VICP Registry Case Source Bundle
Canonical URL: https://vicp-registry.org/case/USCOURTS-cofc-1_19-vv-00929
Package ID: USCOURTS-cofc-1_19-vv-00929
Petitioner: Donald C. Adams
Filed: 2019-06-26
Decided: 2025-09-03
Vaccine: influenza; Pneumovax 23 (pneumococcal polysaccharide, non-covered)
Vaccination date: 2018-10-11
Condition: cardiac arrest, anoxic brain injury, and death
Outcome: denied
Award amount USD: 

AI-assisted case summary:
On June 26, 2019, Abby Adams filed a petition on behalf of the estate of her father, Donald C. Adams. Mr. Adams was 69 years old when he received influenza and Pneumovax 23 vaccinations on October 11, 2018. The pneumococcal polysaccharide vaccine was not itself a covered vaccine under the Program, so the case proceeded on the claim that the covered influenza vaccine caused or significantly aggravated the events that led to his death.

Early the next morning, Mr. Adams felt hot and diaphoretic, had difficulty breathing, and collapsed. He was found in pulseless electrical activity cardiac arrest. Although emergency responders restored circulation, he suffered anoxic brain injury and intracerebral bleeding and died on October 14, 2018. His death certificate identified anoxic brain injury, intracerebral bleeding, coronary artery disease, and diabetes, and classified the manner of death as natural.

Petitioner relied on Dr. Mayer Rashtian, a cardiac electrophysiologist, who proposed that the influenza vaccine produced physiologic stress or immune activation that exacerbated Mr. Adams's cardiac vulnerability and triggered a ventricular arrhythmia, possibly through delayed anaphylaxis, vasovagal reaction, acute pulmonary edema, or cytokine-mediated inflammation. Respondent's expert, Dr. Shane J. LaRue, a cardiologist, responded that the clinical event was PEA arrest rather than ventricular arrhythmia, that the record did not support anaphylaxis or vaccine-caused inflammation, and that treating physicians had considered the vaccine unlikely to explain the arrest.

Special Master Daniel T. Horner denied compensation on September 3, 2025. He found that petitioner had not established a reliable medical theory linking the influenza vaccine to PEA arrest, had not shown a logical sequence of cause and effect in Mr. Adams's case, and had not shown that the next-morning timing itself supplied causation. No compensation was awarded.

Theory of causation field:
Influenza vaccine and Pneumovax 23 on October 11, 2018, age 69, followed by pulseless electrical activity cardiac arrest, anoxic brain injury, and death on October 14, 2018. DENIED. Abby Adams, administrator of Donald C. Adams's estate, argued through cardiac electrophysiologist Dr. Mayer Rashtian that the flu vaccine created physiologic stress, inflammation, delayed anaphylaxis, or a vasovagal response that destabilized Mr. Adams's underlying cardiac substrate and triggered ventricular arrhythmia leading to PEA arrest. Respondent's cardiology expert Dr. Shane J. LaRue rejected a vaccine-mediated mechanism, emphasized that PEA arrest is not ventricular arrhythmia, and noted the death certificate listed natural causes including anoxic brain injury, intracerebral bleeding, coronary artery disease, and diabetes. Special Master Daniel T. Horner found no reliable medical theory, no logical sequence of cause and effect, and no persuasive temporal proof. Decision September 3, 2025. Attorney: Phyllis Widman, Widman Law Firm, Linwood NJ.

Public staged source text:

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DOCUMENT 1: USCOURTS-cofc-1_19-vv-00929-1
Date issued/filed: 2025-09-29
Pages: 28
Docket text: PUBLIC DECISION (Originally filed: 09/03/2025) regarding 101 DECISION of Special Master. Signed by Special Master Daniel T. Horner. (cd) Service on parties made.
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Case 1:19-vv-00929-UNJ Document 103 Filed 09/29/25 Page 1 of 28
In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 19-929V
Filed: September 3, 2025
Special Master Horner
ABBY ADAMS, Administrator of the
Estate of DONALD C. ADAMS,
Petitioner,
v.
SECRETARY OF HEALTH AND
HUMAN SERVICES,
Respondent.
Phyllis Widman, Widman Law Firm, LLC, Linwood, NJ, for petitioner.
Alexa Roggenkamp, U.S. Department of Justice, Washington, DC, for respondent.
DECISION1
On June 26, 2019, petitioner, Abby Adams, filed a petition under the National
Childhood Vaccine Injury Act, 42 U.S.C. § 300aa-10-34 (2012),2 on behalf of her late
father, Donald Adams, alleging that he suffered cardiac arrest and anoxic brain injury
post-cardiac arrest as a result of the pneumococcal and influenza (“flu”) vaccines that
he received on October 11, 2018.3 (ECF No. 1.) Alternatively, petitioner argues that
1 Because this document contains a reasoned explanation for the action taken in this case, it must be
made publicly accessible and will be posted on the United States Court of Federal Claims' website, and/or
at https://www.govinfo.gov/app/collection/uscourts/national/cofc, in accordance with the E-Government
Act of 2002. 44 U.S.C. § 3501 note (2018) (Federal Management and Promotion of Electronic
Government Services). This means the document will be available to anyone with access to the
internet. In accordance with Vaccine Rule 18(b), Petitioner has 14 days to identify and move to redact
medical or other information, the disclosure of which would constitute an unwarranted invasion of privacy.
If, upon review, I agree that the identified material fits within this definition, I will redact such material from
public access.
2 Within this decision, all citations to § 300aa will be the relevant sections of the Vaccine Act at 42 U.S.C.
§ 300aa-10-34.
3 The decedent’s vaccine administration record confirmed that his pneumococcal vaccination was a
“Pneumovax 23” vaccine rather than a “Prevnar” vaccine. However, only pneumococcal conjugate
vaccines are covered by the Vaccine Injury Table, 42 C.F.R. § 100.3(a)(XII), and the Pneumovax 23
vaccine is a polysaccharide rather than conjugate vaccine, e.g., Morrison v. Sec’y of Health & Human
Servs., No. 04-1683V, 2005 WL 2008245 (Fed. Cl. Spec. Mstr. July 26, 2005). Accordingly, this case
turns on whether petitioner can implicate the flu vaccine in particular as a cause of her father’s death.
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Case 1:19-vv-00929-UNJ Document 103 Filed 09/29/25 Page 2 of 28
the pneumococcal and flu vaccines significantly aggravated a pre-existing condition,
leading to Mr. Adams’s untimely death. (Id.) Petitioner clearly suffered a profound loss,
and I offer my sincerest condolences. However, for the reasons set forth below, I
conclude that petitioner is not entitled to an award of compensation.
I. Applicable Statutory Scheme
Under the National Vaccine Injury Compensation Program, compensation
awards are made to individuals who have suffered injuries after receiving vaccines. In
general, to gain an award, a petitioner must make a number of factual demonstrations,
including showing that an individual received a vaccination covered by the statute;
received it in the United States; suffered a serious, long-standing injury or death; and
has received no previous award or settlement on account of the injury. Finally – and the
key question in most cases under the Program – the petitioner must also establish a
causal link between the vaccination and the injury. In some cases, the petitioner may
simply demonstrate the occurrence of what has been called a “Table Injury.” That is, it
may be shown that the vaccine recipient suffered an injury of the type enumerated in
the “Vaccine Injury Table,” corresponding to the vaccination in question, within an
applicable time period following the vaccination also specified in the Table. If so, the
Table Injury is presumed to have been caused by the vaccination, and the petitioner is
automatically entitled to compensation, unless it is affirmatively shown that the injury
was caused by some factor other than the vaccination. § 300aa-13(a)(1)(A);
§ 300aa-11(c)(1)(C)(i); § 300aa-14(a); § 300aa-13(a)(1)(B).
Alternatively, if no injury falling within the Table can be shown, a petitioner could
still demonstrate entitlement to an award by instead showing that the vaccine recipient’s
injury or death was caused-in-fact by the vaccination in question. § 300aa-13(a)(1)(A);
§ 300aa-11(c)(1)(C)(ii). In particular, a petitioner must demonstrate that the vaccine
was “not only [the] but-for cause of the injury but also a substantial factor in bringing
about the injury.” Moberly v. Sec’y of Health & Human Servs., 592 F.3d 1315, 1321-22
(Fed. Cir. 2010) (quoting Shyface v. Sec’y of Health & Human Servs., 165 F.3d 1344,
1352-53 (Fed. Cir. 1999)); Pafford v. Sec’y of Health & Human Servs., 451 F.3d 1352,
1355 (Fed. Cir. 2006). To successfully demonstrate causation-in-fact, petitioner bears a
burden to show: (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 proximate temporal relationship between vaccination
and injury.4 Althen v. Sec’y of Health & Human Servs., 418 F.3d 1274, 1278 (Fed. Cir.
2005).
4 Additionally, where a petitioner in an off-Table case is seeking to prove that a vaccination significantly
aggravated a pre-existing injury, the petitioner must establish the three Althen prongs along with three
additional factors described in the prior Loving case. See Loving ex rel. Loving v. Sec’y of Health &
Human Servs., 86 Fed. Cl. 135, 144 (2009) (combining the first three Whitecotton factors for claims
regarding aggravation of a Table injury with the three Althen factors for off table injury claims to create a
six-part test for off-Table aggravation claims); see also W.C. v. Sec’y of Health & Human Servs., 704 F.3d
1352, 1357 (Fed. Cir. 2013) (applying the six-part Loving test). The additional Loving factors require
petitioners to demonstrate aggravation by showing: (1) the vaccinee’s condition prior to the administration
2

Case 1:19-vv-00929-UNJ Document 103 Filed 09/29/25 Page 3 of 28
In this case, petitioner has not alleged any condition listed on the Vaccine Injury
Table. Accordingly, petitioner must satisfy the above-described Althen test for
establishing causation-in-fact.
Vaccine Program petitioners bear a “preponderance of the evidence” burden of
proof. § 300aa-13(1)(a). That is, a petitioner must offer evidence that leads the “trier of
fact to believe that the existence of a fact is more probable than its nonexistence before
[he] may find in favor of the party who has the burden to persuade the judge of the fact’s
existence.” Moberly, 592 F.3d at 1322 n.2 (alternation in original); see also Snowbank
Enters., Inc. v. United States, 6 Cl. Ct. 476, 486 (1984) (explaining that mere conjecture
or speculation is insufficient under a preponderance standard). Proof of medical
certainty is not required. Bunting v. Sec’y of Health & Human Servs., 931 F.2d 867, 873
(Fed. Cir. 1991). In finding causation, a program fact-finder may rely upon
“circumstantial evidence,” which the court found to be consistent with the “system
created by Congress, in which close calls regarding causation are resolved in favor of
injured claimants.” Althen, 418 F.3d at 1279-80. However, a petitioner may not receive
a Vaccine Program award based solely on her assertions; rather, the petition must be
supported by either medical records or by the opinion of a competent physician.
§ 300aa-13(a)(1). The supporting medical opinion must be based on “sound and
reliable” medical or scientific explanation. Boatmon v. Sec’y of Health & Human Servs.,
941 F.3d 1351, 1359 (Fed. Cir. 2019).
Cases in the Vaccine Program are assigned to special masters who are
responsible for “conducting all proceedings, including taking such evidence as may be
appropriate, making the requisite findings of fact and conclusions of law, preparing a
decision, and determining the amount of compensation, if any, to be awarded.” Vaccine
Rule 3(b)(1). Special masters must ensure each party has had a “full and fair
opportunity” to develop the record. Vaccine Rule 3(b)(2). However, special masters are
empowered to determine the format for taking evidence based on the circumstances of
each case. Vaccine Rule 8(a); Vaccine Rule 8(d). Special masters are not bound by
common law or statutory rules of evidence but must consider all relevant and reliable
evidence in keeping with fundamental fairness to both parties. Vaccine Rule 8(b)(1).
The special master is required to consider “all [] relevant medical and scientific evidence
contained in the record,” including “any diagnosis, conclusion, medical judgment, or
autopsy or coroner’s report which is contained in the record regarding the nature,
causation, and aggravation of the petitioner’s illness, disability, injury, condition, or
death,” as well as the “results of any diagnostic or evaluative test which are contained in
the record and the summaries and conclusions.” § 300aa-13(b)(1)(A). The special
master is required to consider the entire record, draw plausible inferences, and
articulate a rational basis for the decision. Winkler v. Sec’y of Health & Human Servs.,
88 F.4th 958, 963 (Fed. Cir. 2023) (citing Hines ex rel. Sevier v. Sec’y of Health &
Human Servs., 940 F.2d 1518, 1528 (Fed. Cir. 1991)).
of the vaccine, (2) the vaccinee’s current condition, and (3) whether the vaccinee’s current condition
constitutes a “significant aggravation” of the condition prior to the vaccination. Loving, 86 Fed. Cl. at 144.
3

Case 1:19-vv-00929-UNJ Document 103 Filed 09/29/25 Page 4 of 28
II. Procedural History
Petitioner filed medical records marked Exhibits 1-6 between July and October of
2019. (ECF Nos. 7, 14.) Respondent filed his Rule 4 report on June 11, 2020,
recommending against compensation. (ECF No. 22.) Respondent asserted that none
of Mr. Adams’s treating physicians definitively associated his condition with his
vaccination. (Id. at 10-12.) Respondent further asserted that petitioner had not
presented any evidence regarding the natural course of any pre-existing condition or
any evidence to support significant aggravation of a pre-existing condition.5 (Id. at 12-
13.)
In August of 2020, petitioner filed additional medical records, marked Exhibit 7.
(ECF No. 25.) Thereafter, in May of 2022, petitioner filed an expert report by cardiac
electrophysiologist Dr. Mayer Rashtian, along with accompanying medical literature.
(ECF Nos. 39, 41; Exs. 8-18.) On December 14, 2022, petitioner filed additional
medical records, marked Exhibit 19. (ECF No. 48.) Respondent subsequently filed
records from Carlisle Fire Company, marked Exhibit C.6 (ECF No. 67.) Respondent
also filed an expert report by cardiologist Dr. Shane J. LaRue, along with accompanying
medical literature. (ECF No. 62; Ex. A-B.) Thereafter, petitioner filed a supplemental
expert report by Dr. Rashtian. (ECF No. 64, Ex. 21.) Petitioner also filed updated
medical records, marked Exhibit 22, on December 12, 2023. (ECF No. 68.)
Respondent responded to Dr. Rashtian’s supplemental report with a supplemental
expert report by Dr. LaRue, along with accompanying medical literature. (ECF No. 72;
Ex. D.) Finally, petitioner filed medical records marked as Exhibit 23 in May of 2024.
(ECF No. 75.)
An entitlement hearing was held on October 23, 2024. (See Transcript of
Proceedings (“Tr.”), at ECF No. 93.) During the hearing, petitioner testified as well as
Drs. Rashtian and LaRue. (See id.) The parties opted not to file post-hearing briefs.
(ECF No. 91.) Accordingly, the parties have had a full and fair opportunity to develop
the record, and this case is now ripe for resolution.
5 Additionally, respondent initially questioned whether administration of the subject vaccines was
preponderantly established (ECF No. 22, pp. 9-10); however, he later stipulated that the decedent
received the vaccines as alleged (ECF No. 81).
6 On December 19, 2022, petitioner filed a Statement of Unavailability of Records, detailing counsel’s
efforts to locate outstanding medical records. (ECF No. 50.) Petitioner indicated that she had been
unable to locate the EMS transport records. (Id.) Thereafter, respondent was provided an opportunity to
pursue additional avenues of discovery pursuant to Vaccine Rule 7. (Non-PDF Scheduling Order, filed
Dec. 21, 2022.) Respondent indicated his intent to file a motion for leave to issue a subpoena for the
outstanding records and requested that petitioner file all billing records in connection with Mr. Adams’
treatment on October 12, 2018, to assist in his search for the EMS provider to which a subpoena may be
issued. (ECF Nos. 51-52.) Petitioner filed the requested billing records on March 23, 2023. (ECF No.
53.) On April 25, 2023, respondent filed two motions, requesting authorization to issue subpoenas to
Carlisle Fire Co., Inc. and Hart to Heart Transportation, Inc., respectively, which were subsequently
granted. (ECF Nos. 56-59.)
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Case 1:19-vv-00929-UNJ Document 103 Filed 09/29/25 Page 5 of 28
III. Factual History
a. As reflected in the medical records
i. Pre-vaccination
Mr. Adams was born on July 29, 1949. (Ex. 2; Ex. 7, p. 2.) At the time of
vaccination, he was sixty-nine years old. (Ex. 1, p. 1; Ex. 2; Ex. 7, p. 2.) His past
medical history was significant for diabetes mellitus, hypertension, hyperlipidemia,
atypical chest pain, and cigarette smoking. (See generally Ex. 4.)
Mr. Adams underwent an echocardiogram in 2002 that revealed concentric left
ventricular hypertrophy with normal cavity size and preserved systolic function, mild
mitral regurgitation, dilated left atrium, and mild tricuspid regurgitation. (Ex. 4, p. 199.)
At sixty-one years of age, Mr. Adams underwent an electrocardiogram (“EKG”) that
showed sinus rhythm with occasional premature ventricular contractions (“PVCs”) but
was otherwise normal. (Id. at 198.)
On May 3, 2012, Mr. Adams presented to his cardiologist with complaints of a
two-month history of intermittent, left-sided chest pain when coughing. (Ex. 4, p. 175.)
A physical examination and review of his recent laboratory results were unremarkable.
(Id. at 175-78.) His cardiologist’s assessed Mr. Adams with chest pain, hypertension,
hyperlipidemia, diabetes mellitus, tobacco use, and morbid obesity. (Id. at 177-78.) It
was noted that he underwent a stress test in 2010, and he reported that the results were
“fine;” however, there were “[n]o results to review.” (Id. at 178.) He was advised to
undergo a repeat stress test, which he completed on May 31, 2012. (Id. at 171, 178.)
The results of the stress test showed no evidence of dipyridamole induced myocardial
ischemia or scar. (Id. at 171.) Left ventricular ejection fraction was normal at 61%.
(Id.)
Mr. Adams presented to the emergency department on February 13, 2017, with
complaints of a three-day history of numbness and tingling in his right upper extremity.
(Ex. 23, p. 7.) He also reported two days of tingling in his face that had since resolved.
(Id.) He denied headache, speech/vision changes, weakness, chest pain, shortness of
breath, nausea, vomiting, diarrhea, fever, and chills. (Id.) A physical examination was
normal with the exception of elevated blood pressure. (Id. at 8-9.) An EKG revealed
abnormal conduction with an incomplete right bundle branch block and frequent PVCs.
(Id. at 9.) Imaging studies of Mr. Adams’s head, brain, and neck were unremarkable
with the exception of observed atrophy with chronic small vessel ischemic change,
which was seen on CT scan of petitioner’s head without contrast. (Id. at 12-13.)
Although it was recommended that Mr. Adams be admitted for a full stroke work up, he
ultimately opted to be discharged home. (Id. at 13-14.)
Throughout 2017, Mr. Adams presented to his primary care physician for a
nodule in the right lung, tobacco use, hypertension, strain of the right supraspinatus
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tendon, adjustment disorder with mixed anxiety and depressed mood, and type 2
diabetes mellitus with hyperlipidemia. (Ex. 4, pp. 105-35.)
On January 12, 2018, Mr. Adams presented to his primary care provider and
reported increased and worsening episodes of chest palpitations. (Ex. 4, p. 96.) He
described a “buzzing feeling” in his heart and associated fatigue, dizziness, and vision
changes. (Id.) A physical exam was unremarkable. (Id. at 99.) The differential
diagnosis mentioned Mr. Adams’s chronic hypertension and diabetes mellitus. (Id.) It
was also noted that Mr. Adams had recently quit smoking and was experiencing some
exertional dyspnea and atypical chest pain with intermittent cardiac arrhythmia for one
month. (Id.) An EKG, echocardiogram, and Holter monitor were ordered, and Mr.
Adams was referred to a cardiologist. (Id.) Despite the study being technically difficult
with many images being suboptimal in quality, a January 16, 2018 echocardiogram
showed diastolic dysfunction, trace mitral regurgitation, and trace tricuspid regurgitation.
(Id. at 93-95.) Mr. Adams had “low normal” left ventricular systolic function with a left
ventricular ejection fraction of 50-55%. (Id. at 93.)
On January 25, 2018, Mr. Adams saw cardiologist Laeeq Ahmer, M.D., for an
evaluation and management of palpitations, shortness of breath, and coronary artery
disease. (Ex. 4, pp. 54-59.) A history of hypertension, diabetes, and hyperlipidemia, as
well as coronary artery calcification on a prior CT scan of the chest, was noted. (Id. at
54.) Mr. Adams reported intermittent palpitations, which had persisted for several
months, and brief heart flutters, which typically lasted only seconds. (Id.) Although he
had been wearing a Holter monitor, he had not experienced any palpitations in the last
few days. (Id.) Additionally, he was not complaining of chest pain but noted exertional
dyspnea for the past several months. (Id.) His blood pressure was mildly elevated
during this encounter but otherwise well controlled with Coreg, amlodipine, and
lisinopril. (Id.) His lipids were also well controlled on Lipitor. (Id.) A physical
examination was normal. (Id. at 57.) Dr. Ahmer diagnosed Mr. Adams with coronary
artery disease involving native coronary artery of native heart without angina pectoris
and ordered a stress test with myocardial perfusion SPECT. (Id. at 58.) He further
diagnosed palpitations, shortness of breath, hypertension, and hyperlipidemia. (Id. at
58-59.) Mr. Adams underwent a stress test on January 31, 2018, which showed a
medium-sized, partially reversible defect in the inferolateral wall consistent with mild
ischemia as well as mildly depressed left ventricle function. (Id. at 44-45.)
Mr. Adams followed up with Dr. Ahmer on February 9, 2018, to discuss the
results of his stress test and Holter monitor. (Ex. 4, pp. 38-43.) A physical exam was
normal. (Id. at 41.) His mild exertional dyspnea and blood pressure were stable during
this encounter. (Id. at 38.) Mr. Adams noted that his palpitations had gradually
resolved. (Id.) While his Holter monitor uncovered very frequent premature ventricular
contractions, Mr. Adams did not notice any palpitations during monitoring. (Id. at 38,
42.) He also had frequent ventricular triplets and runs of nonsustained ventricular
tachycardia. (Id. at 42.) Dr. Ahmer increased his prescription for Coreg and
recommended an ischemic workup and a repeat Holter monitor. (Id.) Regarding Mr.
Adams’ abnormal stress test, Dr. Ahmer was concerned that he might have silent
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ischemia and suggested that he undergo a cardiac catheterization for further evaluation.
(Id. at 42-43.) Mr. Adams underwent a cardiac catheterization on February 15, 2018,
which showed mild, non-obstructive coronary artery disease by angiography, coronary
artery calcification, and left ventricular ejection fraction of 50%. (Id. at 36-37.) He
followed up with Dr. Ahmer on March 8, 2018, and was noted to be doing well on an
increased dose of Coreg with no further palpitations noted. (Id. at 28-33.) An EKG
performed on that day showed normal sinus rhythm without premature ventricular
contractions and did not show acute ischemia. (Id. at 32.) Mr. Adams denied chest
pain and his lipids and blood pressure were well controlled. (Id. at 31-33.)
On June 8, 2018, Mr. Adams returned to Dr. Ahmer, and it was noted that he was
doing well with only infrequent premature ventricular contractions and no palpitations.
(Ex. 5, pp. 224-5, 229.) He presented to endocrinologist James Hays, M.D., on July 30,
2018, for management of his diabetes. (Ex. 6, pp. 2-5.) Although it was noted that Mr.
Adams had quit smoking approximately one year prior, he was receiving three insulin
injections per day and his glucose monitoring was still labile. (Id. at 5.)
On October 11, 2018, Mr. Adams presented to his primary care provider for a
prescription to control his blood sugar and a referral for a new endocrinologist. (Ex. 4,
p. 1.) He described his diabetes as worsening due to diet noncompliance and missed
medication and being associated with nocturia, peripheral neuropathy, and weight gain.
(Id. at 5.) His hypertension was unchanged and associated with fatigue and vision
changes. (Id. at 5-6.) A physical exam was normal. (Id. at 6-7.) During this encounter,
Mr. Adams received the subject flu and pneumococcal 23-polyvalent vaccines. (Id. at 7;
Ex. 1; Ex. 7.) On the flu vaccine consent form, Mr. Adams denied that he “ever had a
serious allergic reaction to a previous dose of flu vaccine.” (Ex. 1, p. 2.) Mr. Adams’s
primary care physician referred him to an endocrinologist and deferred insulin
management to his new specialist. (Ex. 4, p. 7.) Mr. Adams was also prescribed
empagliflozin7 for management of his diabetes in the interim. (Id.)
ii. Post-vaccination
At around 8:00 p.m. on the day of the vaccination at issue, Mr. Adams
complained that he was tired and decided to watch television in bed. (Ex. 23, p. 161;
see also Ex. 5, p. 262.) At around 2:30 a.m. on October 12, 2018, we awoke not feeling
well. (Ex. 23, p. 161.) He was feeling hot and diaphoretic.8 (Id.) He called his
daughter before dialing 911. (Id.)
At approximately 3:39 a.m., Emergency Medical Services (“EMS”) was
dispatched to Mr. Adams’s home due to reports that he was experiencing difficulty
breathing and a fever. (Ex. C, pp. 2-3.) It was noted that Mr. Adams had received “2
7 Empagliflozin, which is the generic name for Jardiance, is commonly used to help lower blood sugar in
patients with type 2 diabetes. Jardiance (Empagliflozin) – Uses, Side Effects, and More, WEBMD (June
18, 2024), https://www.webmd.com/drugs/2/drug-166762/jardiance-oral/details.
8 Diaphoretic pertains to or is characterized by sweating. Diaphoretic, DORLAND’S MEDICAL DICTIONARY
ONLINE, https://www.dorlandsonline.com/dorland/definition?id=13777 (last visited Aug. 26, 2025).
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shots this morning and believed that he was having a reaction to the shots.” (Id. at 3.)
Upon arrival, Mr. Adams was lying on the floor and was helped to a sitting position in a
chair. (Id.) It was noted that he “stood right up without any problems.” (Id.) Although
Mr. Adams was alert and oriented, his breathing was shallow. (Id.) While attempting to
take Mr. Adams’s vitals, he collapsed in his chair. (Id.; Ex. 23, 135.) Mr. Adams went
into agonal breathing and pulseless electrical activity arrest. (Ex. 23, p. 152.) Mr.
Adams was lowered to the ground, and his pulse was noted to be “no longer strong and
beating adequately.” (Ex. C, p. 3.) He was administered several rounds of epinephrine
and resuscitated by CPR. (Ex. 5, p. 262; Ex. 23, pp. 133, 135, 152.) It was noted that
EMS did not use an automated external defibrillator. (Ex. C, p. 3.) Mr. Adams
“regained pulses and then lost them a short while later.” (Id.; Ex. 23, p. 135.) He was
then transported to the hospital by ambulance. (Ex. C, p. 3; Ex. 23, p. 133.)
During transport, Mr. Adams’s pulse was restored, and he began “breathing on
his own slightly.” (Ex. C, p. 3; Ex. 23, pp. 133, 135.) However, it was noted that Mr.
Adams never regained consciousness. (Ex. 23, p. 161.) Upon arrival at the hospital at
around 5:08 a.m., Mr. Adams was unresponsive with an oropharyngeal airway through
mouth. (Id. at 135-37.) Mr. Adams’s wife informed the emergency department
physician that Mr. Adams had received the flu and pneumococcal vaccines earlier that
day and questioned whether the vaccines could have caused Mr. Adams’s condition.
(Id. at 135.) Mr. Adams was diagnosed with cardiac arrest, hyperglycemia, and
metabolic acidosis with respiratory acidosis. (Id. at 133.) Mr. Adams was subsequently
transferred to the intensive care unit and placed on a ventilator. (Id. at 147, 159.) In the
admission note, Mr. Adams’s diagnoses were pulseless electrical activity (“PEA”)
cardiac arrest of unknown etiology and lactic acidosis secondary to cardiac arrest. (Id.
at 159.)
Throughout the morning of October 12, 2018, Mr. Adams underwent a CT of his
head without contrast, a CT angiogram of his chest with contrast, and an x-ray of his
chest. (Ex. 23, pp. 142-45.) In pertinent part, the CT angiogram showed “[s]mall areas
of ill-defined reticulonodular infiltrate . . . involving the right upper lobe, likely
inflammatory of infectious,” and the x-ray of the chest showed no acute
cardiopulmonary process. (Id. at 143-44.) Mr. Adams’s lab results showed an elevated
white blood count of 19.3 K/μL (reference range of 4.5-11.0 K/μL) with 61.0%
neutrophils (reference range of 50.0-60.0 %). (Id. at 140-41.)
Later that same day, Mr. Adams had a cardiology consult. (Ex. 23, p. 175; see
also Ex. 5, p. 276.) In the history of present illness, it is noted that Mr. Adams went to
bed on the evening of October 11, 2018, “without any complaints” but woke his wife up
early the next morning due to difficulty breathing and a cough. (Ex. 23, p. 176.)
Although he was warm and diaphoretic, his wife stated that he denied chest pain or
palpitations. (Id.) It is noted that the paramedics were called and Mr. Adams’s
“dyspnea got worse rapidly and he collapsed in front of the paramedics.” (Id.)
Pulseless electrical activity was noted, and Mr. Adams was intubated. (Id.) CPR was
performed for several minutes before spontaneous circulation returned. (Id.) However,
no ventricular tachycardia or ventricular fibrillation was noted, and Mr. Adams did not
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required cardioversion during CPR. (Id.) Additionally, while the initial EKG showed
ischemia, a subsequent EKG, which was performed after Mr. Adams’s blood pressure
and oxygen had stabilized, showed no ischemia. (Id. at 176,188.) During this
encounter, Mr. Adams was intubated and unresponsive. (Id. at 176.) It is noted,
Initial cardiac enzymes showed troponin 0.3 which is gradually trending up
and is now 19. Echocardiogram done today shows low normal LV function
and there is no change noted from his prior echocardiogram from January
2018. Patient had been active until recently and according to the family
there was no report of exertional chest pain or shortness of breath in the
last few days.
(Id.) Mr. Adams was diagnosed with cardiopulmonary arrest and there was concern
about significant anoxic brain injury, but the cause of his condition was unclear. (Id. at
188.) It was further noted that the abnormal cardiac enzymes indicated myocardial
infarction, but this was likely secondary to hypoxemia from cardiac arrest. (Id.)
On October 13, 2018, Mr. Adams had an infectious disease consult, during which
his family reported that he had a rection to the flu vaccine “some 10 or 15 yrs ago and
this was his first flu vaccine in several years.” (Ex. 23, p. 161.) It was further noted that
Mr. Adams was recently put on a new medication, Jardiance, for his diabetes mellitus,
and that he had taken one pill only prior to the incident. (Id.) The assessment included
cardiac arrest and “[n]on-ST elevation (NSTEMI) myocardial infarction.” (Id. at 167.)
Pulmonary and cardiology causes were ruled out. (Id.) It was noted that “it is difficult to
say that this was anaphylactic reaction (no wheezing, no [shortness of breath], Vocal
cords normal at intubation)” but whether Mr. Adams’s condition was related to the
vaccinations or the new medication that he started could not be “completely exclude[d].”
(Id.) Mr. Adams was reported as being in a “normal state of health until the day he got
the vaccines.” (Id.) A VAERS report was contemplated. (Id.)
On October 14, 2018, it was noted that Mr. Adams suffered a pulseless electrical
activity cardiac arrest of unknown etiology and had spiked a fever, prompting treatment
with Zosyn and a cooling blanket. (Ex. 23, p. 189.) Following one episode of fever,
which included multiple premature ventricular contractions and nonsustained ventricular
tachycardia, Mr. Adams was treated with Amiodarone. (Id.) It was noted that Mr.
Adams’s elevated white blood count could be secondary to stress as a result of the
cardiac arrest. (Id. at 195.) Mr. Adams’s viral panels were negative and there were no
signs of infection. (Id.) It is noted that Mr. Adams’s family was “informed that it is
unlikely the flu shot can cause [pulseless electrical activity] arrest but cannot totally rule
out.” (Id.) Mr. Adams underwent an MRI of the brain, which showed hypoxic ischemic
injury with mild to moderate diffuse brain edema; moderate new intraventricular
hemorrhage with new hydrocephalus; and acute to early subacute left medial frontal,
bilateral punctate frontal, and right pontine infarcts. (Id. at 196, 243-44.) The radiologist
indicated that the bleeding could be secondary to the diffuse hypoxic ischemic injury.
(Id. at 196.) Mr. Adams’s family decided not to pursue aggressive intervention or
hospice care and to instead switch his code status to “do not resuscitate with comfort
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care.” (Id.) He was disconnected from the ventilator and started on a morphine drip for
respiratory distress. (Id. at 151, 196.) Mr. Adams was pronounced deceased at 8:40
p.m. on October 14, 2018. (Id. at 151; Ex. 2.) His death certificate lists his cause of
death as anoxic brain injury, intracerebral bleeding, coronary artery disease, and
diabetes, and classifies his manner of death as natural. (Ex. 2.) No autopsy was
performed. (Id.)
b. Testimony
Petitioner authored one affidavit in this case. (Ex. 24.) She also provided
testimony at the hearing. (Tr. 8-25.) Petitioner explained that, at around 4:00 a.m. on
October 12, 2018, she received a phone call from Mr. Adams, stating that he was
“having some kind of attack” and requesting that she come over. (Ex. 24, ¶ 4; Tr. 16.)
When petitioner arrived at her father’s house, Mr. Adams was laying on the ground and
indicating that he could not breathe. (Ex. 24, ¶ 6; Tr. 16-17.) His wife informed
petitioner that Mr. Adams had been complaining that he was hot all night and required
multiple electric fans. (Ex. 24, ¶ 7.) Petitioner decided to call 911, and the paramedics
arrived thereafter. (Id. ¶¶ 7-8; but see Tr. 17 (unable to recall whether EMTs arrived
first).) Petitioner avers that, at some point, Mr. Adams’s wife informed the paramedics
that he had just been to the doctor and received the flu and pneumonia vaccines. (Ex.
24, ¶ 9.) She further describes the paramedics helping Mr. Adams sit up in a chair after
he indicated that he could not do it himself. (Id. ¶¶ 10-11; Tr. 18.) Mr. Adams was
sitting with one hand on his knee for support and his head in his other hand when
talking to the paramedics. (Ex. 24, ¶ 11.) “At that point, [Mr. Adams] fell forward onto
the floor and his heart stopped.” (Id. ¶ 12; Tr. 18-19.) The paramedics that were
already there began performing CPR and additional paramedics arrived. (Ex. 24, ¶ 13;
Tr. 19-20.) Mr. Adams was then transported by ambulance to the hospital. (Ex. 24,
¶ 16; Tr. 19.) After the paramedics left, petitioner recalls counting five vials of
epinephrine “or whatever drug it is they use to try to restart a heart.” (Ex. 24, ¶ 15.)
She states her understanding is that Mr. Adams regained a pulse while still at the house
but lost the pulse during transport to the hospital. (Id. ¶¶ 15-16.)
Petitioner avers that Mr. Adams never regained consciousness. (Ex. 24, ¶ 17;
Tr. 22.) She describes how she felt that they made eye contact at one point during his
hospitalization, but notes that he could not speak, and that she has “no basis to believe
he was conscious.” (Ex. 24, ¶ 17.) She states that Mr. Adams’s physicians eventually
stopped running tests and seemed to be waiting for him to regain consciousness to
know whether he suffered any brain damage due to lack of oxygen as a result of his
cardiac arrest. (Id. ¶ 18; Tr. 22-23.) The following day, petitioner states that “a doctor
talked to us about our concerns about the vaccines my dad had received, but said
nothing conclusive.” (Ex. 24, ¶ 20.) She further avers that “[n]othing seemed to be
happening with respect to his care.” (Id. ¶ 21.) That night, Mr. Adams “had a fitful night”
and spiked a fever. (Id. ¶ 23.) Petitioner recalls being very uncomfortable while
watching Mr. Adams’s feet move in apparent reflex without the ability to speak. (Id.; Tr.
23.) She was concerned that he was in pain with no way to communicate. (Ex. 24,
¶ 23.) She requested that the attending physicians run additional tests or transfer Mr.
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Adams to a different hospital because “[i]t seemed they were just waiting for him to die.”
(Id. ¶ 25.) She was informed that, although another hospital would likely refuse to admit
him in his condition, one hospital had agreed to the transfer. (Id. ¶ 26.) Before deciding
whether to transfer him, they ran additional tests, and the results were grave. (Id.
¶¶ 27-28.) Petitioner avers that “[t]here was nothing that could be done that would
enable him to regain any form of life that he would want to live, if he would ever regain
consciousness.” (Id. ¶ 28.) Mr. Adams passed away very soon after his family made
the decision to withdraw life support. (Id. ¶ 29.)
Petitioner describes,
[m]y father was himself leading up to this. He had quit smoking. He took
care of himself more than many, in that he did go to the doctor, and he
followed up when he was told to. He almost never missed a day of work.
He always got up early – 4 a.m. and started working, took notes of his days,
drove to his various meetings throughout his territory, and came home for
dinner. He called his sister, Sherry, every day. He called me almost every
day, just to check if I “needed anything.” He was the kind of person who
loved to cut grass, and his yard was very well-maintained. He always had
a clean car and always polished his shoes, which I attribute to his service
in the Navy. I last saw him no more than a week before. He would often
stop by my house for a chat or I would go to his house for Sunday dinner. I
saw no changes in him, and he said nothing to me about feeling bad prior
to that terrifying phone call.
(Ex. 24, ¶ 31.)
IV. Expert Opinions
a. Petitioner’s Expert, Cardiac Electrophysiologist Mayer Rashtian,
M.D., F.A.C.C., F.H.R.S.9
9 Dr. Rashtian received his medical degree from Drexel University in Philadelphia, Pennsylvania in 1988,
before going on to complete an internship and residency in internal medicine at Loma Lina University
Medical Center in Loma Linda, California in 1989 and 1991, respectively; a fellowship in cardiology at LA
County-USC Medical Center in Los Angeles, California in 1994; and a fellowship in cardiac
electrophysiology at Kaiser Permanente Hospital in Los Angeles, California in 1995. (Ex. 9, p. 1.) He is
board certified in cardiovascular disease and clinical cardiac electrophysiology and maintains an active
medical license in California, where he practices cardiac electrophysiology at Foothill Cardiology Medical
Group. (Id. at 2-3; Ex. 8, p. 2.) Additionally, Dr. Rashtian is an Assistant Clinical Professor of Medicine at
Keck School of Medicine at the University of Southern California, an Assistant Clinical Professor of
Nursing at University of California at Los Angeles, and the Medical Director of the Cardiac
Electrophysiology Department at Huntington Memorial Hospital in Pasadena, California. (Ex. 9, p. 3; Ex.
8, p. 2.) Dr. Rashtian states that an integral part of his practice includes caring for patients who have
suffered from cardiac arrest; identifying the risk factors, causes, and triggers of cardiac arrest; and
prescribing appropriate therapies. (Ex. 8, p. 2.) Another significant part of his practice includes screening
patients who are at increased risk of sudden cardiac death and ordering various screening tests to define
the substrates that can increase the risk of sudden cardiac death. (Id.) He states that he commonly
works with patients, such as Mr. Adams, that have been diagnosed with frequent premature ventricular
contractions and nonsustained ventricular tachycardia and who continue to have symptoms despite
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Dr. Rashtian authored two expert reports on behalf of petitioner in this case.
(Exs. 8, 21.) He also provided expert testimony at the hearing. (Tr. 27-77, 127-36.) Dr.
Rashtian opines that “the stress of the flu vaccine” caused Mr. Adams to suffer a
sudden cardiac death. (Ex. 8, p. 5.) He explains that, prior to the flu vaccine, Mr.
Adams had “some form of idiopathic [ventricular arrhythmia],” which was “stable” and
included premature ventricular contractions (“PVCs”) and nonsustained ventricular
tachycardia. (Id. at 4-5; Tr. 35.) Dr. Rashtian notes that Mr. Adams was doing very well
on a small dose of beta blockers. (Ex. 8, p. 5.) However, following vaccination, Mr.
Adams’s underlying PVCs and nonsustained ventricular tachycardia were
“exacerbated,” inducing sudden cardiac death. (Id.; Tr. 37-39.)
Although he noted that he agreed with respondent’s summary of the medical
records in this case (Ex. 8, p. 4), Dr. Rashtian provided a summary of the relevant
chronology of events that led up to Mr. Adams’s death. (Tr. 35-36; see also Ex. 10.)
He explains that Mr. Adams’s had an underlying medical history of “stable
nonobstructive coronary artery disease with established known ventricular arrhythmia,
PVC, and nonsustained ventricular tachycardia.” (Tr. 35.) When Mr. Adams visited his
primary care doctor in October of 2018, he received the pneumovax and flu vaccines
and was also started on a new medication for his diabetes. (Id.) Within 14 to 18 hours
after this encounter, Mr. Adams started to feel unwell and experienced shortness of
breath. (Id. at 35-36.) By the time the paramedics arrived, Mr. Adams collapsed and
was in pulseless electrical activity (“PEA”). (Id. at 36.) As a result of his PEA, Mr.
Adams received CPR and epinephrine before subsequently being transported to the
hospital. (Id.) Upon arrival at the hospital, Mr. Adams was intubated and put on life
support. (Id.) Dr. Rashtian specifically notes that Mr. Adams had “more evidence of
ventricular arrhythmia, nonsustained ventricular tachycardia” at the hospital, and was
put on intravenous Amiodarone to suppress that arrhythmia. (Id.) After an MRI showed
findings indicating that Mr. Adams was essentially brain dead, the family withdrew care
and extubated him, and he died shortly thereafter. (Id.)
Dr. Rashtian provides an overview of ventricular arrhythmias. (Ex. 8, pp. 2-4.)
He explains that ventricular arrhythmia is an umbrella term that includes PVCs, which
are extra heartbeats that begin in one of the heart’s two lower pumping chambers and
disrupt the regular heart rhythm, causing a sensation of “fluttering” or “skipped beat” in
the chest. (Id. at 2.) The clinical presentation of ventricular arrhythmia can range from
asymptomatic to cardiac arrest with the most life-threatening ventricular arrhythmia
being associated with ischemic heart disease, particularly in older patients. (Id.) Risk
factors for ventricular arrhythmia and sudden cardiac death vary based on underlying
cardiac conditions, family history, and genetic variants. (Id. at 3.) Long-term monitoring
demonstrates that PVCs are found in about 50% of all people with or without heart
disease. (Id.) However, frequent PVCs – defined as the presence of at least one PVC
medical therapy. (Id.) Dr. Rashtian has published 25 articles and 5 abstracts, and he has participated in
30 research experiences. (Ex. 9, pp. 4-9.) Dr. Rashtian was proffered without objection as an expert in
cardiology and cardiac electrophysiology. (Tr. 33-34.)
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on 12-lead ECG or over 30 PVCs per hour – are associated with increased
cardiovascular risk and mortality. (Id.) Moreover, in some populations, nonsustained
ventricular tachycardia has been independently associated with increased risk of death
and other cardiovascular adverse outcomes. (Id.) As PVCs and nonsustained
ventricular tachycardia are common in cardiovascular disease and have been
associated with adverse cardiovascular outcomes, detection of PVCs is generally
considered a risk factor for such adverse outcomes and useful in prompting additional
testing to determine the presence of underlying conditions. (Id.) One such outcome,
which is a common consequence of ventricular arrhythmia, is sudden cardiac death.
(Id.) This outcome accounts for approximately 50% of all cardiovascular deaths. (Id.)
Dr. Rashtian describes the mechanisms of ventricular arrhythmia as including
enhanced normal automaticity, abnormal automaticity, triggered activity induced by
early or late afterdepolarizations, and reentry. (Ex. 8, p. 4.) With regard to reentry, Dr.
Rashtian explains that this mechanism requires a trigger to initiate the arrhythmia and a
substrate to sustain it. (Id.) A potential trigger could be a PVC, which may be due to
automaticity. (Id.) A potential substrate could be structural remodeling secondary to an
underlying disease process, a scar secondary to a prior myocardial infarction or surgical
repair, or patchy fibrosis in the setting of cardiomyopathy or hypertrophy. (Id.) The
electrophysiological substrate is dynamically influenced by a variety of factors including
cardiac metabolism, electrolytes, signaling pathways, and autonomic effects. (Id.) With
regard to enhanced automaticity and abnormal automaticity, ventricular arrhythmia may
arise from subordinate pacemaker cells in the His-Purkinje system or ventricular
myocardium. (Id.) Ventricular arrhythmia that is not associated with underlying
structural heart disease or genetic arrhythmia syndrome is commonly referred to as
idiopathic. (Id.) Idiopathic ventricular arrhythmia tends to be monomorphic and based
on a focal mechanism of triggered activity or abnormal automaticity with a few being the
result of reentry. (Id.) Dr. Rashtian opines that Mr. Adams suffered from an idiopathic
ventricular arrhythmia as his cardiac structure was unremarkable, and he did not have
previous myocardial infarction. (Id.)
Substrate is the underlying pathology of an individual with abnormal cardiac
status. (Tr. 39-40.) In this case, Dr. Rashtian notes that Mr. Adams’s substrate refers
to his stable underlying coronary artery disease with frequent PVCs and nonsustained
tachycardia and slightly reduced ejection fraction. (Id. at 41; Ex. 8, p. 5.) While Mr.
Adams’s underlying cardiac condition was stable at the time of vaccination, Dr. Rashtian
notes that his substrate left him more susceptible to injury. (Tr. 41, 58.) Specifically, he
states that “if you look at 1,000 patients like him, by virtue of having the lower ejection
fraction and the PVCs, he would be higher risk of a future cardiac arrest.” (Id. at 70-71.)
Moreover, Dr. Rashtian recognizes that many different factors can impact the type of
substrate that Mr. Adams had. (Ex. 8, p. 4; Tr. 71.) Accordingly, for patients with a
substrate similar to Mr. Adams who experience an acute cardiac event such as PEA, it
is not uncommon for the triggering event to be indeterminable. (Tr. 72-74.)
Dr. Rashtian agrees that Mr. Adams died from a complication of his PEA cardiac
arrest. (Tr. 43, 75-76.) He explains that PEA occurs when the heart has a rhythm but
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there is no pulse or circulation. (Id. at 36.) Essentially, PEA is the end result of a very
bad case of hypotension. (Id. at 38, 128.) While Dr. Rashtian notes that Mr. Adams
was in a PEA cardiac arrest when the paramedics arrived (Id. at 36, 38; Ex. 21, p. 3), he
acknowledges that it is impossible to determine exactly what was going on before his
PEA and the arrival of the paramedics (Tr. 38, 46-47, 59). Therefore, his proposed
causal theory focuses on providing “a probable cause and explanation for what
preceded the PEA cardiac arrest.” (Id. at 43.)
Although Dr. Rashtian agrees that Mr. Adams experienced a PEA cardiac arrest
that ultimately led to his death (Tr. 43, 75-76), he opines that Mr. Adams likely first
experienced ventricular arrhythmia, such as ventricular fibrillate or ventricular
tachycardia, that evolved into a PEA cardiac arrest by the time the paramedics arrived.
(Ex. 21, p. 3; Tr. 43-46, 75-76.) While he acknowledges that there is no evidence that
Mr. Adams was experiencing ventricular tachycardia when EMS arrived (Tr. 45), Dr.
Rashtian notes that it is established that Mr. Adams experienced ventricular tachycardia
prior to his vaccination and while hospitalized after his cardiac arrest (Id. at 46).
Therefore, he contends it is “very likely” that Mr. Adams had ventricular tachycardia
before his PEA arrest. (Id. at 45, 59.) Specifically, Dr. Rashtian opines that the insult
and stress of the flu vaccine combined with his underlying cardiac conditions could have
caused Mr. Adams to experience “prolonged nonsustained ventricular tachycardia” that
resolved by the time the paramedics arrived and degenerated into PEA. (Id. at 44-45,
58.) He contends that any ventricular arrhythmia cardiac arrest that is shockable will
degenerate to PEA arrest if not attended to and treated promptly. (Ex. 21, p. 3.)
However, Dr, Rashtian concedes it is not common for ventricular tachycardia to
degenerate into PEA (Tr. 60-61), noting that “[u]sually a ventricular tachycardia does not
terminate in the PEA . . . It degenerates to – usually to a systolic cardiac arrest.” (Id. at
47.)
Dr. Rashtian’s opinion implicates the flu vaccine, stating that an acute
immunological reaction to the flu vaccine in a patient with an underlying substrate for
increased risk of sudden cardiac death is what triggered Mr. Adams’s PEA cardiac
arrest. (Ex. 8, p. 5; Tr. 37-39, 58, 75-76.) As a general matter, Dr. Rashtian recognizes
the benefits of the flu vaccine, especially for vulnerable cardiac patients, and attests that
he strongly advocates the flu vaccine for all his patients, especially those with
underlying congestive heart failure, coronary disease, heart attack, and individuals with
pacemakers and defibrillators. (Tr. 50-51; Ex. 8, p. 6.) He indicates that based on Mr.
Adams’s status at the time of vaccination, “[t]here was no reason not to give him the flu
vaccine.” (Tr. 52.) However, he acknowledges that some patients unfortunately suffer
an adverse reaction to the flu vaccine. (Id. at 51-53.)
Describing the flu vaccine as “both a trigger and aggravation,” Dr. Rashtian
contends that the stress of the flu vaccine, acute leukocytosis, and acute inflammatory
reaction turned Mr. Adams’s stable substrate into an acutely unstable arrhythmia, which
led to his PEA cardiac arrest. (Ex. 8, p. 5; Tr. 37-39.) He explains that Mr. Adams’s
reaction to the immune response produced by the vaccine “was too much stress for his
heart.” (Tr. 75.) Dr. Rashtian opines that Mr. Adams’s immune response to the flu
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vaccine could have exacerbated his underlying PVCs that grew into “long runs of
nonsustained ventricular tachycardia that was probably terminated on its own before the
paramedic arrived.” (Id.; Ex. 8, p. 5.) This sequence of events disturbed the equilibrium
of Mr. Adams’s heart and resulted in PEA arrest. (Tr. 75-76; Ex. 8, p. 5.) Moreover, he
characterizes his proposed causal hypothesis as “common sense and basic medical
theory,” citing Halverson v. Secretary of Health & Human Services, No. 15-227V, 2020
WL 992588 (Fed. Cl. Spec. Mstr. Feb. 4, 2020) as support. (Ex. 8, p. 5.) However, Dr.
Rashtian also concedes that none of the medical literature filed by petitioner mentions
or discusses the flu vaccine as a cause of ventricular arrhythmia, nor does it implicate
ventricular arrhythmia as a cause of PEA. (Tr. 60-64 (discussing Sana M. Al-Khatib et
al., 2017 AHA/ACC/HRS Guideline for Management of Patients with Ventricular
Arrhythmias and the Prevention of Sudden Cardiac Death, 138 CIRCULATION e272
(2018) (Ex. 11); Steven J. Compton, Ventricular Tachycardia, MEDSCAPE,
https://emedicine.medscape.com/article/159075 (last updated Dec. 5, 2017) (Ex. 12)).)
Dr. Rashtian contends that the flu vaccine induces a release of cytokines, and
vulnerable individuals, such as Mr. Adams, can experience a reaction to this immune
response that aggravates and makes an underlying condition more unstable. (Tr. 37-
39, 75.) However, he also indicates that nobody can say for certain that Mr. Adams did
not suffer a delayed anaphylactic reaction to the flu vaccine. (Id. at 38.) Dr. Rashtian
states that we know Mr. Adams was hypotensive and short of breath prior to his PEA
and stresses that these symptoms are consistent with a delayed anaphylactic reaction.
(Id. at 38-39.) In the case of a delayed anaphylactic reaction to the vaccine, Dr.
Rashtian notes that Mr. Adams’s underlying coronary artery disease and ventricular
arrhythmias would have prevented him from tolerating and appropriately responding to
the anaphylaxis. (Id.) Regardless of whether Mr. Adams’s reaction to the vaccine is
characterized as anaphylaxis, Dr. Rashtian opines that it is more probable than not that
the vaccination triggered Mr. Adam’s PEA arrest and death. (Id. at 74-76.)
However, Dr. Rashtian also notes that he is not providing one direct cause of Mr.
Adams’s PEA and death. (Tr. 134.) Rather, he offers a series of possible contributory
factors that led to the PEA arrest, noting that Mr. Adams could have experienced “a
combination of a nonsustained ventricular tachycardia, delayed anaphylactic reaction, a
delayed severe vasovagal reaction, some immune reaction, acute pulmonary edema,
any of those or in combination.” (Id. at 65.) Dr. Rashtian notes that the symptoms Mr.
Adams experienced before his PEA, specifically the elevated temperature, shortness of
breath, and hypotension, are indicative of delayed anaphylaxis but also consistent with
tachycardia. (Id. at 45-46.) He states that Mr. Adams could have been experiencing a
cytokine reaction, delayed anaphylaxis, and/or runs of nonsustained ventricular
tachycardia, and that all of these clinical scenarios “would give the same symptoms.”
(Id. at 46.) Therefore, Dr. Rashtian opines that “the combinations of vaccine reaction,
cytokine release, runs of a ventricular arrhythmia, possible anaphylactic reaction to [the
vaccines], all in combination” more likely than not triggered Mr. Adams’s PEA. (Id. at
65; see also id. at 37-39, 43-49, 62, 65, 129.)
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b. Respondent’s Expert, Cardiologist Shane J. LaRue, M.D., M.P.H.S.10
Dr. LaRue authored two expert reports on behalf of petitioner in this case. (Exs.
A, D.) He also provided expert testimony at the hearing. (Tr. 78-126.) Dr. LaRue
opines that the subject flu vaccine did not have any bearing on Mr. Adams’s clinical
course and death. (Ex. A, p. 10; Ex. D, p. 2; Tr. 82-83.)
Dr. LaRue begins by providing a summary of the pertinent medical facts in this
case. (Ex. A, pp. 2-5; Tr. 82-83, 91-93.) He notes that Mr. Adams had a medical
history significant for non-obstructive coronary artery disease, hypertension, diabetes,
mild left ventricular dysfunction, premature ventricular contractions (“PVCs”), and
nonsustained ventricular tachycardia. (Ex. A, p. 2.) However, Dr. LaRue agrees with
Dr. Rashtian that Mr. Adams’s clinical presentation from a cardiac standpoint was stable
at the time of vaccination. (Tr. 94.) He describes how Mr. Adams was initially feeling
well after receiving the subject vaccination, but notes that he awoke pale, diaphoretic,
and warm in the early morning of the day after vaccination. (Ex. A, pp. 4-5 (citing Ex. 5,
pp. 237, 267); Tr. 82-83, 95.) Although Mr. Adams did not report chest pain or
palpitations, he complained of progressively worsening shortness of breath until he lost
consciousness and suffered a PEA cardiac arrest in the presence of EMS personnel.
(Ex. A, p. 5 (citing Ex. 5, p. 276); Tr. 83, 95.) Mr. Adams required prolonged
resuscitation which led to a brain injury and his ultimate death. (Ex. A, p. 5; Tr. 83.)
Dr. LaRue provides an overview of PEA. (Ex. A, pp. 6-7; Tr. 88-89.) He defines
PEA as “any one of a heterogeneous group of organized ECG rhythms without sufficient
mechanical contraction of the heart to produce a palpable pulse or measurable blood
pressure.” (Ex. A, p. 6 (citing Jonathon Elmer, Advanced Cardiac Life Support (ACLS)
in Adults, UPTODATE (July 13, 2023) (Ex. A, Tab 1; see also Ex. D, Tab 1)).) Further, he
notes that, by definition, PEA is a non-perfusing rhythm that requires immediate
initiation of CPR. (Ex. A, p. 6 (citing Elmer, supra, at Ex. A, Tab 1).) Dr. LaRue
explains that with PEA the heart has an electrical pattern but is not actually pumping
blood due to an electromechanical dissociation. (Tr. 88.) PEA does not respond to
defibrillation because the heart rhythm is not the issue causing the arrest as PEA is a
mechanical problem. (Ex. A, p. 6.) Dr. LaRue notes that PEA manifests as a form of
cardiac arrest because the heart is not actually circulating blood. (Tr. 88-89.) There are
“myriad causes of PEA,” and the associated symptoms depend on the underlying
cause. (Id. at 89.) Dr. LaRue lists a series of common causes of PEA arrests, including
10 Dr. LaRue received his medical degree in 2005 from the Medical College of Wisconsin in Milwaukee,
before going on to complete an internship and residency in internal medicine at the University of
Wisconsin Hospitals and Clinics in Madison in 2006 and 2008, respectively, as well as a cardiology
fellowship at Washington University School of Medicine in St. Louis, Missouri in 2012. (Ex. B, pp. 1-2.)
He is board certified in cardiovascular disease and advanced heart failure and transplant cardiology, and
he maintains an active medical license in Missouri and Illinois. (Id. at 3.) He currently works as the
director of Heart Failure Cardiology at St. Luke’s Hospital in Chesterfield, Missouri. (Id. at 1; Ex. A, p. 1.)
He has authored 40 peer-reviewed articles, covering aspects of advanced heart failure, as well as 4 book
chapters, specifically addressing acute systolic heart failure and cardiomyopathy. (Ex. A, p. 1; Ex. B, pp.
7-10.) Dr. LaRue was proffered as an expert in cardiology without objection. (Tr. 81.)
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hypovolemia, hypoxia, hydrogen ion acidosis, hyperkalemia, hypokalemia, hypothermia,
hypoglycemia, toxins, tamponade, tension PTX, coronary thrombosis, pulmonary
thrombosis, and trauma. (Ex. A, p. 7 (citing Laszlo Littmann et al., A Simplified and
Structured Teaching Tool for the Evaluation and Management of Pulseless Electrical
Activity, 23 MED. PRINCIPLES & PRAC. 1 (2014) (Ex. A, Tab 2)).)
In contrast, Dr. LaRue notes that with ventricular arrhythmia such as ventricular
tachycardia, the heart rhythm is the issue and is thus an electrical problem. (Ex. A, p. 6;
Tr. 85.) He explains that ventricular tachycardia is a specific kind of fast heart rhythm
where the ventricles are beating on their own without anything telling them to. (Tr. 85.)
Ventricular tachycardia exists on a spectrum and can manifest in different ways with
different heart rates and for different durations. (Id.) An individual can experience short
runs of ventricular tachycardia known as nonsustained ventricular tachycardia, or it can
be sustained where it does not stop on its own. (Id. at 85-86.) Dr. LaRue notes that
individuals experiencing ventricular tachycardia may report buzzing or fluttering
sensations in their chest, as Mr. Adams reported to his cardiologist during an encounter
prior to vaccination. (Id. at 86.) Ventricular arrhythmias can cause cardiac arrest and
sudden cardiac death where a person is conscious with a perfusing heart rhythm in one
moment and then they collapse because their ventricular arrhythmia is unable to pump
blood to the brain. (Ex. A, p. 6.) Because the heart rhythm is the problem with
ventricular arrythmias, they are treated with an external heart shock known as direct
current cardioversion. (Id.) Dr. LaRue emphasizes that ventricular arrhythmias are not
classified as PEA and are not recognized as a potential cause of PEA. (Id.) Rather,
ventricular arrhythmias and PEA are recognized as the two different types of cardiac
arrest. (Tr. 89-90.)
Dr. LaRue agrees that Mr. Adams suffered a PEA arrest that ultimately led to his
death. (Ex. A, pp. 5, 7, 10; Ex. D, p. 2; Tr. 82-83, 96.) Specifically, he indicates that Mr.
Adams’s PEA cardiac arrest occurred at the point when Mr. Adams “was sitting, talking
to EMS and lost consciousness.” (Tr. 95.) Dr. LaRue opines that Mr. Adams’s PEA
arrest is of unknown etiology (Id. at 106), and he does not offer a theory as to what
caused the PEA (Id. at 113). However, he stresses that no specific cause of Mr.
Adams’s PEA arrest was ever suggested by any of his treating providers. (Ex. A, p. 7.)
Additionally, he indicates that it is not uncommon for the cause of a PEA that occurs
outside of the hospital to remain idiopathic. (Tr. 121-22.) Dr. LaRue opines that the
available evidence does not strongly implicate a specific cause of Mr. Adams’s PEA,
and that sometimes you are left not knowing definitively what caused the cardiac event.
(Id. at 118-22.)
Dr. LaRue acknowledges that the symptoms Mr. Adams experienced prior to his
PEA, including shortness of breath, elevated temperature, and sweating, are not
specific symptoms indicative of a specific cause of his PEA. (Tr. 95-96.) However, he
contends that the objective data and clinical evidence do not support Dr. Rashtian’s
opinion that Mr. Adams suffered from ventricular arrhythmia prior to his PEA. (Ex. A, p.
8; Tr. 97.) He emphasizes that, although Mr. Adams required prolonged CPR and
multiple rounds of epinephrine, his arrest was characterized as PEA, no ventricular
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tachycardia or ventricular fibrillation was noted, and no defibrillator shocks were
administered during his resuscitation. (Ex. A, p. 5 (citing Ex. 5, p. 276); Tr. 97-99.) Dr.
LaRue explains that ventricular tachycardia and ventricular fibrillation can be treated
with defibrillator shocks or direct current cardioversion (i.e., external heart shock). (Ex.
A, pp. 5-6 (citing Elmer, supra, at Ex. A, Tab 1); Tr. 90, 97-99, 123-24.) Therefore, he
suggests that the fact that Mr. Adams did not receive any defibrillator shocks implies
that he did not have ventricular tachycardia or ventricular fibrillation. (Ex. A, pp. 5-6; Tr.
97-99.) Additionally, Dr. LaRue stresses that when Mr. Adams experienced ventricular
tachycardia and PVCs prior to vaccination, he described feeling buzzing sensations and
palpitations in his chest. (Tr. 98; Ex. A, p. 3 (citing Ex. 4, p. 96).) However, Mr. Adams
did not complain of any fluttering or buzzing sensations on the morning he suffered his
PEA arrest, and he specifically denied experiencing chest pain or palpitations. (Tr. 95-
96, 98; Ex. A, p. 5.) While Dr. LaRue acknowledges that an arrest due to ventricular
arrhythmia could “in theory” represent an exacerbation of Mr. Adams’s PVCs and
nonsustained ventricular tachycardia, Mr. Adams suffered a PEA arrest that is, by
definition, not related to a ventricular arrhythmia. (Ex. A, p. 8.) In sum, Dr. LaRue
opines that there is no specific evidence demonstrating that Mr. Adams’s PEA arrest
was due to an exacerbation of his underlying ventricular arrhythmias. (Id. at 9; Tr. 97-
99.)
Furthermore, Dr. LaRue opines that the fact that Mr. Adams experienced
ventricular tachycardia after his PEA when he was in the hospital is not of any
significance because it happened after the arrest and resuscitation. (Tr. 96.) Further,
he notes that the EMS personnel were monitoring Mr. Adams and did not detect any
arrhythmias when they resuscitated him or in transport to the hospital. (Id. at 96-97.)
There were other stressors, such as the fevers Mr. Adams experienced while
hospitalized, that certainly could have brought on the ventricular arrhythmias he
experienced after his cardiac arrest. (Id. at 97.) However, the fact that Mr. Adams
experienced ventricular tachycardia while hospitalized does not indicate that he arrested
from a ventricular arrhythmia. (Id.)
Moreover, Dr. LaRue specifically contests Dr. Rashtian’s assertion that “any
ventricular arrhythmia cardiac arrest that is shockable will degenerate to PEA arrest if
not attend[ed] to and treated promptly.” (Ex. D, pp. 1-2.) He states that, in theory, it is
possible that a ventricular arrhythmia could be followed by PEA arrest where an
individual who experienced a sustained ventricular tachycardia and arrested is shocked
back to a normal cardiac rhythm, but their heart nonetheless cannot pump. (Tr. 90.)
However, while conceding that it is not impossible, Dr. LaRue notes that this
phenomenon, generally speaking, is “not likely or doesn’t happen.” (Id.) In the context
of this case, he explains that, although Mr. Adams was feeling unwell, he was still alert
when the paramedics arrived. (Ex. D, p. 1 (citing Ex. 5, p. 237); Tr. 97.) Therefore, any
ventricular tachycardia that Mr. Adams would have been experiencing prior to his PEA
would have been perfusing. (Tr. 97.) Dr. LaRue opines that from a physiological
perspective, Dr. Rashtian’s theory is missing a step, noting he doesn’t “understand how
a person would go from having [ventricular tachycardia] that was perfusing, . . . and
then go back into a normal rhythm and then arrest from a PEA mechanism. (Id.) While
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he acknowledges that some patients may remain alert for a time while experiencing
ventricular tachycardia, Dr. LaRue opines that “there is not a conceivable mechanism
for a person to transition from alert with ventricular tachycardia to collapsed with PEA in
the presence of EMS personnel.” (Ex. D, p. 1.) Rather, when left unattended,
ventricular tachycardia may degenerate to asystole, and asystole is not a rhythm that is
classified as a cause of PEA. (Id. at 1-2; Tr. 87-88.)
Dr. LaRue opines that there is no scientific evidence of a causal relationship
between the flu vaccine and PEA arrest. (Ex. A, p. 7; Tr. 102-103.) He cites a systemic
review of flu vaccine literature by Beyer et al., which makes no mention of PEA arrest as
a complication of flu vaccination. (Ex. A, p. 7 (citing W.E.P. Beyer et al.,
Immunogenicity and Safety of Inactivated Influenza Vaccines in Primed Populations: A
Systematic Literature Review and Meta-Analysis, 29 VACCINE 5785 (2011) (Ex. A, Tab
3)).) He further cites a study that looked at VAERS reports over a 23-month period and
found no mention of pulseless electrical activity arrest in association with the flu
vaccine. (Ex. A, p. 7 (citing 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 (2016)
(Ex. A, Tab 4)).) Moreover, Dr. LaRue indicates that a study filed by petitioner
concluded that the flu vaccine was associated with a reduced risk of primary cardiac
arrest. (Tr. 101-02 (discussing David S. Siscovic et al., Influenza Vaccination and the
Risk of Primary Cardiac Arrest, 152 AM. J. EPIDEMIOLOGY 674 (2000) (Ex. 16)).)
In this case, Dr. LaRue disagrees with Dr. Rashtian’s proposed theories that the
stress of the flu vaccine, acute leukocytosis, acute inflammatory reaction, and possible
delayed anaphylaxis caused Mr. Adams’s stable substrate to become unstable and
induce his ultimate PEA arrest. (Tr. 99-101; Ex. A, p. 8.) First, he notes that there is no
evidence to suggest that Mr. Adams suffered from any kind of inflammation reaction as
a result of vaccination. (Ex. A, p. 8; Tr. 99.) There was no localized inflammation at the
vaccination site, and Mr. Adams’s elevated white blood count is to be expected
following any kind of cardiac arrest and prolonged resuscitation. (Ex. A, p. 8 (citing Ex.
5, pp. 241-43, 260); Tr. 99-100.) With respect to anaphylaxis, Dr. Rashtian notes that
an anaphylactic reaction generally occurs within minutes to hours of exposure, not 12
hours after exposure. (Tr. 100; Ex. A, p. 7.) While he acknowledges that a delayed
anaphylactic reaction may be possible, Dr. LaRue notes that further investigation and
research are necessary to determine whether the specific timing in this case could be
consistent with a delayed anaphylactic reaction. (Tr. 112-13.) Additionally, he stresses
that there is no clinical evidence suggestive of an anaphylactic reaction, noting that
there was no wheezing, no vocal fold swelling, and no shortness of breath at the time of
intubation. (Id. at 100; Ex. A, p. 7 (discussing Ex. 5, p. 268).) Furthermore, none of Mr.
Adams’s treating physicians suggested that Mr. Adams suffered an anaphylactic
reaction, and Dr. LaRue highlights that his treating physicians specifically documented
that an anaphylactic reaction was unlikely given the lack of clinical evidence. (Tr. 100-
01; Ex. A, p. 7.)
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In sum, Dr. LaRue notes that Mr. Adams experienced a PEA arrest of unknown
etiology which ultimately led to his death. (Ex. D, p. 2; Tr. 82-83, 106.) He stresses that
Mr. Adams’s PEA arrest “was unequivocally not related to any ventricular arrhythmia
and thus does not represent any exacerbation of his prior ventricular arrhythmias.” (Ex.
A, p. 10; Ex. D, p. 2.) Dr. LaRue opines that there is no evidence to suggest or support
the conclusion of that Mr. Adams’s flu vaccine played any role in his clinical course and
ultimate death. (Ex. A, p. 10; Ex. D, p. 2; Tr. 82-83, 106-07.)
V. Analysis
a. Althen prong one (theory of causation)
Under Althen prong one, petitioner must provide a “reputable medical theory,”
demonstrating that the subject vaccine can cause the type of injury alleged. Pafford,
451 F.3d at 1355-56 (quoting Pafford v. Sec’y of Health & Human Servs., No. 01-
0165V, 2004 WL 1717359, at *4 (Fed. Cl. Spec. Mstr. July 16, 2004)). Such a theory
must only be “legally probable, not medically or scientifically certain.” Knudsen v. Sec’y
of Health & Human Servs., 35 F.3d 543, 548-49 (Fed. Cir. 1994). Petitioner may satisfy
the first Althen prong without resort to medical literature, epidemiological studies,
demonstration of a specific mechanism, or a generally accepted medical theory. See
Andreu v. Sec’y of Health & Human Servs., 569 F.3d 1367, 1378-79 (Fed. Cir. 2009)
(citing Capizzano v. Sec’y of Health & Human Servs., 440 F.3d 1317, 1325-26 (Fed. Cir.
2006)). However, “[a] petitioner must provide a ‘reputable medical or scientific
explanation’ for [their] theory.” Boatmon, 941 F.3d at 1359 (quoting Moberly, 592 F.3d
at 1322). “While it does not require medical or scientific certainty, it must still be ‘sound
and reliable.’” Id. (quoting Knudsen, 35 F.3d at 548-49).
Both parties’ experts agree that Mr. Adams died as a result of PEA cardiac
arrest. (Tr. 43, 75-76, 96, 106.) However, PEA arrest is only a final result, the moment
when blood stops circulating as a result of “myriad” underlying causes. (Id. at 48, 89.)
Thus, Dr. Rashtian’s theory of causation is intended to explain what occurred prior to
the ultimate PEA arrest. (Id. at 43.) During the course of the hearing, he discussed a
number of theoretical propositions as underlying his theory of causation, often returning
to the notion that what he proposes is multifactorial. (E.g., id. at 131-33.) However, two
shortcomings are dispositive with respect to Althen prong one. First, Dr. Rashtian is
unpersuasive in seeking to explain how the flu vaccine could be the initiating cause of
the cardiologic effects he is positing. He is vague with respect to the relevant
immunology as a general matter and admits to being unable to substantiate the flu
vaccine as a cause of ventricular arrhythmia in particular. Second, even if Dr. Rashtian
had succeeded in suggesting that a post-vaccination process could result in a loss of
cardiac equilibrium leading to ventricular arrhythmia, he has not preponderantly
established that such an arrhythmia would result in the PEA cardiac arrest at issue in
this case.
Dr. Rashtian opines as a general matter that vaccines, including the flu vaccine,
can aggravate and worsen underlying conditions. (Tr. 37-38.) However, Dr. Rashtian is
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not trained in immunology (Id. at 135), and his opinion was either vague or inconsistent
with respect to the nature of the immune reaction potentially at issue. Initially he cited a
post-vaccination release of cytokines. (Id. at 37-38.) Later, he suggested that “nobody
can say for sure that . . . [Mr. Adams] didn’t have an anaphylactic reaction.” (Id. at 38.)
He then backtracked on the proposed anaphylactic reaction, indicating his theory would
remain operative “whether it was delayed anaphylactic or a systemic reaction or
cytokine reaction.” (Id. at 45.) Later, on cross examination, he stated that he was
relying on “a combination of a nonsustained ventricular tachycardia, delayed
anaphylactic [reaction], a delayed severe vasovagal reaction, some immune reaction,
acute pulmonary edema, any of those, or in combination.” (Id. at 65.) Ultimately, in
response to the undersigned’s questions, Dr. Rashtian suggested that, absent an
anaphylactic response, an “appropriate” cytokine response to vaccination would be
sufficient to disturb Mr. Adams’s cardiac equilibrium given his underlying susceptibility.
(Id. at 74-75.)
However, even acknowledging that the vaccine can induce some inflammatory
immune response, mere invocation of a vaccine’s intended immune response is not in
and of itself sufficient to carry petitioner’s burden under Althen prong one. See Elvira ex
rel. D.E. v. Sec’y of Health & Human Servs., No. 17-531V, 2024 WL 4966035, at *20
(Fed. Cl. Spec. Mstr. Nov. 6, 2024); Vanore v. Sec’y of Health & Human Servs., No. 21-
0870V, 2024 WL 3200287, at *18 (Fed. Cl. Spec. Mstr. May 31, 2024); Kalajdzic ex rel.
A.K. v. Sec’y of Health & Human Servs., No. 17-792V, 2022 WL 2678877, at *23-24
(Fed. Cl. Spec. Mstr. June 17, 2022), mot. for rev. denied, 2024 WL 4524777 (Fed. Cl.
Oct. 18, 2024), aff’d, No. 2023-1321, 2024 WL 3064398 (Fed. Cir. June 20, 2024);
Cordova v. Sec’y of Health & Human Servs., No. 17-1282V, 2021 WL 3285367, at *17
(Fed. Cl. Spec. Mstr. June 23, 2021). There must be some additional evidence linking
the vaccine’s immune response to the pathology of petitioner’s actual condition. For
example, the Chief Special Master has observed:
I have on many occasions considered theories asserting a vaccine-caused,
cytokine-driven process led to injury, but have repeatedly deemed such
theories wanting, absent evidence connecting the process (no matter how
scientifically plausible it might be) with additional proof sufficient to render it
“more likely than not” that the immune processes outlined could be rendered
pathogenic by introduction of a vaccine. Otherwise, such a theory only
attempts to transmute the expected reaction to a vaccine into pathology.
M.R. v. Sec’y of Health & Human Servs., No. 16-1024V, 2023 WL 4936727, at *27 (Fed.
Cl. Spec. Mstr. June 30, 2023) (citing Dean v. Sec'y of Health & Human Servs., No. 13-
808V, 2017 WL 2926605, at *17 (Fed. Cl. Spec. Mstr. June 9, 2017); see also
Kaltenmark v. Sec’y of Health & Human Servs., No.17-1362V, 2023 WL 8870299, at
*28 (Fed. Cl. Spec. Mstr. Nov. 27, 2023) (the undersigned observing that, “[e]ven where
there is some reason to suspect a condition may be cytokine mediated, this does not
automatically lead to the conclusion that vaccines can cause the injury merely because
vaccines produce some cytokine elevations”).
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Here, despite being unable to implicate any specific immune process, Dr.
Rashtian nonetheless opined without any apparent support that the flu vaccine can
cause or trigger ventricular arrhythmia, which he opined is the primary concern for
patients with Mr. Adams’s substrate. (Tr. 58, 72-73.) He stated that “any stress or
injury or anything – stress can initiate and trigger a ventricular tachycardia in a patient
who has the appropriate substrate and appropriate treatment triggers.” (Id. at 58.)
However, he agreed that patients with a substrate similar to that of Mr. Adams – a lower
ejection fraction of 41 to 50 percent along with frequent PVCs and nonsustained
ventricular tachycardia – are at higher risk for a future cardiac event across the board.
(Id. at 70-71.) He acknowledged that a number of factors can affect this substrate and
that it is “not uncommon” for the trigger to remain unknown. (Id. at 71, 73; Ex. 8, p. 4.)
Moreover, he acknowledged that the literature he has cited does not implicate the flu
vaccine as a cause of ventricular arrhythmia (Tr. 60-62 (discussing Al-Khatib et al.,
supra, at Ex. 11; Compton, supra, at Ex. 12)), and conceded that “[y]ou’re not going to
find” articles that “say that [a] vaccine caused the ventricular tachycardia” (Id. at 62).
Dr. Rashtian has otherwise himself opined that the flu vaccine is cardio-protective. (Id.
at 50-52; Ex. 8, p. 6.) In his first report indicated that “as a cardiologist/cardiac
electrophysiologist, I am a passionate advocate of administering yearly flu vaccines to
older patients and to patients with underlying cardiac structure abnormality, to reduce
their risk of cardiac events and total mortality and even reduce the total number of
cardiac arrests per year.” (Ex. 8, p. 6.)
In general, petitioners have not been able to preponderantly establish that the flu
vaccine can cause acute cardiovascular events. Goff v. Sec’y of Health & Human
Servs., No. 17-259V, 2025 WL 431582 (Fed. Cl. Spec. Mstr. Jan. 13, 2025) (stroke),
mot. for rev. denied, 2025 WL 2081262 (Fed. Cl. July 9, 2025); Druery v. Sec’y of
Health & Human Servs., No. 17-1213V, 2023 WL 5094088 (Fed. Cl. Spec. Mstr. July
11, 2023) (heart attack), mot. for rev. denied, 169 Fed. Cl. 557 (2024); Singleton v.
Sec’y of Health & Human Servs., No. 17-1474V, 2023 WL 3595653 (Fed. Cl. Spec.
Mstr. May 23, 2023 (stroke); Baldwin v. Sec’y of Health & Human Servs., No. 13-957V,
2020 WL 4197937 (Fed. Cl. Spec. Mstr. June 4, 2020) (cardiac arrest), mot. for rev.
denied, 151 Fed. Cl. 431 (2020); Schultz v. Sec’y of Health & Human Servs., No. 16-
539V, 2020 WL 1039161 (Fed. Cl. Spec. Mstr. Jan. 24, 2020) (stroke); Sokol v. Sec’y of
Health & Human Servs., No. 16-1631V, 2020 WL 553842 (Fed. Cl. Spec. Mstr. Jan. 9,
2020) (stroke); Hayward v. Sec’y of Health & Human Servs., No. 15-005V, 2018 WL
2772495 (Fed. Cl. Spec. Mstr. May 4, 2018) (cerebral vascular accident); but see Irwin
v. Sec’y of Health & Human Servs., No. 16-1454V, 2024 WL 863690 (Fed. Cl. Spec.
Mstr. Jan. 23, 2024) (stroke); Halverson v. Sec’y of Health & Human Servs., No. 15-
227V, 2020 WL 992588 (Fed. Cl. Spec. Mstr. Feb. 4, 2020) (cardiac arrest).
Even if petitioner had been successful in identifying the flu vaccine as a likely
cause of ventricular arrhythmia, Dr. LaRue would still be persuasive in disputing the
relevance of ventricular arrhythmia as an underlying cause of PEA arrest. Dr. LaRue
explained that ventricular tachycardia and PEA are “big picture, the two different kinds
or types of cardiac arrest.” (Tr. 89-90.) In his supplemental report, Dr. Rashtian
asserted that “I am certain that Dr. LaRue agrees that any ventricular arrhythmia cardiac
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arrest that is shockable will degenerate to PEA arrest if not attended to and treated
promptly.” (Ex. 21, p. 3.) In response, however, Dr. LaRue explained that unattended
ventricular tachycardia degenerates to asystole, which is a complete absence of cardiac
rhythm due to the absence of electrical activity in the heart. (Ex. D, pp. 1-2; Tr. 87-88.)
PEA arrest, by contrast, is effectively the inverse, constituting “a heterogenous group of
organized rhythms without sufficient mechanical contraction of the heart to produce a
palpable pulse or measurable blood pressure.” (Ex. D, p. 2 (citing Elmer, supra, at Ex.
D, Tab 1).) Ultimately, Dr. Rashtian conceded during the hearing that “[u]sually a
ventricular tachycardia does not terminate in the PEA . . . It degenerates to – usually to
a systolic cardiac arrest.” (Tr. 47.) And, during cross examination, Dr. Rashtian
discussed the fact that, despite presenting literature touching on the diagnosis and
management of ventricular arrhythmias, these papers do not describe PEA as a
potential consequence of ventricular tachycardia. (Id. at 60-64 (discussing Al-Khatib et
al., supra, at Ex. 11; Compton, supra, at Ex. 12).)
As Dr. LaRue explains it, the only way that sustained ventricular tachycardia
could be followed by PEA would be for a resuscitative shock to bring the cardiac rhythm
back to normal, but in so doing nonetheless find that the heart could not pump. (Tr. 90.)
While not impossible, he opined that “generally speaking, it’s not likely or doesn’t
happen.” (Id.) And, as applied to this specific case, because Mr. Adams was conscious
and talking prior to his PEA, this would mean that any ventricular tachycardia would
have been perfusing, meaning blood was still supplied to the heart and the brain. (Id. at
97-98.) Thus, there is a “missing step” physiologically in terms of how blood could have
been perfusing during the ventricular tachycardia but then stop perfusing and result in
PEA arrest only after the heart rhythm had returned to normal. (Id.) Despite
acknowledging that what he proposed was “not common” (Id. at 60-61), and despite
opining that Mr. Adams’ hypothesized tachycardia resolved prior to the arrival of
paramedics (Id. at 45, 130), Dr. Rashtian never addressed this point by Dr. LaRue.
Instead, Dr. Rashtian simply reasoned that, because Mr. Adams experienced ventricular
tachycardia on separate occasions both before and after the cardiac arrest, it is
probable that he also suffered the same tachycardia in the context of his PEA. (Id. at
59.) However, despite submitting two reports, testifying at the hearing, and having the
last word in the form of his rebuttal testimony, Dr. Rashtian never explained how
ventricular tachycardia would degenerate to PEA.
For all these reasons, petitioner has not met her preponderant burden of proof
under Althen prong one.
b. Althen prong two (logical sequence of cause and effect)
The second Althen prong requires proof of a logical sequence of cause and
effect, usually supported by facts derived from a petitioner’s medical records. Althen,
418 F.3d at 1278; Andreu, 569 F.3d at 1375-77; Capizzano, 440 F.3d at 1326-27; Grant
v. Sec’y of Health & Human Servs., 956 F.2d 1144, 1147-48 (Fed. Cir. 1992). Medical
records are generally viewed as particularly trustworthy evidence. Cucuras v. Sec’y of
Health & Human Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993). However, medical
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records and/or statements of a treating physician’s views do not per se bind the special
master. See § 300aa-13(b)(1) (providing that “[a]ny such diagnosis, conclusion,
judgment, test result, report, or summary shall not be binding on the special master or
court”); Snyder v. Sec’y of Health & Human Servs., 88 Fed. Cl. 706, 745 n.67 (2009)
(“[T]here is nothing . . . that mandates that the testimony of a treating physician is
sacrosanct—that it must be accepted in its entirety and cannot be rebutted.”). A
petitioner may support a cause-in-fact claim through either medical records or expert
medical opinion. § 300aa-13(a). The special master is required to consider all the
relevant evidence of record, draw plausible inferences, and articulate a rational basis for
the decision. Winkler, 88 F.4th at 963 (citing Hines, 940 F.2d at 1528).
In this case, there is no evidence from Mr. Adams’s medical records to suggest
that any of his treating physicians would support the causal relationship petitioner is
alleging. In fact, the medical records tend to suggest they would not agree. First, none
of the treating physicians recorded any opinion endorsing Mr. Adams’s vaccination as a
causal factor in his condition despite the fact that this was repeatedly questioned by his
family. (E.g., Ex. 23, pp. 135, 161, 228.) Second, the medical records indicate that, to
the contrary, during a multidisciplinary evaluation in the intensive care unit, “[the]
patient[’s] family [was] informed that it is unlikely the flu shot can cause PEA arrest.”11
(Id. at 195.) Thus, Mr. Adams’s treating cardiologist opined that the cause of his PEA
was “unclear.” (Id. at 188; see also Tr. 106 (Dr. LaRue similarly opining).) Third,
whereas Dr. Rashtian’s expert opinion incorporates a potential anaphylactic reaction
into his explanation, Mr. Adams’s treating physicians did not think that an anaphylactic
injury was likely, having observed no wheezing, no shortness of breath, and normal
vocal cords upon intubation.12 (Ex. 23, pp. 167, 195; see also Tr. 99-101 (Dr. LaRue
agreeing).)
Of course, as noted above, petitioner can also substantiate a logical sequence of
cause and effect based on expert opinion. § 300aa-13(a). Here, however, Dr.
Rashtian’s opinion effectively amounts to speculation. During the hearing, Dr. Rashtian
stressed that both he and Dr. LaRue agree that Mr. Adams died as a result of PEA
arrest (Tr. 43), and that “when the paramedic arrived, he was in a PEA cardiac arrest.
We don’t know exactly what was going on that one hour before or the day before . . .”
(Id. at 38). Upon questioning from the undersigned, Dr. Rashtian confirmed during the
11 In the interest of completeness, I also note that the same statement goes on to state that they “cannot
totally rule out” that Mr. Adams’s condition is due to adverse effects of the vaccine. (Ex. 23, p. 195.)
However, when reading the statement as a whole, it is clear that the overarching point is that the
proposed causal relationship is unlikely.
12 Specifically, the medical record indicates that they “cannot completely exclude” an anaphylactic
reaction but indicates that “it is difficult to say that this was anaphylactic reaction.” (Ex. 23, p. 167.)
Again, as indicated above, while this record is nuanced, the overarching point is that an anaphylactic
reaction was considered unlikely. See supra note 11. Moreover, to the extent an anaphylactic reaction
was considered, the treating physicians suggested that it would not necessarily have been due to the
vaccination, noting that Mr. Adams had also started a new medication. (Ex. 23, p. 167; see also Ex. 4, p.
7 (newly prescribing empagliflozin at the same medical encounter at which the vaccine at issue was
administered).)
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hearing that it is “absolutely correct” that once Mr. Adams entered PEA arrest, his
theory could neither be proven nor disproven. (Id. at 69-70.) In that regard, Dr. LaRue
persuasively explained that the symptoms Mr. Adams experienced prior to his PEA
(elevated temperature and shortness of breath) were nonspecific and that PEA has
many causes. (Id. at 89, 95-96.) Moreover, Dr. LaRue explained that clinically it is not
unusual for the cause of PEA to remain unknown when it occurs outside of a hospital
setting, as it did in this case. (Id. at 121-22.) Although Dr. Rashtian sought to reason
out what probably happened to the decedent prior to his PEA arrest, he acknowledged
multiple times during the hearing that the nature of what happened prior to the arrival of
the paramedics simply remains unknown. (Id. at 38, 46-47, 59.)
Moreover, Dr. Rashtian’s opinion relies on a jumble of potential contributing
factors, none of which are especially well substantiated. During the hearing, Dr.
Rashtian stated that he’s “not giving one direct cause.” (Tr. 134.) Instead, he’s “trying
to give medical probability of what led before the PEA. And I’m saying the combinations
of vaccine reaction, cytokine release, runs of a ventricular arrhythmia, possible
anaphylactic reaction to them, all in combination” contributed. (Id.) However, none of
these specific factors are preponderantly supported. Although Dr. Rashtian opined that
petitioner’s symptoms of shortness of breath and elevated temperature are consistent
with hypotension, which can in turn be consistent with anaphylaxis, he also indicated
that these symptoms can otherwise be consistent with tachycardia. (Id. at 38-39, 45-46,
127-28.) Ultimately, Dr. LaRue is persuasive in opining that the symptoms are
nonspecific. Apart from these two nonspecific symptoms, there is no clinical evidence
to support the presence of a vaccine reaction, cytokine release, ventricular arrhythmia,
or anaphylaxis, either individually or in combination. To be sure, the fact that these
purported events would have occurred before the arrival of paramedics means that the
dearth of confirmed clinical findings could not necessarily have been avoided.
However, whereas specific findings to support petitioner’s theory are lacking, Dr.
Rashtian otherwise agreed that that any number of factors can affect the type of
substrate that Mr. Adams had and that “if you look at 1,000 patients like him, by virtue of
him having the lower ejection fraction and the PVCs, he would be [at] higher risk of a
future cardiac arrest.” (Id. at 70-71; see also Ex. 8, p. 4.) Even if the decedent had
experienced a tachycardic event, Dr. Rashtian opined that it would not be uncommon
for the underlying cause to remain a mystery. (Tr. 72-73.)
And, finally, the one key causal factor that remains clear throughout Dr.
Rashtian’s opinion – the role of ventricular tachycardia – is unpersuasive. As discussed
under Althen prong one, Dr. Rashtian’s suggestion that PEA arrest would result from
ventricular tachycardia is in itself unlikely. Thus, it is noteworthy that the treating
physicians suggested that arrhythmia had been ruled out. (Ex. 23, p. 167.) In
particular, Mr. Adams’s treating cardiologist made note of the fact that “[n]o VT or V. fib
was noted [by paramedics] and patient did not require cardioversion during CPR.” (Id.
at 176.) Furthermore, the treating cardiologist explained that Mr. Adams had not
complained of any chest pain or palpitations prior to his PEA, concluding that “[h]e did
not have chest pain or cardiac arrhythmias before the PEA.” (Id. at 176, 188.)
Therefore, contrary to Dr. Rashtian’s opinion, the treating cardiologist concluded that
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“[t]he cause of PEA cardiac arrest is not clear.” (Id. at 188.) While Dr. Rashtian relies in
part on Mr. Adams’s prior history of nonsustained ventricular tachycardia to infer the
underlying cause of his PEA, Dr. LaRue is more persuasive in noting that in the hours
leading up to PEA, Mr. Adams did not complain of the symptoms he had previously
attributed to his tachycardia. (Tr. 95-96.)
Given the temporal proximity, it is, of course, easy to see why Mr. Adams’s family
initially focused on his vaccinations as a potential cause of his PEA cardiac arrest and
ultimate death. Moreover, when they approached his physicians about that concern,
they received measured responses indicating that, while the proposed causal
connection was unlikely, it “cannot [be] completely exclude[d]” or “cannot [be] totally
rule[d] out.” (Ex. 23, pp. 167, 195.) Thus, it is hardly a surprise that petitioner filed this
action. Throughout the course of this proceeding, the parties’ experts have likewise
been measured in their assessments. Both experts have stressed that it is impossible
to know what happened prior to the point at which Mr. Adams first received paramedic
attention. (Tr. 38, 46-47, 59, 95-96, 118-21.) Importantly, however, it is petitioner who
bears the preponderant burden of proof, and the Federal Circuit has explained that
“[a]lthough probative, neither a mere showing of a proximate temporal relationship
between vaccination and injury, nor a simplistic elimination of other potential causes of
the injury suffices, without more, to meet the burden of showing actual causation.”
Althen, 418 F.3d at 1278 (citing Grant, 956 F.2d at 1149). While the treating physicians
reasonably suggested that it is difficult, if not impossible, to prove a negative, the fact
that they could not rule out or completely exclude Mr. Adams’s vaccination as a cause is
not tantamount to preponderant evidence supporting that causal relationship. And,
while the cause of Mr. Adams’s PEA cardiac arrest remains unknown, for all the
reasons discussed above, petitioner’s expert’s explanation of events is not
preponderantly supported.
For all these reasons, petitioner has not met her preponderant burden of proof
under Althen prong two.13
13 There has been ambiguity in this case with respect to whether the case should be addressed under
Athen or Loving. In her pre-hearing brief, petitioner framed the case as one of significant aggravation,
contending with respect to the first three Loving prongs that Mr. Adams had pre-existing PVC and
nonsustained ventricular tachycardia with a stable substrate, which was significantly aggravated by the
vaccination leading to an acutely unstable arrhythmia inducing sudden cardiac death. (ECF No. 87, pp.
16-17.) However, in respondent’s pre-hearing brief, he argues that “[t]o the extent that Mr. Adams had a
cardiac arrest, this injury occurred in its entire[t]y after vaccination. While Mr. Adams had predisposing
factors for the cardiac arrest, there is insufficient evidence that those risk factors materially changed after
vaccination.” (ECF No. 86, p. 14 n.7.) During the hearing, petitioner’s expert, Dr. Rashtian, described the
vaccination at issue as “both a trigger and aggravation.” (Tr. 37.) He described the vaccine as creating
an immune response that Mr. Adams could not tolerate due to his underlying condition. (Id. at 37-39.) I
note, however, that it is immaterial whether the alleged logical sequence of cause and effect is evaluated
as part of a vaccine-triggered injury under Althen prong two or as part of a significant aggravation under
Loving prong five. The analysis herein indicates that, regardless of whether Mr. Adams’s pre-existing
PVC and nonsustained ventricular tachycardia are viewed as a condition to be aggravated or merely as
potential predisposing factors, there is inadequate evidence to implicate any arrhythmia as the cause of
his PEA cardiac arrest.
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c. Althen prong three (proximate temporal relationship)
The third Althen prong requires establishing a “proximate temporal relationship”
between the vaccination and the injury alleged. Althen, 418 F.3d at 1278. A petitioner
must offer “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).
In this case, petitioner relies on the notion that “[r]esearch supports that
significant inflammatory reactions can arise within hours of vaccination, particularly in
patients with pre-existing conditions. This aligns with the understanding of how
vaccines can influence cardiovascular stability.” (ECF No. 87, p. 21.) However, neither
Dr. Rashtian’s testimony nor the literature he cited support these points.
Though petitioner has failed to develop the record on this point, it is not
necessarily controversial that a cytokine response would begin within approximately 12
hours of vaccination as a general matter. However, petitioner has not substantiated that
this fact alone is dispositive of timing appropriate for a causal inference relative to the
actual injury at issue. For example, in Hayward, a case involving a stroke occurring
about 12 hours post-vaccination, the special master noted that petitioner’s immunology
expert had explained that proinflammatory cytokines begin to increase within six hours
of vaccination, but found that the record as a whole supported the conclusion that it
would take longer than half a day for such cytokines to increase to pathologic levels and
further that relevant literature otherwise supported a longer latency between
inflammatory triggers and cerebral vascular accidents. 2018 WL 2772495, at *8, *19.
Here, petitioner and her expert essentially take for granted that the timing of onset is
appropriate for a causal inference.
But in any event, for the reasons discussed under Althen prong one, Dr. Rashtian
has not meaningfully addressed how a transient cytokine response to vaccination would
result in either ventricular tachycardia specifically or PEA arrest. Thus, this shortcoming
prevents petitioner from meeting her burden of proof under Althen prong three. The
explanation for what is a medically acceptable timeframe must coincide with the theory
of how the relevant vaccine can cause an injury (Althen prong one’s requirement). de
Bazan, 549 F.3d at 1352; Shapiro v. Sec’y of Health & Human Servs., 101 Fed. Cl. 532,
542 (2011), mot. for recons. denied after remand, 105 Fed. Cl. 353 (2012), aff’d, 503 F.
App’x 952 (Fed. Cir. 2013); Koehn v. Sec’y of Health & Human Servs., No. 11-355V,
2013 WL 3214877, at *26 (Fed. Cl. Spec. Mstr. May 30, 2013), aff’d, 773 F.3d 1239
(Fed. Cir. 2014).
Additionally, Dr. Rashtian raised for the first time during the hearing that the
decedent may have experienced a delayed anaphylactic reaction. (Tr. 38-39.) As with
the proposed cytokine response more generally, Dr. Rashtian has not actually
substantiated that 12 hours post-vaccination is the appropriate timing for onset of such
a reaction. Although Dr. LaRue agreed in general that a delayed anaphylactic reaction
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can occur, he did not agree, in the absence of relevant research, that the specific timing
in this case would be appropriate for such a reaction. (Id. at 112-13.) But in any event,
he did not agree based on the decedent’s clinical presentation that an anaphylactic
reaction is implicated. (Id. at 99-101, 122-23.) Because I have credited Dr. LaRue’s
opinion that anaphylaxis is not implicated under Althen prong two, his opinion likewise
refutes the notion that the appropriate timing for an anaphylactic injury is informative
under Althen prong three.
For all these reasons, petitioner has not met her preponderant burden of proof
under Althen prong three.
VI. Conclusion
As noted at the outset, I offer my sincerest condolences to petitioner for her loss.
However, for all of the reasons described above, I find that petitioner has not met her
burden of proof. Therefore, pursuant to § 300aa-12(d)(3)(A) and Vaccine Rule 10, this
decision concludes that petitioner is not entitled to an award of compensation. Absent a
timely motion for review, the Clerk is directed to enter judgment dismissing this case for
insufficient proof in accordance with Vaccine Rule 11(a).
IT IS SO ORDERED.
s/Daniel T. Horner
Daniel T. Horner
Special Master
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