temporal Relationship
Dr. Stark stated that the “four-day proximate temporal relationship” supports his opinion
that Mrs. Halverson’s vaccine on January 9, 2013 “significantly aggravated her atrial fibrillation,
myocardial infarction and death.” Pet. Ex. 18 at 4.
Dr. Stark explained that Fluzone elicits an “enhanced systemic inflammatory response”
which generally occurs three to seven days after immunization, the same length of time between
Mrs. Halverson’s receipt of Fluzone and her subsequent cardiac arrest. Pet. Ex. 19 at 1. At hearing,
he discussed the amount of time it takes for an inflammatory response to develop following
Fluzone. Dr. Stark testified, “…beginning at day three or three (sic) four [after vaccination], you
are getting an inflammatory response and the effect on the heart is such that if your heart was
jumpy to begin with, that you had extra heartbeats, you had arrhythmias, which are bad, jazzing
up the heart by – with inflammation makes those extra beats be even more frequent and a rhythm
is more likely.” Tr. 93. He added, “The local inflammation [in the arm where the vaccine was
injected] begins in 10 hours after the immunization, but the production of antibodies and
inflammation goes seven, 10, 14 days.” Tr. 93.
For support, Dr. Stark cited to the package insert for Fluzone, noting that the “label
indicates that the vaccine may cause Guillain-Barre syndrome for up to 6 weeks after
administration.” Pet. Ex. 18 at 4, citing Pet. Ex. 31. Dr. Stark concluded, “It is well-established
that reactions to the influenza vaccines manifest up to weeks after the administration of the vaccine
and adverse events often manifest in a shorter timeframe.” Id.
32
Dr. Rose testified that it takes four to six days for the immune system to generate antibodies
to Fluzone. Tr. 259. He stated that a local reaction to Fluzone, evidenced by swelling and redness
at the injection site, “will generally go for maybe two to four days, depending again on the intensity
of the inflammatory response.” Tr. 262. Dr. Rose did not address whether four days is an
appropriate amount of time for a person to develop a systemic inflammatory reaction.
According to Dr. Murphy, the temporal relationship between Mrs. Halverson’s receipt of
Fluzone and subsequent cardiac arrest can be adequately explained by her history of long standing
cardiac, diabetic, hypertensive and renal disease. Resp. Ex. O at 9. Dr. Murphy opined that
congestive heart failure and atrial fibrillation are common diseases in the elderly “and would be
expected to frequently occur proximate to influenza vaccination by chance alone.” Id. at 8.
According to Dr. Murphy, the coincidence of flu vaccination and heart failure or atrial fibrillation
in the elderly population is so common that the “determination of a causal relationship. . . would
be almost impossible.” Id. He provided statistics in support of his opinion, stating that there are
5.7 million heart failure patients in the United States; about 50% of patients with heart failure die
within 5 years of diagnosis. Resp. Ex. A at 4; Resp. Ex. G at 1.51 Dr. Murphy estimated that a 50%
mortality rate over five years is equivalent to about 500,000 deaths due to heart failure every year.
Resp. Ex. A at 4. During the 2013-2014 flu season, 46% of people in the U.S. received the flu
vaccine. Resp. Ex. F at 1. If 46% of heart failure patients were vaccinated, then about 230,000
vaccinated heart failure patients die annually. Resp. Ex. A at 4. By what he called a “back of the
envelope calculation” from data of peer reviewed literature, Dr. Murphy stated that in “a 6-month
window for influenza vaccination, the estimated number of US heart failure patients who will die
within one week of influenza vaccination based solely on chance and not causally related to
influenza vaccination is estimated at 8,000-9,000 annually.” Id. Dr. Murphy did not submit any
studies where individuals suffering from an upper respiratory infection who also had a fragile
cardiovascular system received Fluzone without event.
Althen Prong 3/Loving Factor 6: Discussion
Mrs. Halverson had a URI when she received Fluzone on January 9, 2014. Later that
evening, she began vomiting and developed a severe cough. On January 10, 2014, she had
numbness and tingling in her arms, fatigue, malaise, weakness, and shortness of breath. She
deteriorated and, three days later, suffered a cardiac arrest and died.
Petitioner’s experts opined that there is a temporal relationship between Mrs. Halverson’s
receipt of Fluzone and her development of SIRS. Dr. Stark pointed to the Fluzone package insert,
which, among other warnings, included the onset of systemic adverse events usually within three
days of vaccination. See Pet. Ex. 31 at 3. Dr. Murphy did not address whether four days was
appropriate for a systemic inflammatory response; rather, he viewed Mrs. Halverson’s death four
days after Fluzone as coincidental and solely due to her heart conditions. Dr. Rose did not discuss
the length of time required for a systemic inflammatory reaction to develop, but he did state that it
takes four to six days for the immune system to generate antibodies to Fluzone. This opinion
implies that Mrs. Halverson’s symptoms began too rapidly to be a response to her receipt of
Fluzone. However, I have previously found that administration of a flu vaccine in the setting of a
51
CDC Heart Failure Fact Sheet, filed as “Resp. Ex. G.”
33
preexisting URI can cause an increased immune response resulting in a more rapid onset of
symptoms, based on the concession made by respondent’s expert in that case. See Lehrman v.
Sec’y of Health & Human Servs., No. 13-901V, 2018 WL 1788477, at *19 (Fed. Cl. Spec. Mstr.
Mar. 19, 2018) (Finding a temporal relationship existed between petitioner’s flu vaccine and
development of GBS symptoms within 24 hours, when the petitioner had recently suffered a URI
at the time of his vaccination).
Furthermore, Mrs. Halverson’s clinical course is analogous to that experienced by the
vaccinee in Bragg v. Sec’y of Health & Human Services. In Bragg, the vaccinee “felt ill 30 minutes
after receiving the flu vaccination. He never felt any better but continued to get worse until he
died.” 2012 WL 404773, at *26 (Fed. Cl. Spec. Mstr. Jan. 18, 2012). The special master found that
there was a temporal connection between the vaccinee’s flu vaccine and his development of SIRS:
The timing is compelling in this case….When someone becomes ill with a vaccine
injury and worsens day by day until he dies, a reasonable conclusion is that the
immunologic challenge caused the illness.…In the instant action, the timing of
decedent’s onset of his mortal illness is consistent with systemic inflammation
response syndrome, the response being to flu vaccination.
Id. at *26-27. Notably, the vaccinee’s symptoms began shortly after vaccination and continued to
progress until his death five days post-vaccination. Id. at *1. The timing of Mrs. Halverson’s
clinical course is very similar, with an already fulminating upper respiratory infection and an onset
of vomiting, coughing, and progressive deterioration the day of vaccination, culminating in death
four days later. Like the special master in Bragg, I find the timing of Mrs. Halverson’s receipt of
Fluzone and subsequent deterioration quite compelling. According to petitioner’s experts, it is
medically acceptable to infer a temporal relationship between Fluzone and Mrs. Halverson’s
development of SIRS and subsequent death. Respondent’s experts did little to dispel petitioner’s
argument. Accordingly, petitioner has satisfied Althen prong 3/Loving factor 6.
D. Loving Factor 1: Mrs. Halverson’s Condition Prior to Fluzone
As detailed in the facts section above, prior to her receipt of Fluzone, Mrs. Halverson had
a host of co-morbidities. See Pet. Ex. 3 at 2-7; Pet. Ex. 4 at 7, 11; Pet. Ex. 7 at 1, 5. She also had a
history of heart issues as documented at length throughout this Ruling. See Pet. Ex. 3 at 2; Pet. Ex.
4 at 27; Pet. Ex. 7 at 5, 24-29, 41, 91-92, 104, 154-55.
When she presented for placement of a permanent biventricular AICD in September of
2013, Mrs. Halverson’s expected survival was greater than one year. Pet. Ex. 7 at 104. The AICD
was recommended due to Mrs. Halverson’s potential for sudden cardiac related to her episodes of
ventricular tachycardia. Id. at 7-8.
As the medical records reflect, after placement of the AICD, Mrs. Halverson’s health
improved. She had more energy and wanted to walk more. Tr. 42. At a visit with Dr. Arluck in
November of 2013, Mrs. Halverson reported that she no longer had nocturnal dyspnea but still had
shortness of breath when walking. Pet. Ex. 6 at 19; Pet. Ex. 7 at 14. An echocardiogram showed
that she had atrial and biventricular racing. Pet. Ex. 4 at 4. Petitioner recalled that petitioner saw
34
Dr. Arluck in December of 2013; he stated that Mrs. Halverson was “doing fine” and told her to
return in four months. Tr. 9.
According to petitioner, Mrs. Halverson developed a slight cold around January 7 and 8,
with cough, sneezing, and congestion. Tr. 8, 47. He did not recall her being fatigued or having
shortness of breath or having a similar cold himself. Tr. 24-26.
Upon presenting to Dr. Sparagna on January 9, 2014, Mrs. Halverson was noted to have
nasal congestion, a loose but non-productive cough, and a scratchy throat. Pet. Ex. 3 at 5. She
reported “clogged” ears and difficulty hearing but no ear pain. Id. She complained of fatigue and
was noted to walk with a cane for balance. Id. She did not have difficulty breathing at that
examination. Id. Dr. Sparagna diagnosed her with an upper respiratory. Id. at 5, 7. She was
administered a Fluzone vaccine. Id. at 2.
E. Loving Factor 2: Mrs. Halverson’s Condition Following Fluzone
Petitioner stated that Mrs. Halverson experienced “rapid degeneration” following Fluzone;
he recalled that she began vomiting later the day of the vaccine, after dinner, and continued to
vomit through the night, culminating in dry heaves the following morning. Tr. 11, 28. According
to petitioner, Mrs. Halverson had started to lose her voice and her hearing. Tr. 12. Her arms were
numb and tingling, “like when your foot goes to sleep.” Tr. 12. Petitioner described her as “zombie-
like,” with “less than half of her normal energy.” Tr. 12, 14.
Mrs. Halverson deteriorated in the following days and petitioner finally convinced her to
go to the hospital on January 13, but she wanted to change her clothes first. Tr. 15-16. She
collapsed while in the bathroom and could not be resuscitated. Tr. 16; Pet. Ex. 9 at 16-17; 20-21.
Her immediate cause of death was listed as cardiac arrest due to ischemic heart disease. Pet. Ex. 2
at 1.
F. Loving Factor 3: Significant Aggravation vs. Natural Progression of Disease
Dr. Murphy submitted that Mrs. Halverson’s death was the result of the natural progression
of her severe cardiac disease combined with her comorbidities. In his opinion, Mrs. Halverson
suffered from a “constellation of medical conditions” which placed her “at high risk of sudden
cardiac death without the need to invoke a vaccine specific etiology for her untimely death.” Resp.
Ex. A at 3. In his opinion, her sudden death was typical of the natural course of the patient with
severe structural cardiac disease with recurrent episodes of heart failure and poor left ventricular
function compounded by insulin-dependent diabetes and chronic renal failure. Resp. Ex. A at 4.
1. Respondent submits that Mrs. Halverson was in poor cardiac condition prior to Fluzone
Dr. Murphy thoroughly discussed Mrs. Halverson’s medical history in his reports and at
hearing. He noted that she likely had underlying suspected coronary artery disease based on her
history of smoking, insulin-dependent diabetes, hyperlipidemia, hypertension, and renal failure.
Resp. Ex. A at 3. Dr. Murphy clarified that she was only “suspected” to have coronary artery
disease because her doctors did not do a coronary angiogram, which, in Dr. Murphy’s opinion,
35
“you would typically do [here].” Tr. 166; Resp. Ex. A at 3. Dr. Murphy suggested that Mrs.
Halverson’s doctors “were afraid that they would precipitate a further decline in her kidney
function, because the x-ray dye tends to be toxic to the kidneys.” Tr. 166.
A nuclear stress test in 2013 showed that Mrs. Halverson had abnormal ventricular function
with multiple regional wall motion abnormalities but no definitive evidence of myocardial
ischemia. Resp. Ex. A at 3. According to Dr. Murphy, this did not exclude occult coronary artery
disease. Id. She had a permanent pacemaker due to heart block in 2001 and biventricular
pacemaker/defibrillator in 2013. Id.
Dr. Murphy noted that, after Mrs. Halverson received the AICD, her ejection fraction
improved, though it was still below normal. Tr. 168-69. It went from 25 to 30 percent up to 45
percent. Tr. 172-73. She had an EKG on December 12, 2013 which showed an ejection fraction of
45 to 50 percent, “which is much better than the 25 to 30 percent previously.” Tr. 183. According
to Dr. Murphy, Mrs. Halverson had “a reasonably good response” to the AICD. Tr. 183. He added,
“[T]he ejection fraction is useful, but there are limitations to how effective it is. And just because
your ejection fraction is normal doesn’t mean that you’re okay.” Tr. 169. Dr. Murphy conceded
that, “[T]he fact that her ejection fraction got better would reduce the risk of sudden death.” Tr.
177.
Mrs. Halverson had an echocardiogram on December 12, which showed “abnormal
diastolic function, which is typical of patients who have long-standing hypertension, and patients
with kidney disease.” Tr. 185. Dr. Murphy estimated that the abnormal diastolic function was long-
standing. Tr. 185. He observed that her pulmonary valve, aorta, and pericardium were normal. Tr.
186. He further noted that she had signs of an old heart attack. Tr. 186.
According to Dr. Murphy, it is possible but unproven that Mrs. Halverson may have had a
myocardial infarction. Resp. Ex. A at 22. In his opinion, it is more likely that she had ventricular
fibrillation secondary to her underlying ventricular dysfunction and congestive heart failure. Id.
“A relatively normal clinical examination does not exclude the possibility of sudden cardiac
arrhythmia in a very high-risk patient, such as Mrs. Halverson.” Id. He noted that the rhythm strip
from her ER admission showed ventricular fibrillation. Id.; see also Pet. Ex. 9 at 8. In Dr. Murphy’s
opinion, “She died of a cardiac arrest” caused by ventricular fibrillation. Tr. 211, 222.
Additionally, Dr. Murphy added that Mrs. Halverson was short of breath prior to
vaccination, “which was probably an exacerbation of her congestive heart failure. Thus she was
not [in] stable condition prior to her vaccination.” Resp. Ex. A at 21. The medical records indicate
that Mrs. Halverson routinely reported shortness of breath beginning in 2010. See Pet. Ex. 4 at 44-
45, 59-60.
2. Respondent submits that Mrs. Halverson was at a high risk for sudden death
In Dr. Murphy’s opinion, Mrs. Halverson was at a high risk for sudden death prior to her
receipt of the Fluzone vaccine. At hearing, Dr. Murphy explained that 50 percent of patients with
heart failure die within five years. According to Dr. Murphy, Mrs. Halverson’s heart failure began
36
“several years” before her death in 2013 and was the natural progression of disease for a person
with heart failure. Tr. 202.
To support his opinion, Dr. Murphy offered multiple statistics on heart failure. He
explained that sudden death is common in patients with congestive heart failure, occurring at a rate
of six to nine times that of the general population. Resp. Ex. A at 5. Heart failure contributes to
287,000 deaths a year; in 2009, one in nine deaths was attributed to heart failure. Id. 50% of
patients who develop heart failure die within five years. Id. More than five percent of people age
60 to 69 have congestive heart failure, and 10 per 1,000 people older than age 65 have congestive
heart failure. Id. Heart failure is responsible for 11 million medical visits each year and more
hospitalizations than all forms of cancer combined. Id. One-fifth of all hospitalizations have heart
failure as the primary or secondary diagnosis. Id. Based on these statistics, he was confident that
Mrs. Halverson had a high risk of sudden death prior to receiving the Fluzone vaccine and that her
sudden death four days after Fluzone did not imply a causal relationship. Resp. Ex. O at 9.
Dr. Murphy further submitted that Mrs. Halverson had an expected five-year mortality of
50 to 70% based on end stage kidney disease. Resp. Ex. A at 4. She was given a diagnosis of stage
IV kidney disease in 2011. Pet. Ex. 4 at 37-38. According to her records, she had not progressed
to stage V, or “end stage” kidney disease, which requires dialysis.52 The experts did not discuss
whether renal failure could cause cardiac arrest, but Dr. Murphy stated that one possibility for Mrs.
Halverson’s symptoms following Fluzone was progression of her renal dysfunction. Tr. 198.
However, there are no medical records indicating that Mrs. Halverson’s renal disease was
worsening at that time.
Dr. Murphy concluded, “I think the cause of her death was the natural history of her
multiple comorbidities, particularly her heart disease, her renal failure, her diabetes, and more
likely than not, that was the cause of this poor lady’s death.” Tr. 202.
Dr. Patel agreed that heart failure and renal failure can also cause immunostimulation. Tr.
66. However, he noted that Mrs. Halverson appeared to improve following the implantation of the
AICD and her deterioration occurred shortly after vaccine administration. Tr. 66-67.
In response to Dr. Murphy’s opinion that Mrs. Halverson’s death was secondary to her
long term underlying cardiac risk factors, Dr. Stark pointed out that for 65 years she had been
successfully treated for each of her medical problems. Pet. Ex. 19 at 1.
3. Loving Factor 3: Discussion
While Mrs. Halverson suffered from a number of conditions, including diabetes, renal
failure, atrial fibrillation, and congestive heart failure, she had been living with these conditions
for years. She worked to maintain her health, regularly presenting for care to her cardiologist,
primary care physician, and other specialists. Following the implantation of an AICD in September
of 2013, Mrs. Halverson had more energy and was more active. Approximately one month before
she received the Fluzone vaccine, she had an echocardiogram, which showed that her left
52
“Stage 5 [of chronic kidney disease] has a GFR below 15 (end-stage renal disease), and patients require
dialysis.” Chronic kidney disease, DORLAND’S at 530.
37
ventricular systolic function had markedly improved since the last study. Her cardiologist said she
was “doing fine.” Overall, it appears that her heart condition, while serious, was stable.
When she presented to Dr. Sparagna on January 9, 2014 with an upper respiratory infection,
Mrs. Halverson reported nasal congestion, a loose but non-productive cough, scratchy throat,
numbness in her feet, fatigue, and difficulty hearing; she did not complain of vomiting, severe
cough, weakness, or malaise. Pet. Ex. 3 at 5-7. She was not “zombie-like.” She walked into the
doctor’s office of her own accord and went to the pharmacy with petitioner to purchase the
medication prescribed. Her health took a rapid and markedly devastating turn that evening after
receiving the Fluzone vaccination. Tr. 10-17; Pet. Ex. 9 at 16-17.
Dr. Stark and Dr. Murphy agree that Mrs. Halverson’s immediate cause of death was
cardiac arrest but differ as to the cause of said cardiac arrest. In Dr. Stark’s opinion, the
combination of Fluzone, a high-dose flu vaccine, and URI caused Mrs. Halverson to develop SIRS,
which strained her heart and caused cardiac arrest. According to Dr. Murphy, Mrs. Halverson’s
cardiac arrest occurred as the natural progression of her preexisting heart conditions. Dr. Murphy
based this opinion on the statistical likelihood that Mrs. Halverson would die within five years of
being diagnosed with congestive heart failure. However, the Federal Circuit has rejected
arguments put forth by petitioners which rely heavily on statistical likelihood as proof of causation.
See, e.g., Boatmon v. Sec’y of Health & Human Servs., 941 F.3d 1351, 1363 (Fed. Cir. 2019)
(rejecting petitioners’ theory due to expert’s reliance on statistics that a brainstem defect is found
in 50-70% of SIDS cases, and that, given these statistics, the vaccinee likely had a defect);
Knudsen, 35 F.3d at 550 (rejecting the government’s alternative cause theory based on “[t]he bare
statistical fact that there are more reported cases of viral encephalopathies than there are reported
cases of DTP encephalopathies”). While I acknowledge that the burden here lies with petitioner
rather than respondent, the Federal Circuit has rejected arguments relying on statistics from both
petitioners and respondent. Based on the totality of the circumstances, I find petitioner’s expert
more persuasive.
Based on the above, petitioner has proffered preponderant evidence that Mrs. Halverson’s
death was not the natural progression of her heart disease, but rather a combination of the Fluzone
and her upper respiratory infection that significantly aggravated her preexisting heart disease,
resulting in her death.
G. Respondent’s Burden to Show Unrelated Factors
Because petitioner has established a prima facie case of causation/significant aggravation,
he is entitled to compensation unless respondent can show by the preponderance of the evidence
that Mrs. Halverson’s injury was caused by a factor unrelated to the Fluzone vaccine. Deribeaux
ex rel. Deribeaux v. Sec’y of Health & Human Servs., 717 F.3d 1363, 1367 (Fed. Cir. 2013) (citing
§ 13(a)(1)(B)). To meet this standard, respondent must “present sufficient evidence to prove that
the alternative factor was the sole substantial factor in bringing about the injury.” Id. at 1368. The
Vaccine Act limits the scope of unrelated factors by excluding any “idiopathic, unexplained,
unknown, hypothetical, or undocumentable cause, factor, injury, illness or condition.” §
13(a)(2)(A). “In other words, alternative causes that are ‘idiopathic, unexplained, unknown,
38
hypothetical or undocumentable’ cannot overcome a petitioner’s prima facie case.” Doe v. Sec’y
of Health & Human Servs., 601 F.3d 1349, 1357 (Fed. Cir. 2010) (quoting § 13(a)(2)(A)).
As discussed above, respondent submitted that Mrs. Halverson’s death was the result of
her preexisting heart disease, which predisposed her to sudden cardiac death. Dr. Rose testified
that he had “no theory to explain her death.” Tr. 299. Dr. Murphy conceded that he would not have
vaccinated her if she was his patient but would have waited a week and reexamined her before
giving the vaccination. While refusing to concede Fluzone’s role in Mrs. Halverson’s death, Dr.
Murphy agreed that he could not parse out among her comorbidities and Fluzone any one thing to
attribute her death to. Having determined that Mrs. Halverson’s death was the result of a significant
aggravation of her cardiac condition by Fluzone rather than the natural progression of her
condition, I find that respondent has failed to demonstrate that Mrs. Halverson’s preexisting heart
disease was the sole substantial factor in bringing about her death on January 13, 2014.
VII. Conclusion
I extend my sympathies to petitioner for the loss of his wife. Upon careful evaluation of all
of the evidence submitted in this matter, I find that petitioner has established entitlement to
compensation under the Vaccine Act. Accordingly, this case shall proceed to damages. In matters
such as this one, where the vaccinee is deceased at the time of a compensation award, the estate
can recover the death benefit of $250,000 as well as “pain and suffering and emotional distress
from the time of the injury until the date of death.” Tembenis v. Sec’y of Health & Human Servs.,
733 F.3d 1190, 1193 (Fed. Cir. 2013) (citing Zatuchni v. Sec’y of Health & Human Servs., 516
F.3d 1312, 1318-19 (Fed. Cir. 2008) (discussing damages available to a petitioner’s estate where
the petitioner had established vaccine-related injuries and vaccine-caused death).
IT IS SO ORDERED.
s/ Mindy Michaels Roth
Mindy Michaels Roth
Special Master
39