Latest CDC Data Shows FULLY Vaccinated Children Have Higher Covid Infection Rates Than Unvaccinated Children

Authors:  Julian Conradson Published May 18, 2022  The Gateway Pundit

As the Biden Administration green-lights another experimental jab of mRNA for 5-11-year-olds, the latest CDC data reveals children of that age have a higher Covid infection rate than their unvaccinated peers. In other words, kids who are jabbed are more likely to catch Covid, which also means the vaccinated are spreading the virus more than the unvaccinated.

So, these kids must take their boosters… Must be that dang science again.

According to the latest CDC data, children aged 5-11 have been contracting Covid at a higher rate if they have been fully vaccinated since February, which is the first time the agency recorded more vaccinated Covid cases than unvaccinated.

On Feb. 12, the CDC reported a weekly case rate among fully vaccinated children aged 5-11 of 250.02 per 100,000, compared to 245.82 among the unvaccinated children in the same age group.

Although the vaccines were billed as and promised to be ‘effective,’ they definitely aren’t living up to being anything close to it. Since February, the infection rate among vaccinated children remained higher through the third week of March, which is the latest available data published – and things are trending in the wrong direction.

As of March, the difference in the case rates has nearly doubled, with the most recent numbers showing a -11 gap (36.23 per 100,000 [vaxxed] / 26.98 per 100,000[unvaxxed]).

The breakdown of the case rate for 5-11-year-olds between Feb. and Mar. is as follows:

February 19: 136.61 per 100,000 [vaxxed] / 120.63 per 100,000[unvaxxed]

February 26: 71.81 per 100,000 [vaxxed] / 61.52 per 100,000[unvaxxed]

March 5: 56.67 per 100,000 [vaxxed] / 40.61 per 100,000[unvaxxed]

March 12: 42.56 per 100,000 [vaxxed] / 28.75 per 100,000[unvaxxed]

March 19: 36.23 per 100,000 [vaxxed] / 26.98 per 100,000[unvaxxed]

The Biden Administration and the FDA authorized the experimental vaccine for children in this age group in November of 2021. In just three short months, enough children had become vaccinated and the case rate flipped. Any protection the jab provided quickly wore off, making the fully vaccinated children more susceptible to and more likely to spread the virus than the unvaccinated.

In all, there are over 28 million children aged 5-11 in the United States. Unfortunately, a whopping ~8 million of them (or 28.8%) have been fully vaccinated already, according to the Mayo Clinic. Not only is the virus proven to be effectively non-lethal for children, especially ones of this young age (99.995% or higher recovery rate), but the experimental vaccine has proven to have negative effectiveness – aka higher infection rate – across multiple age groups.

In addition to the poor results, the mRNA vaccine has been directly linked to serious and life-threatening side effects that have become prevalent in the wake of its rollout. Most concerningly of which – myocarditis – is popping up at an unprecedented rate in otherwise healthy children and young people all across the world. According to heart experts like Dr. Peter McCullough, who is the most published Cardiologist in the world, “an extraordinary number of young individuals that are going to have permanent heart damage” because of this experimental jab. 

Keep in mind, Fauci, Biden, and the rest of the tyrannical public health bureaucracy just Ok’d boosters for 5-11-year-olds. Considering everything that’s publicly available, let alone what the federal government has compiled, this is beyond criminal. How much more data is needed to pull these shots off the market?

Growing Number Of COVID-19 Deaths Among Vaccinated People: Federal Data

Authors: Katabella Roberts via The Epoch Times MY 13, 2022

An increasing number of COVID-19 deaths are occurring among individuals in the United States who have been vaccinated, according to federal data.

In August of 2021, roughly 18.9 percent of COVID-19 deaths happened among individuals who were vaccinated, an ABC News analysis of the data shows. Six months later in February 2022, that figure had risen to over 40 percent as the highly-transmissible Omicron variant made its way across the globe.

Similarly, in September 2021, just 1.1 percent of COVID-19 deaths occurred among Americans who had been fully vaccinated and boosted once. Five months later in February, that percentage had jumped to about 25 percent, according to ABC News.

A separate analysis of federal data by CNN shows that in the second half of September 2021—when the Delta variant was at its peak—less than a quarter of all COVID-19 deaths were among individuals who were vaccinated with at least two doses of the Moderna or Pfizer/BioNTech mRNA vaccines or a single dose of the Johnson & Johnson vaccine. However, just months later in January and February as Omicron surged, that figure had jumped to 40 percent.

Some experts believe the increase in deaths among fully vaccinated people or “breakthrough infections” in those who have received all their shots is not overly concerning, saying it is because while more and more people become fully vaccinated, new variants emerge and vaccine protection begins to wane as fewer people continue to get booster shots.

These data should not be interpreted as vaccines not working. In fact, these real-world analyses continue to reaffirm the incredible protection these vaccines afford especially when up to date with boosters,” said John Brownstein, an epidemiologist at Boston Children’s Hospital and an ABC News contributor.

Despite an increasing number of deaths among the vaccinated, the Centers for Disease Control and Prevention (CDC) states that vaccines are safe and effective. Data from the government agency says that overall, the risk of death from COVID-19 is roughly five times higher in unvaccinated individuals than in those who have had at least their initial dose of a vaccine.

However, in some cases, serious adverse events such as thrombosis with thrombocytopenia syndrome (blood clots), myocarditis (inflammation of the heart muscle), and pericarditis (inflammation of the outer lining of the heart) have been documented.

As of May 4, around 257.9 million people in the United States, or 77.7 percent of the total population in the nation have received at least one dose of vaccine, while roughly 219.9 million people, or 66.2 percent of the total U.S. population, have been fully vaccinated.

Around 100.9 million of those who are fully vaccinated have received a booster shot, while 49.4 percent of those eligible for booster shots have not yet had one.

As the Omicron variant swept through the nation, an increasing number of vulnerable, older populations were being hospitalized, and 73 percent of deaths have been among those 65 and older, despite the fact that 90 percent of seniors have had all of their vaccine shots.

However, a large percentage—a third of them—have not yet had their booster jab.

“This trend in increased risk among the elderly further supports the need for community-wide immunization,” Brownstein said. “Older populations, especially those with underlying conditions, continue to be at great risk of severe complications, especially as immunity wanes. The best way to protect them is to make sure everyone around them is fully immunized.”

The data comes a month after pharmaceutical and biotechnology company Moderna said that preliminary results from its study on a COVID-19 vaccine intended to protect against variants showed that it outperformed the company’s currently authorized booster shot, mRNA-1273.

Moderna said on April 19 that its mRNA-1273.211 shot, its first bivalent booster vaccine candidate, showed “superiority” against the Beta, Delta, and Omicron variants of the virus one month after being administered, compared to the booster shot of its original vaccine currently in use.

SARS-CoV-2 mRNA Vaccination-Associated Myocarditis in Children Ages 12-17: A Stratified National Database Analysis

Authors: RALPH TURCHIANO    • 


Establishing the rate of post-vaccination cardiac myocarditis in the 12-15 and 16-17-year-old population in the context of their COVID-19 hospitalization risk is critical for developing a vaccination recommendation framework that balances harms with benefits for this patient demographic. Design, Setting and Participants: Using the Vaccine Adverse Event Reporting System (VAERS), this retrospective epidemiological assessment reviewed reports filed between January 1, 2021, and June 18, 2021, among adolescents ages 12-17 who received mRNA vaccination against COVID-19. Symptom search criteria included the words myocarditis, pericarditis, and myopericarditis to identify children with evidence of cardiac injury. The word troponin was a required element in the laboratory findings. Inclusion criteria were aligned with the CDC working case definition for probable myocarditis. Stratified cardiac adverse event (CAE) rates were reported for age, sex and vaccination dose number. A harm-benefit analysis was conducted using existing literature on COVID-19-related hospitalization risks in this demographic. Main outcome measures: 1) Stratified rates of mRNA vaccine-related myocarditis in adolescents age 12-15 and 16-17; and 2) harm-benefit analysis of vaccine-related CAEs in relation to COVID-19 hospitalization risk. Results: A total of 257 CAEs were identified. Rates per million following dose 2 among males were 162.2 (ages 12-15) and 94.0 (ages 16-17); among females, rates were 13.0 and 13.4 per million, respectively. For boys 12-15 without medical comorbidities receiving their second mRNA vaccination dose, the rate of CAE is 3.7-6.1 times higher than their 120-day COVID-19 hospitalization risk as of August 21, 2021 (7-day hospitalizations 1.5/100k population) and 2.6-4.3-fold higher at times of high weekly hospitalization risk (2.1/100k), such as during January 2021. For boys 16-17 without medical comorbidities, the rate of CAE is currently 2.1-3.5 times higher than their 120-day COVID-19 hospitalization risk, and 1.5-2.5 times higher at times of high weekly COVID-19 hospitalization. Conclusions: Post-vaccination CAE rate was highest in young boys aged 12-15 following dose two. For boys 12-17 without medical comorbidities, the likelihood of post vaccination dose two CAE is 162.2 and 94.0/million respectively. This incidence exceeds their expected 120-day COVID-19 hospitalization rate at both moderate (August 21, 2021 rates) and high COVID-19 hospitalization incidence. Further research into the severity and long-term sequelae of post-vaccination CAE is warranted. Quantification of the benefits of the second vaccination dose and vaccination in addition to natural immunity in this demographic may be indicated to minimize harm.

Millennials Experienced the “Worst-Ever Excess Mortality in History” – An 84% Increase In Deaths After Vaccine Mandates

The most recent data from the CDC shows that U.S. millennials, aged 25-44, experienced a record-setting 84% increase in excess mortality during the final four months of 2021, according to the analysis of financial expert and Blackrock whistleblower, Edward Dowd,

Dowd, with the assistance of an insurance industry expert, compiled data from the CDC showing that, in just the second half of 2021, the total number of excess deaths for millennials was higher than the number of Americans who died in the entirety of the Vietnam War. Between August and December, there were over 61,000 deaths in this age group, compared to 58,000 over the course of 10 years in Vietnam.

In all, excess death among those who are traditionally the healthiest Americans is up by 84%.

Colchicine: A Possible COVID-19 Long haul Cardiac Therapy

Last Updated: December 16, 2021

Last Updated: December 16, 2021

Colchicine is an anti-inflammatory drug that is used to treat a variety of conditions, including gout, recurrent pericarditis, and familial Mediterranean fever.1 Recently, the drug has been shown to potentially reduce the risk of cardiovascular events in those with coronary artery disease.2 Colchicine has several potential mechanisms of action, including reducing the chemotaxis of neutrophils, inhibiting inflammasome signaling, and decreasing the production of cytokines, such as interleukin-1 beta.3 When colchicine is administered early in the course of COVID-19, these mechanisms could potentially mitigate or prevent inflammation-associated manifestations of the disease. These anti-inflammatory properties coupled with the drug’s limited immunosuppressive potential, favorable safety profile, and widespread availability have prompted investigation of colchicine for the treatment of COVID-19.


  • The COVID-19 Treatment Guidelines Panel (the Panel) recommends against the use of colchicine for the treatment of nonhospitalized patients with COVID-19, except in a clinical trial (BIIa).
  • The Panel recommends against the use of colchicine for the treatment of hospitalized patients with COVID-19 (AI).


For Nonhospitalized Patients With COVID-19

COLCORONA, a large randomized placebo-controlled trial that evaluated colchicine in outpatients with COVID-19, did not reach its primary efficacy endpoint of reducing hospitalizations and death.4 However, in the subset of patients whose diagnosis was confirmed by a positive SARS-CoV-2 polymerase chain reaction (PCR) result from a nasopharyngeal (NP) swab, a slight reduction in hospitalizations was observed among those who received colchicine.

PRINCIPLE, another randomized, open-label, adaptive-platform trial that evaluated colchicine versus usual care, was stopped for futility when no significant difference in time to first self-reported recovery from COVID-19 between the colchicine and usual care recipients was found.5

The PRINCIPLE trial showed no benefit of colchicine, and the larger COLCORONA trial failed to reach its primary endpoint, found only a very modest effect of colchicine in the subgroup of patients with positive SARS-CoV-2 PCR results, and reported more gastrointestinal adverse events in those receiving colchicine. Therefore, the Panel recommends against the use of colchicine for the treatment of COVID-19 in nonhospitalized patients, except in a clinical trial (BIIa).

For Hospitalized Patients With COVID-19

In the RECOVERY trial, a large randomized trial in hospitalized patients with COVID-19, colchicine demonstrated no benefit with regard to 28-day mortality or any secondary outcomes.6 Based on the results from this large trial, the Panel recommends against the use of colchicine for the treatment of COVID-19 in hospitalized patients (AI).

Clinical Data for COVID-19

Colchicine in Nonhospitalized Patients With COVID-19


The COLCORONA trial was a contactless, double-blind, placebo-controlled, randomized trial in outpatients who received a diagnosis of COVID-19 within 24 hours of enrollment. Participants were aged ≥70 years or aged ≥40 years with at least 1 of the following risk factors for COVID-19 complications: body mass index ≥30, diabetes mellitus, uncontrolled hypertension, known respiratory disease, heart failure or coronary disease, fever ≥38.4°C within the last 48 hours, dyspnea at presentation, bicytopenia, pancytopenia, or the combination of high neutrophil count and low lymphocyte count. Participants were randomized 1:1 to receive colchicine 0.5 mg twice daily for 3 days and then once daily for 27 days or placebo. The primary endpoint was a composite of death or hospitalization by Day 30; secondary endpoints included components of the primary endpoint, as well as the need for mechanical ventilation by Day 30. Participants reported by telephone the occurrence of any study endpoints at 15 and 30 days after randomization; in some cases, clinical data were confirmed or obtained by medical chart reviews.4


  • The study enrolled 4,488 participants.
  • The primary endpoint occurred in 104 of 2,235 participants (4.7%) in the colchicine arm and 131 of 2,253 participants (5.8%) in the placebo arm (OR 0.79; 95% CI, 0.61–1.03; P = 0.08).
  • There were no statistically significant differences in the secondary outcomes between the arms.
  • In a prespecified analysis of 4,159 participants who had a SARS-CoV-2 diagnosis confirmed by PCR testing of an NP specimen (93% of those enrolled), those in the colchicine arm were less likely to reach the primary endpoint (96 of 2,075 participants [4.6%]) than those in the placebo arm (126 of 2,084 participants [6.0%]; OR 0.75; 95% CI, 0.57–0.99; P = 0.04). In this subgroup of patients with PCR-confirmed SARS-CoV-2 infection, there were fewer hospitalizations (a secondary outcome) in the colchicine arm (4.5% of patients) than in the placebo arm (5.9% of patients; OR 0.75; 95% CI, 0.57–0.99).
  • More participants in the colchicine arm experienced gastrointestinal adverse events, including diarrhea which occurred in 13.7% of colchicine recipients versus 7.3% of placebo recipients (P < 0.0001). Unexpectedly, more pulmonary emboli were reported in the colchicine arm than in the placebo arm (11 events [0.5% of patients] vs. 2 events [0.1% of patients]; P= 0.01).


  • Due to logistical difficulties with staffing, the trial was stopped at approximately 75% of the target enrollment, which may have limited the study’s power to detect differences for the primary outcome.
  • There was uncertainty as to the accuracy of COVID-19 diagnoses in presumptive cases.
  • Some patient-reported clinical outcomes were potentially misclassified.


PRINCIPLE is a randomized, open-label, platform trial that evaluated colchicine in symptomatic, nonhospitalized patients with COVID-19 who were aged ≥65 years or aged ≥18 years with comorbidities or shortness of breath, and who had symptoms for ≤14 days. Participants were randomized to receive colchicine 0.5 mg daily for 14 days or usual care. The coprimary endpoints, which included time to first self-reported recovery or hospitalization or death due to COVID-19 by Day 28, were analyzed using a Bayesian model. Participants were followed through symptom diaries that they completed online daily; those who did not complete the diaries were contacted by telephone on Days 7, 14, and 29. The investigators developed a prespecified criterion for futility, specifying a clinically meaningful benefit in time to first self-reported recovery as a hazard ratio ≥1.2, corresponding to about 1.5 days of faster recovery in the colchicine arm.


  • The study enrolled 4,997 participants: 212 participants were randomized to receive colchicine; 2,081 to receive usual care alone; and 2,704 to receive other treatments.
  • The prespecified primary analysis included participants with SARS-CoV-2 positive test results (156 in the colchicine arm; 1,145 in the usual care arm; and 1,454 in the other treatments arm).
  • The trial was stopped early because the criterion for futility was met; the median time to self-reported recovery was similar in the colchicine arm and the usual care arm (HR 0.92; 95% CrI, 0.72–1.16).
  • Analyses of self-reported time to recovery and hospitalizations or death due to COVID-19 among concurrent controls also showed no significant differences between the colchicine and usual care arms.
  • There were no statistically significant differences in the secondary outcomes between the colchicine and usual care arms in both the primary analysis population and in subgroups, including subgroups based on symptom duration, baseline disease severity, age, or comorbidities.
  • The occurrence of adverse events was similar in the colchicine and usual care arms.


  • The design of the study was open-label treatment.
  • The sample size of the colchicine arm was small.

Colchicine in Hospitalized Patients With COVID-19


In the RECOVERY trial, hospitalized patients with COVID-19 were randomized to receive colchicine (1 mg loading dose, followed by 0.5 mg 12 hours later, and then 0.5 mg twice daily for 10 days or until discharge) or usual care.6


  • The study enrolled 11,340 participants.
  • At randomization, 10,603 patients (94%) were receiving corticosteroids.
  • The primary endpoint of all-cause mortality at Day 28 occurred in 1,173 of 5,610 participants (21%) in the colchicine arm and 1,190 of 5,730 participants (21%) in the placebo arm (rate ratio 1.01; 95% CI, 0.93–1.10; P = 0.77).
  • There were no statistically significant differences between the arms for the secondary outcomes of median time to being discharged alive, discharge from the hospital within 28 days, and receipt of mechanical ventilation or death.
  • The incidence of new cardiac arrhythmias, bleeding events, and thrombotic events was similar in the 2 arms. Two serious adverse events were attributed to colchicine: 1 case of severe acute kidney injury and one case of rhabdomyolysis.


  • The trial’s open-label design may have introduced bias for assessing some of the secondary endpoints.

The GRECCO-19 Trial

GRECCO-19 was a small, prospective, open-label randomized clinical trial in 105 patients hospitalized with COVID-19 across 16 hospitals in Greece. Patients were assigned 1:1 to receive standard of care with colchicine (1.5 mg loading dose, followed by 0.5 mg after 60 minutes and then 0.5 mg twice daily until hospital discharge or for up to 3 weeks) or standard of care alone.7


  • Fewer patients in the colchicine arm (1 of 55 patients) than in the standard of care arm (7 of 50 patients) reached the primary clinical endpoint of deterioration in clinical status from baseline by 2 points on a 7-point clinical status scale (OR 0.11; 95% CI, 0.01–0.96).
  • Participants in the colchicine group were significantly more likely to experience diarrhea (occurred in 45.5% of participants in the colchicine arm vs. 18.0% in the standard of care arm; P = 0.003).


  • The overall sample size and the number of clinical events reported were small.
  • The study design was open-label treatment assignment.

The results of several small randomized trials and retrospective cohort studies that have evaluated various doses and durations of colchicine in hospitalized patients with COVID-19 have been published in peer-reviewed journals or made available as preliminary, non-peer-reviewed reports.8-11 Some have shown benefits of colchicine use, including less need for supplemental oxygen, improvements in clinical status on an ordinal clinical scale, and reductions in certain inflammatory markers. In addition, some studies have reported higher discharge rates or fewer deaths among patients who received colchicine than among those who received comparator drugs or placebo. However, the findings of these studies are difficult to interpret due to significant design or methodological limitations, including small sample sizes, open-label designs, and differences in the clinical and demographic characteristics of participants and permitted use of various cotreatments (e.g., remdesivir, corticosteroids) in the treatment arms.

Adverse Effects, Monitoring, and Drug-Drug Interactions

Common adverse effects of colchicine include diarrhea, nausea, vomiting, abdominal cramping and pain, bloating, and loss of appetite. In rare cases, colchicine is associated with serious adverse events, such as neuromyotoxicity and blood dyscrasias. Use of colchicine should be avoided in patients with severe renal insufficiency, and patients with moderate renal insufficiency who receive the drug should be monitored for adverse effects. Caution should be used when colchicine is coadministered with drugs that inhibit cytochrome P450 (CYP) 3A4 and/or P-glycoprotein (P-gp) because such use may increase the risk of colchicine-induced adverse effects due to significant increases in colchicine plasma levels. The risk of myopathy may be increased with the concomitant use of certain HMG-CoA reductase inhibitors (e.g., atorvastatin, lovastatin, simvastatin) due to potential competitive interactions mediated by CYP3A4 and P-gp pathways.12,13 Fatal colchicine toxicity has been reported in individuals with renal or hepatic impairment who received colchicine in conjunction with P-gp inhibitors or strong CYP3A4 inhibitors.

Considerations in Pregnancy

There are limited data on the use of colchicine in pregnancy. Fetal risk cannot be ruled out based on data from animal studies and the drug’s mechanism of action. Colchicine crosses the placenta and has antimitotic properties, which raises a theoretical concern for teratogenicity. However, a recent meta-analysis did not find that colchicine exposure during pregnancy increased the rates of miscarriage or major fetal malformations. There are no data for colchicine use in pregnant women with acute COVID-19. Risks of use should be balanced against potential benefits.12,14

Considerations in Children

Colchicine is most commonly used in children to treat periodic fever syndromes and autoinflammatory conditions. Although colchicine is generally considered safe and well tolerated in children, there are no data on the use of the drug to treat pediatric acute COVID-19 or multisystem inflammatory syndrome in children (MIS-C).


  1. van Echteld I, Wechalekar MD, Schlesinger N, Buchbinder R, Aletaha D. Colchicine for acute gout. Cochrane Database Syst Rev. 2014(8):CD006190. Available at:
  2. Xia M, Yang X, Qian C. Meta-analysis evaluating the utility of colchicine in secondary prevention of coronary artery disease. Am J Cardiol. 2021;140:33-38. Available at:
  3. Reyes AZ, Hu KA, Teperman J, et al. Anti-inflammatory therapy for COVID-19 infection: the case for colchicine. Ann Rheum Dis. 2021 May;80(5):550-557. Available at:
  4. Tardif JC, Bouabdallaoui N, L’Allier PL, et al. Colchicine for community-treated patients with COVID-19 (COLCORONA): a phase 3, randomised, double-blinded, adaptive, placebo-controlled, multicentre trial. Lancet Respir Med. 2021;9(8):924-932. Available at:
  5. PRINCIPLE Trial Collaborative Group, Dorward J, Yu L, et al. Colchicine for COVID-19 in adults in the community (PRINCIPLE): a randomised, controlled, adaptive platform trial. medRxiv. 2021;Preprint. Available at:
  6. RECOVERY Collaborative Group. Colchicine in patients admitted to hospital with COVID-19 (RECOVERY): a randomised, controlled, open-label, platform trial. Lancet Respir Med. 2021;Published online ahead of print. Available at:
  7. Deftereos SG, Giannopoulos G, Vrachatis DA, et al. Effect of colchicine vs standard care on cardiac and inflammatory biomarkers and clinical outcomes in patients hospitalized with coronavirus disease 2019: the GRECCO-19 randomized clinical trial. JAMA Netw Open. 2020;3(6):e2013136. Available at:
  8. Brunetti L, Diawara O, Tsai A, et al. Colchicine to weather the cytokine storm in hospitalized patients with COVID-19. J Clin Med. 2020;9(9). Available at:
  9. Sandhu T, Tieng A, Chilimuri S, Franchin G. A case control study to evaluate the impact of colchicine on patients admitted to the hospital with moderate to severe COVID-19 infection. Can J Infect Dis Med Microbiol. 2020. Available at:
  10. Lopes MI, Bonjorno LP, Giannini MC, et al. Beneficial effects of colchicine for moderate to severe COVID-19: a randomised, double-blinded, placebo-controlled clinical trial. RMD Open. 2021;7(1). Available at:
  11. Salehzadeh F, Pourfarzi F, Ataei S. The impact of colchicine on the COVID-19 patients; a clinical trial. Research Square. 2020;Preprint. Available at:
  12. Colchicine (Colcrys) [package insert]. Food and Drug Administration. 2012. Available at:
  13. American College of Cardiology. AHA statement on drug-drug interactions with statins. 2016. Available at: Accessed November 2, 2021.
  14. Indraratna PL, Virk S, Gurram D, Day RO. Use of colchicine in pregnancy: a systematic review and meta-analysis. Rheumatology (Oxford). 2018;57(2):382-387. Available at:

www.covid19treatmentguidelines.nih.govAn official website of the National Institutes of Health

Association of Myocarditis With BNT162b2 Messenger RNA COVID-19 Vaccine in a Case Series of Children

Authors: Audrey Dionne, MD1,2Francesca Sperotto, MD1,2Stephanie Chamberlain1,2et alAnnette L. Baker, MSN, CPNP1,2Andrew J. Powell, MD1,2Ashwin Prakash, MD1,2Daniel A. Castellanos, MD1,2Susan F. Saleeb, MD1,2Sarah D. de Ferranti, MD, MPH1,2Jane W. Newburger, MD, MPH1,2Kevin G. Friedman, MD1,2

JAMA Cardiol. 2021;6(12):1446-1450. doi:10.1001/jamacardio.2021.347

Question  What are the findings on cardiac imaging in children with myocarditis after COVID-19 vaccination?

Findings  In this case series of 15 children who were hospitalized with myocarditis after receipt of the BNT162b2 messenger RNA COVID-19 vaccine for 1 to 5 days, boys were most often affected after the second vaccine dose, 3 patients had ventricular systolic dysfunction, and 12 patients had late gadolinium enhancement on cardiac magnetic resonance imaging. There was no mortality, and all but 1 patient had normal echocardiogram results on follow-up 1 to 13 days after discharge.

Meaning  COVID-19 vaccine-associated myocarditis may have a benign short-term course in children; however, the long-term risks remain unknown.Abstract

Importance  The BNT162b2 (Pfizer-BioNTech) messenger RNA COVID-19 vaccine was authorized on May 10, 2021, for emergency use in children aged 12 years and older. Initial reports showed that the vaccine was well tolerated without serious adverse events; however, cases of myocarditis have been reported since approval.

Objective  To review results of comprehensive cardiac imaging in children with myocarditis after COVID-19 vaccine.

Design, Setting, and Participants  This study was a case series of children younger than 19 years hospitalized with myocarditis within 30 days of BNT162b2 messenger RNA COVID-19 vaccine. The setting was a single-center pediatric referral facility, and admissions occurred between May 1 and July 15, 2021.

Main Outcomes and Measures  All patients underwent cardiac evaluation including an electrocardiogram, echocardiogram, and cardiac magnetic resonance imaging.

Results  Fifteen patients (14 male patients [93%]; median age, 15 years [range, 12-18 years]) were hospitalized for management of myocarditis after receiving the BNT162b2 (Pfizer) vaccine. Symptoms started 1 to 6 days after receipt of the vaccine and included chest pain in 15 patients (100%), fever in 10 patients (67%), myalgia in 8 patients (53%), and headache in 6 patients (40%). Troponin levels were elevated in all patients at admission (median, 0.25 ng/mL [range, 0.08-3.15 ng/mL]) and peaked 0.1 to 2.3 days after admission. By echocardiographic examination, decreased left ventricular (LV) ejection fraction (EF) was present in 3 patients (20%), and abnormal global longitudinal or circumferential strain was present in 5 patients (33%). No patient had a pericardial effusion. Cardiac magnetic resonance imaging findings were consistent with myocarditis in 13 patients (87%) including late gadolinium enhancement in 12 patients (80%), regional hyperintensity on T2-weighted imaging in 2 patients (13%), elevated extracellular volume fraction in 3 patients (20%), and elevated LV global native T1 in 2 patients (20%). No patient required intensive care unit admission, and median hospital length of stay was 2 days (range 1-5). At follow-up 1 to 13 days after hospital discharge, 11 patients (73%) had resolution of symptoms. One patient (7%) had persistent borderline low LV systolic function on echocardiogram (EF 54%). Troponin levels remained mildly elevated in 3 patients (20%). One patient (7%) had nonsustained ventricular tachycardia on ambulatory monitor.

Conclusions and Relevance  In this small case series study, myocarditis was diagnosed in children after COVID-19 vaccination, most commonly in boys after the second dose. In this case series, in short-term follow-up, patients were mildly affected. The long-term risks associated with postvaccination myocarditis remain unknown. Larger studies with longer follow-up are needed to inform recommendations for COVID-19 vaccination in this population.Introduction

SARS-CoV-2 was first identified in China and evolved rapidly to a global pandemic. Vaccines to prevent SARS-CoV-2 infection are the current standard approach for curbing the pandemic. In the US, the BNT162b2 messenger RNA (mRNA) (Pfizer-BioNTech), mRNA-1273 (Moderna), and Ad26.COV2.S (Janssen) vaccines were granted emergency use authorization for adults. On May 10, 2021, the emergency use authorization for the BNT162b2 vaccine was extended to children aged 12 years and older.1

Myocarditis has been reported as a rare complication of vaccination against other viruses.2 It was not reported in the initial messenger RNA COVID-19 vaccine trials, although the ability to detect rare events was limited by sample size. Since the emergency use authorization, myocarditis in adolescents and young adults after COVID-19 vaccine has been reported.35 In this series, we detail the occurrence of myocarditis after COVID-19 vaccination in an adolescent population, including comprehensive cardiac imaging evaluation and follow-up.MethodsPopulation

This case series included all patients younger than 19 years admitted at our center with acute myocarditis after COVID-19 vaccination. Myocarditis was defined as chest pain and an elevated troponin level in the absence of an alternative diagnosis. The institutional review board at Boston Children’s Hospital approved this study and granted an exemption from informed consent owing to use of deidentified data and the requirements of 45 CFR §46. This study followed the reporting guideline for case series.Data Collection and Definitions

Clinical data elements including demographic characteristics, laboratory values, and hospital course were collected from the electronic medical record. Patients’ race and ethnicity were self-reported by patients or parents according to the US Census categories6 and were collected because of their known association with COVID-19–related illnesses. Elevated troponin T level was defined as a troponin value greater than 0.01 ng/mL. Cardiac evaluation for all patients included electrocardiogram (ECG), echocardiogram, and cardiac magnetic resonance (CMR) imaging. Ventricular systolic dysfunction was defined as a left ventricular (LV) ejection fraction equal to or greater than 55% on echocardiogram or CMR results. Echocardiographic peak global longitudinal strain was measured from an apical 4-chamber view and peak global circumferential strain from a parasternal short-axis view at the midpapillary level using software (Tom Tec Image Arena, version 4.6; TOMTEC). Strain values were considered abnormal if the z score was less than or equal to −2 for age. Diastolic dysfunction was defined as a z score less than or equal to −2 for age, for septal e′ tissue Doppler, LV free wall e′, or the E/e′ ratio. CMR assessment included LV ejection fraction, T2-weighted myocardial imaging, LV global native T1, LV global T2, extracellular volume fraction, and late gadolinium enhancement (LGE).Statistical Analysis

Descriptive statistics were calculated for all study variables. Quantitative variables were summarized as median and range and categorical variables as frequencies and percentages.Results

Fifteen patients were admitted at the Department of Cardiology, Boston Children’s Hospital for management of myocarditis after COVID-19 vaccination between May 1 and July 15, 2021. The median age was 15 years (range, 12-18 years), and most patients were male (n = 14 [93%]). Patients self-identified as non-Hispanic White (n = 8 [53%]), Hispanic White (n = 2 [15%]), other Hispanic (n = 1 [8%]), other non-Hispanic (n = 1 [8%]), and unknown (n = 3 [20%]) (Table). All patients received the BNT162b2 mRNA vaccine. Symptoms occurred after the second dose of the vaccine in all but 1 case. No patients had a known prior COVID-19 infection, although 1 had reactive SARS-CoV-2 antibodies to the nucleocapsid protein.

Chest pain in 15 of 15 patients (100%) started at median 3 days (range, 1-6 days) after receiving the vaccine and lasted 1 to 9 days. Other symptoms included fever in 10 patients (67%), myalgia in 8 patients (53%), and headache in 6 patients (40%). Seven patients (47%) were treated with intravenous immunoglobulins (2 g/kg) and methylprednisolone (1 mg/kg/dose twice a day, transitioned to prednisone at time of discharge). Hospital length of stay was a median of 2 days (range, 1-5 days), and no patients required intensive care unit admission.Troponin

Troponin levels were elevated in all patients at admission (median, 0.25 ng/mL [range, 0.08-3.15 ng/mL]) and peaked 0.1 to 2.3 days after admission (Table). At the time of discharge, the troponin level had substantially decreased but remained elevated in all patients (Figure 1).Echocardiogram

On admission echocardiogram, 3 patients (20%) had global LV systolic ventricular dysfunction (EF 44%, 49%, and 53%), one of whom also had regional wall motion abnormality at the apex. Two patients (13%) with systolic dysfunction had abnormal diastolic function indices, and 1 patient (7%) with borderline EF (55%) had evidence of diastolic dysfunction. Five patients (33%) had abnormal global longitudinal or global circumferential strain (Figure 2; eFigure 1 and eTable in the Supplement). No patients had a coronary artery aneurysm or pericardial effusion.Electrocardiogram

The most frequent finding was diffuse ST-segment elevation consistent with pericarditis, present on admission in 6 patients (40%), and at some time during hospital admission in 8 patients (53%). Four additional patients had nonspecific ST segment changes. One patient (normal systolic and diastolic ventricular function; LGE on CMR) had nonsustained ventricular tachycardia during hospital admission. ST-T wave changes persisted at time of hospital discharge in 9 patients (69%). No patient had PR interval, QRS duration, or QTc duration prolongation.Cardiac Magnetic Resonance

CMR imaging was performed in all patients 1 to 7 days after the onset of symptoms. Systolic LV dysfunction was present in 3 patients (25%). Findings consistent with myocarditis were found in 13 patients (87%). LGE was present in 12 patients, and most often found in the inferolateral (n = 3) and anterolateral (n = 4) regions (eTable and eFigure 2 in the Supplement). The extracellular volume fraction was borderline elevated (28%-30%) in 4 patients (27%) and elevated (>30%) in 3 patients (25%). LV global native T1 was borderline elevated (1080-1100 milliseconds) in 2 patients and elevated (>1100 milliseconds) in 2 patients. Two patients had regional hyperintensity on T2-weighted imaging. LV global T2 was borderline elevated (56-60 milliseconds) in 1 patient.Follow-up

Follow-up information after hospital discharge was available for all patients (virtual visit in 1 patient; in-person with testing in 14 patients) and occurred 1 to 13 days after discharge. Four patients (27%) were asymptomatic with normal troponin level, ECG, and echocardiogram results.

Four patients (27%) had persistent symptoms, including fatigue in 3 patients (25%) and continued chest pain in 1 patient (7%). None of the patients with persistent symptoms had decreased EF at time of initial presentation (1 with abnormal strain) and 3 patients (75%) had abnormal CMR results with LGE.

One asymptomatic patient (7%) had persistent borderline low LV EF (54%), reduced circumferential strain (z score, −2.3), and reduced lateral e′ velocity (z score, −2.8) measured by echocardiogram at 8 days after discharge; all other patients had normal echocardiogram results. Ventricular systolic function recovered (EF>55%) in 2 to 11 days (Figure 1).

ECG changes persisted in 4 patients (33%) and included nonspecific ST-T wave changes in 4 patients (33%) or new T-wave inversion in 3 patients (20%). One patient (7%) with nonsustained ventricular tachycardia during hospital admission had recurrence of nonsustained ventricular tachycardia on 6 days of ambulatory ECG monitoring, despite initiation of β-blocker therapy.

Troponin levels remained mildly elevated at follow-up in 3 patients (20%) (Figure 1). One patient (7%) with a persistently elevated troponin level (0.05 ng/mL) had continuing fatigue. All patients with persistently elevated troponin levels had had prior abnormalities on CMR (2 patients with LGE, 1 patient with elevated extracellular volume fraction).Discussion

In this early experience of 15 cases, myocarditis typically occurred in male patients after the second dose of the COVID-19 vaccine. All patients in this series had a benign course; none required intensive care unit admission and all were discharged alive from the hospital within 5 days. LV systolic function at presentation was normal in most patients and normalized within a few days in all but 1 patient who had persistent borderline low LV function. This finding differs from other forms of myocarditis in which LV systolic dysfunction and arrhythmias are more common, with 50% of children requiring intensive care unit admission, a mean hospital length of stay of 14.4 days, and a mortality rate of 7.8%.79

Although vaccine-associated cases of myocarditis to date have had uncomplicated short-term course, the long-term prognosis remains unclear. Of note, CMR LGE was a frequent finding at time of diagnosis. In this clinical setting, LGE reflects an increased volume of distribution of the gadolinium-based contrast agent in the affected region likely related to myocyte necrosis and/or extracellular edema. In nonvaccine-associated myocarditis, the presence of LGE is associated with increased risk for adverse cardiovascular events during follow-up.1012 Thus, longitudinal studies of patients with myocarditis after COVID-19 vaccine will be important to better understand long-term risks.

To date, there have been 1226 reports of myocarditis after messenger RNA vaccination to the Vaccine Adverse Event Reporting System (VAERS), including 687 in persons aged less than 30 years.13 Crude reporting rates using vaccine administration data estimates the highest rate among male individuals aged 12 to 17 years (62.8 cases per million), similar to our observations. Despite the risks of myocarditis associated with vaccination, the benefits of vaccination likely outweigh risks in children and adolescents. It is estimated that COVID-19 vaccination in males aged 12 to 29 years can prevent 11 000 COVID-19 cases, 560 hospitalizations, 138 intensive care unit admissions, and 6 deaths compared with 39 to 47 expected myocarditis cases.Limitations

This study has limitations. Limitations to this series include the lack of COVID-19 vaccine administration data, which does not permit calculation of incidence or identification of risk factors for myocarditis. Mild cases may have been missed due to the novelty of this complication and the lack of routine screening.Conclusions

Myocarditis may be a rare complication after COVID-19 vaccination in patients aged less than 19 years. In this case series study, the short-term clinical course was mild in most patients; however, the long-term risks remain unknown. Risks and benefits of COVID-19 vaccination must be considered to guide recommendations for vaccination in this population.Back to topArticle Information

Accepted for Publication: July 20, 2021.

Published Online: August 10, 2021. doi:10.1001/jamacardio.2021.3471

Study: Myocarditis risk 37 times higher for children with COVID-19 than uninfected peers

Authors: Melissa Jenco, News Content Editor August 31, 2021

The risk of myocarditis for children under 16 years is 37 times higher for those infected with COVID-19 than those who haven’t been infected with the virus, according to a new study.

Authors from the Centers for Disease Control and Prevention (CDC) said the study provides more evidence that the benefits of the vaccine outweigh a small risk of myocarditis after vaccination.

Researchers analyzed data from more than 900 hospitals and found inpatient visits for myocarditis were 42% higher in 2020 compared to 2019, according to a new Morbidity and Mortality Weekly Report.

Among 36 million patients, about 0.01% had myocarditis between March 2020 and February 2021. The median age of people with myocarditis was 54 years, and 59% were male.

About 42% of patients with myocarditis had a history of COVID-19, mostly within the same month. The team determined the risk of myocarditis to be 0.146% among those with COVID-19 and 0.009% among those not diagnosed with COVID-19.

Across all ages, the risk of myocarditis was almost 16 times higher for people with COVID-19 compared to those who aren’t infected. The myocarditis risk is 37 times higher for infected children under 16 years and seven times higher for infected people ages 16-39 compared to their uninfected peers.

Some of the myocarditis cases seen in children with COVID-19 may be cases of multisystem inflammatory syndrome, according to the study.

Authors noted the study could not prove COVID-19 causes myocarditis, but the findings of a link between the two are consistent with several other studies.

In recent months, there has been concern about a small risk of myocarditis after receiving an mRNA COVID-19 vaccine. A June study showed among males ages 12-29 years — the group with the highest rates of myocarditis after vaccination — there would be an estimated 39 to 47 cases of myocarditis for every million second doses of vaccine. Authors of the new study say their findings support health officials’ assertions that the benefits of vaccination outweigh the risks.

“These findings underscore the importance of implementing evidence-based COVID-19 prevention strategies, including vaccination, to reduce the public health impact of COVID-19 and its associated complications,” they wrote.Resources

Copyright © 2021 American Academy of Pediatrics

Former Senior FDA Official: Manufacturers, FDA Negligent In Not Investigating Covid-19 Vaccine Risks To Heart Health


Manufacturers, FDA, and CDC must investigate serious cardiovascular incidents related to the Pfizer and Moderna Covid vaccines.

From day ,one the U.S. Food and Drug Administration knew the Covid-19 vaccine was linked to serious heart trouble in recipients. The FDA medical officer review of Pfizer’s original Covid-19 application notes “clinically important serious adverse reactions [included] anaphylaxis and myocarditis/pericarditis”—that is, severe allergic reactions and inflammation of the heart and or the sac containing the heart, respectively. As of this writing, FDA has not released its review of the Moderna “Spikevax” mRNA vaccine application despite having granted emergency use authorization well more than a year ago and full approval late last month.

The Vaccine Adverse Event Reporting System (VAERS), jointly run by FDA and the Centers for Disease Control, lists a long and impersonal number of cardiovascular-related events in young, healthy people. Without reading the underlying narratives submitted with the reports, it’s hard to establish the precise causal links regarding these adverse events. Still, there are thousands of reports of heart attacks, myocarditis, and pericarditis in the United States alone, which should have spurred manufacturers and the FDA into full investigation mode.

Studies acknowledged by FDA officials show that the FDA’s various safety databases only collect an estimated 1 to 13 percent of all adverse events that occur. Multiple FDA drug safety epidemiologists have stated during official FDA presentation that it only takes a single well-documented adverse event to justify a safety signal investigation and in turn to warn the American public of the potential risk.

Historically, the FDA has sought safety warnings on labels, up to and including a “black boxed warning” and a prescribing restriction known as a Risk Evaluation and Mitigation Strategy (REMS) for much less. For instance, in 2008, after fewer than 200 spontaneous VAERS reports of tendon rupture following administration of the class of antibiotics known as fluoroquinolones, FDA added a “black box warning” and REMS prescribing restrictions.

Yet thousands of serious, debilitating, and deadly safety VAERS reports following Covid vaccines and boosters are not being held to the same regulatory standards. If approximately 1 to 13 percent of adverse events are reported, extrapolating those numbers means the actual number of adverse health events could easily be in the hundreds of thousands in the United States and many millions worldwide.

In addition to VAERS, the CDC’s Vaccine Safety Datalink indicates an excess risk of myocarditis and pericarditis in recipients following the Pfizer and Moderna vaccines. The cardiovascular risk after any mRNA vaccine is high, but with Moderna it’s approximately four times higher than Pfizer’s.

Other public health agencies with much tinier budgets and staff compared to our FDA’s took action on this months ago. In October, DenmarkFinlandNorway, and Sweden suspended the use of the Moderna vaccine for young people, but it’s still full speed ahead here in the United States.

Since then, more data has been released affirming the same: On Jan. 25, 2022, a CDC and FDA study published in JAMA shows the risk of myocarditis following any kind of mRNA Covid vaccination is greater than the background risk in the population, with the largest proportions of cases of myocarditis occurring among white males.

A comprehensive study out of Britain from December 2021 examined data from more than 42 million people who have taken a Covid-19 shot found a noteworthy increase in myocarditis with mRNA vaccines that persisted and increased with every dose and booster. “An association between Covid-19 infection and myocarditis was observed in all ages for both sexes,” the study’s abstract states. “These findings have important implications for public health and vaccination policy.” Indeed they do—especially in light of the questionable way the FDA approved vaccines in kids from 5 to 13 years old, and the pending FDA applications to approve vaccination in babies starting at 6 months old.

The FDA, CDC, and manufacturers have access to VAERS and additional high-quality denominator-based vaccine safety systems including the Biologics Effectiveness and Safety Initiative (BEST) and the Vaccine Safety Datalink (VSD), respectively. Have manufacturers and our health agencies used these tools and others to fully investigate the cardiovascular health risks of the vaccine? There is reason to doubt, given the political pressure the Biden administration has put on the agencies to advocate for taking the vaccine while almost never mentioning safety.

Myocarditis and pericarditis have historically been rare. They are defined as inflammation of the heart muscle or layers of the pericardial sac, respectively. Both conditions cause easily recognizable ECG changes and have ambiguous symptoms that include shortness of breath and chest pain. Myocarditis and pericarditis can easily be diagnosed clinically with echocardiograms and can be treated by inexpensive pharmacology and bedrest, but for that to happen, people need to know to seek medical diagnosis and care. 

Therein is the problem: providers and patients are not being adequately warned to monitor for cardiovascular symptoms despite the increased incidence. Since there is a failure of manufacturers and the FDA to address this and other untoward effects of mRNA utility and mandates, outside drug safety experts need to publicly address mRNA Covid vaccine safety immediately.

On February 4, 2022, a CDC advisory committee proposed extending the gap between Covid-19 shots to mitigate the cardiovascular damage of the vaccine. This indicates the federal government is aware of the serious risk. Yet rather than addressing the risk head-on by communicating the facts to the public, they seem to be taking a “half measure” of changing the interval and hoping to mitigate risk without evidence it will have any effect on outcome.

In the very recent past, anyone warning about the exact same cardiovascular risk that this advisory panel spoke about less than a week ago were shamed and banned on social media by “big tech” “fact checkers.”

Vaccines are one of the most important inventions in human history, having saved millions of lives. That does not mean every person should get every vaccine. Also, like every drug out there, it is critically important to quickly detect and report safety problems. Now we have a federally mandated vaccine that is clearly no longer effective, and potentially causing additional illness and death.

The failure to adequately monitor and warn for Covid vaccine adverse events has served to harden not only Covid vaccine hesitancy but has shredded the credibility of public health authorities. The failure to openly talk about known adverse reactions erodes trust.

In the 1950s physicians used to not tell patients when they had terminal cancer because they thought it was for their own good. We are long past the day when hiding information from the public is considered good for public health. It never is. It is not only unethical and insulting, it’s dangerous.

To See 1,000 Peer Reviewed Articles on COVID-19 Adverse Events Click Below

Long-term cardiovascular outcomes of COVID-19


The cardiovascular complications of acute coronavirus disease 2019 (COVID-19) are well described, but the post-acute cardiovascular manifestations of COVID-19 have not yet been comprehensively characterized. Here we used national healthcare databases from the US Department of Veterans Affairs to build a cohort of 153,760 individuals with COVID-19, as well as two sets of control cohorts with 5,637,647 (contemporary controls) and 5,859,411 (historical controls) individuals, to estimate risks and 1-year burdens of a set of pre-specified incident cardiovascular outcomes. We show that, beyond the first 30 d after infection, individuals with COVID-19 are at increased risk of incident cardiovascular disease spanning several categories, including cerebrovascular disorders, dysrhythmias, ischemic and non-ischemic heart disease, pericarditis, myocarditis, heart failure and thromboembolic disease. These risks and burdens were evident even among individuals who were not hospitalized during the acute phase of the infection and increased in a graded fashion according to the care setting during the acute phase (non-hospitalized, hospitalized and admitted to intensive care). Our results provide evidence that the risk and 1-year burden of cardiovascular disease in survivors of acute COVID-19 are substantial. Care pathways of those surviving the acute episode of COVID-19 should include attention to cardiovascular health and disease.


Post-acute sequelae of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)—the virus that causes coronavirus disease 2019 (COVID-19)—can involve the pulmonary and several extrapulmonary organs, including the cardiovascular system1. A few studies have investigated cardiovascular outcomes in the post-acute phase of the COVID-19; however, most were limited to hospitalized individuals (who represent the minority of people with COVID-19), and all had a short duration of follow-up and a narrow selection of cardiovascular outcomes2,3,4,5. A comprehensive assessment of post-acute COVID-19 sequelae of the cardiovascular system at 12 months is not yet available, and studies of post-acute COVID-19 sequelae across the spectrum of care settings of the acute infection (non-hospitalized, hospitalized and admitted to intensive care) are also lacking. Addressing this knowledge gap will inform post-acute COVID-19 care strategies.

In this study, we used the US Department of Veterans Affairs national healthcare databases to build a cohort of 153,760 US veterans who survived the first 30 d of COVID-19 and two control groups: a contemporary cohort consisting of 5,637,647 users of the US Veterans Health Administration (VHA) system with no evidence of SARS-CoV-2 infection and a historical cohort (pre-dating the COVID-19 pandemic) consisting of 5,859,411 non-COVID-19-infected VHA users during 2017. These cohorts were followed longitudinally to estimate the risks and 12-month burdens of pre-specified incident cardiovascular outcomes in the overall cohort and according to care setting of the acute infection (non-hospitalized, hospitalized and admitted to intensive care).


There were 153,760, 5,637,647 and 5,859,411 participants in the COVID-19, contemporary control and historical control groups, respectively (Fig. 1). Median follow-up time in the COVID-19, contemporary control and historical control groups was 347 (interquartile range, 317–440), 348 (318–441) and 347 (317–440) d, respectively. The COVID-19, contemporary control and historical control groups had 159,366, 5,854,288 and 6,082,182 person-years of follow-up, respectively, altogether corresponding to 12,095,836 person-years of follow-up. The demographic and health characteristics of the COVID-19, contemporary control and historical control groups before and after weighting are presented in Supplementary Tables 1 and 2, respectively.

figure 1
Fig. 1: Flowchart of cohort construction.

Incident cardiovascular diseases in COVID-19 versus contemporary control

Assessment of covariate balance after application of inverse probability weighting suggested that covariates were well balanced (Extended Data Fig. 1a).

We estimated the risks of a set of pre-specified cardiovascular outcomes in COVID-19 versus contemporary control; we also estimated the adjusted excess burden of cardiovascular outcomes due to COVID-19 per 1,000 persons at 12 months on the basis of the difference between the estimated incidence rate in individuals with COVID-19 and the contemporary control group. Risks and burdens of individual cardiovascular outcomes are provided in Fig. 2 and Supplementary Table 3 and are discussed below. Risks and burdens of the composite endpoints are provided in Fig. 3 and Supplementary Table 3.

figure 2
Fig. 2: Risks and 12-month burdens of incident post-acute COVID-19 cardiovascular outcomes compared with the contemporary control cohort.
figure 3
Fig. 3: Risks and 12-month burdens of incident post-acute COVID-19 composite cardiovascular outcomes compared with the contemporary control cohort.

Cerebrovascular disorders

People who survived the first 30 d of COVID-19 exhibited increased risk of stroke (hazard ratio (HR) = 1.52 (1.43, 1.62); burden 4.03 (3.32, 4.79) per 10,00 persons at 12 months; for all HRs and burdens, parenthetical ranges refer to 95% confidence intervals (CIs)) and transient ischemic attacks (TIA) (HR = 1.49 (1.37, 1.62); burden 1.84 (1.38, 2.34)). The risks and burdens of a composite of these cerebrovascular outcomes were 1.53 (1.45, 1.61) and 5.48 (4.65, 6.35).


There were increased risks of atrial fibrillation (HR = 1.71 (1.64, 1.79); burden 10.74 (9.61, 11.91)), sinus tachycardia (HR = 1.84 (1.74, 1.95); burden 5.78 (5.07, 6.53)), sinus bradycardia (HR = 1.53 (1.45, 1.62); burden 4.62 (3.90, 5.38)), ventricular arrhythmias (HR = 1.84 (1.72, 1.98); burden 4.18 (3.56, 4.85)); and atrial flutter (HR = 1.80 (1.66, 1.96); burden 3.10 (2.55, 3.69)). The risks and burdens of a composite of these dysrhythmia outcomes were 1.69 (1.64, 1.75), and 19.86 (18.31, 21.46).

Inflammatory disease of the heart or pericardium

Inflammatory disease of the heart or pericardium included pericarditis (HR = 1.85 (1.61, 2.13)); burden 0.98 (0.70, 1.30) and myocarditis (HR = 5.38 (3.80, 7.59); burden 0.31 (0.20, 0.46)). The risks and burdens of a composite of these inflammatory diseases of the heart or pericardium were 2.02 (1.77, 2.30) and 1.23 (0.93, 1.57).

Ischemic heart disease

Ischemic heart disease included acute coronary disease (HR = 1.72 (1.56, 1.90); burden 5.35 (4.13, 6.70)), myocardial infarction (HR = 1.63 (1.51, 1.75); burden 2.91 (2.38, 3.49)), ischemic cardiomyopathy (HR = 1.75 (1.44, 2.13); burden 2.34 (1.37, 3.51)) and angina (HR = 1.52 (1.42, 1.64); burden 2.50 (2.00, 3.03)). The risks and burdens of a composite of these ischemic heart disease outcomes were 1.66 (1.52, 1.80) and 7.28 (5.80, 8.88).

Other cardiovascular disorders

Other cardiovascular disorders included heart failure (HR = 1.72 (1.65, 1.80); burden 11.61 (10.47, 12.78)), non-ischemic cardiomyopathy (HR = 1.62 (1.52, 1.73); burden 3.56 (2.97, 4.20)), cardiac arrest (HR = 2.45 (2.08, 2.89); burden 0.71 (0.53, 0.93)) and cardiogenic shock (HR = 2.43 (1.86, 3.16); burden 0.51 (0.31, 0.77)). The risks and burdens of a composite of these other cardiovascular disorders were 1.72 (1.65, 1.79) and 12.72 (11.54, 13.96).

Thromboembolic disorders

Thromboembolic disorders included pulmonary embolism (HR = 2.93 (2.73, 3.15); burden 5.47 (4.90, 6.08)); deep vein thrombosis (HR = 2.09 (1.94, 2.24); burden 4.18 (3.62, 4.79)) and superficial vein thrombosis (HR = 1.95 (1.80, 2.12); burden 2.61 (2.20, 3.07)). The risks and burdens of a composite of these thromboembolic disorders were 2.39 (2.27, 2.51) and 9.88 (9.05, 10.74).

Additional composite endpoints

We then examined the risks and burdens of two composite endpoints, including major adverse cardiovascular event (MACE)—a composite of myocardial infarction, stroke and all-cause mortality—and any cardiovascular outcome (defined as the occurrence of any incident pre-specified cardiovascular outcome included in this study). Compared to the contemporary control group, there were increased risks and burdens of MACE (HR = 1.55 (1.50, 1.60); burden 23.48 (21.54, 25.48)) and any cardiovascular outcome (HR = 1.63 (1.59, 1.68); burden 45.29 (42.22, 48.45)).

Subgroup analyses

We examined the risks of incident composite cardiovascular outcomes in subgroups based on age, race, sex, obesity, smoking, hypertension, diabetes, chronic kidney disease, hyperlipidemia and cardiovascular disease. The risks of incident composite cardiovascular outcomes were evident in all subgroups (Fig. 4 and Supplementary Table 4),

figure 4
Fig. 4: Subgroup analyses of the risks of incident post-acute COVID-19 composite cardiovascular outcomes compared with the contemporary control cohort.

We examined the risks and burdens of the pre-specified outcomes in a cohort of people without any cardiovascular disease at baseline; the results were consistent with those shown in the primary analyses (Extended Data Figs. 2 and 3 and Supplementary Table 5).

Incident cardiovascular diseases in COVID-19 versus contemporary control by care setting of the acute infection

We further examined the risks and burdens of cardiovascular diseases in mutually exclusive groups by the care setting of the acute infection (that is, whether people were non-hospitalized (n = 131,612), hospitalized (n = 16,760) or admitted to intensive care (n = 5,388) during the acute phase of COVID-19); demographic and health characteristics of these groups before weighting can be found in Supplementary Table 6 and after weighting in Supplementary Table 7. Assessment of covariate balance after application of weights suggested that covariates were well balanced (Extended Data Fig. 1b). Compared to the contemporary control group, the risks and 12-month burdens of the pre-specified cardiovascular outcomes increased according to the severity of the acute infection (Fig. 5 and Supplementary Table 8); results for the composite outcomes are shown in Fig. 6 and Supplementary Table 8.

figure 5
Fig. 5: Risks and 12-month burdens of incident post-acute COVID-19 cardiovascular outcomes compared with the contemporary control cohort by care setting of the acute infection.
figure 6
Fig. 6: Risks and 12-month burdens of incident post-acute COVID-19 composite cardiovascular outcomes compared with the contemporary control cohort by care setting of the acute infection.

Incident cardiovascular diseases in COVID-19 versus historical control

We then examined the associations between COVID-19 and the pre-specified outcomes in analyses considering a historical control group as the referent category; the characteristics of the exposure groups were balanced after weighting (Extended Data Fig. 1c and Supplementary Table 2). The results were consistent with analyses using the contemporary control as the referent category and showed increased risks and associated burdens of the pre-specified outcomes in comparisons of COVID-19 versus the overall historical control group (Extended Data Figs. 4 and 5 and Supplementary Table 9). Using the historical control as the referent category, we examined the risks in subgroups and separately in people without any prior cardiovascular disease; the results were consistent with those undertaken versus the contemporary control (Extended Data Figs. 68 and Supplementary Tables 10 and 11). Associations between COVID-19 and our pre-specified outcomes based on care setting of the acute infection were also assessed using the historical control group as the referent category; demographic and clinical characteristics are presented before weighting in Supplementary Table 12 and after weighting in Supplementary Table 13. Characteristics of the exposure groups were balanced after weighting (Extended Data Fig. 1d). The risks and 12-month burdens of the pre-specified outcomes by care setting of the acute infection were also consistent with those shown in analyses considering COVID-19 versus contemporary control (Extended Data Figs. 9 and 10 and Supplementary Table 14).

Cardiovascular diseases before and after COVID-19

To better understand the change in the relative rates of incident cardiovascular outcomes before and after the COVID-19 exposure, we developed a difference-in-differences analysis to estimate the adjusted incident rate ratios of the cardiovascular outcomes relative to both the contemporary and historical control groups in the pre-COVID-19 and post-COVID-19 exposure periods. The results showed that the adjusted incident rate ratios of cardiovascular outcomes in the post-COVID-19 exposure period were significantly higher than those in the pre-exposure period (ratios of incident rate ratios for all cardiovascular outcomes were significantly higher than 1) and exhibited a graded increase by severity of the acute phase of the disease (Supplementary Tables 1518).

Sensitivity analyses

We tested robustness of results in several sensitivity analyses involving the outcomes of MACE and any cardiovascular outcome (Supplementary Tables 17 and 18). The sensitivity analyses were performed in comparisons involving COVID-19 versus the contemporary control and COVID-19 versus the historical control and, additionally, COVID-19 by care setting versus both controls. (1) To test whether the inclusion of additional algorithmically selected covariates would challenge the robustness of study results, we selected and used 300 high-dimensional variables (instead of the 100 used in the primary analyses) to construct the inverse probability weighting. (2) We then also tested the results in models specified to include only pre-defined covariates (that is, without inclusion of algorithmically selected covariates) to build the inverse probability weighting. Finally, (3) we changed the analytic approach by using the doubly robust method (instead of the inverse weighting method used in primary analyses) to estimate the magnitude of the associations between COVID-19 exposure and the pre-specified outcomes. All sensitivity analyses yielded results consistent with those produced using the primary approach (Supplementary Tables 19 and 20).

Risk of myocarditis and pericarditis without COVID-19 vaccination

Because some COVID-19 vaccines might be associated with a very rare risk of myocarditis or pericarditis, and to eliminate any putative contribution of potential vaccine exposure to the outcomes of myocarditis and pericarditis in this study, we conducted two analyses. First, we censored cohort participants at the time of receiving the first dose of any COVID-19 vaccine. Second, we adjusted for vaccination as a time-varying covariate. Both analyses were conducted versus both the contemporary and historical control groups. The results suggested that COVID-19 was associated with increased risk of myocarditis and pericarditis in both analyses (Supplementary Tables 2124).

Positive and negative outcome controls

To assess whether our data and analytic approach would reproduce known associations, we examined the association between COVID-19 and the risk of fatigue (known to be a signature sequela of post-acute COVID-19) as a positive outcome control. The results suggested that COVID-19 was associated with a higher risk of fatigue (Supplementary Table 25).

We then examined the association between COVID-19 and a battery of seven negative-outcome controls where no prior knowledge suggests that an association is expected. The results yielded no significant association between COVID-19 and any of the negative-outcome controls, which were consistent with a priori expectations (Supplementary Table 25).

Negative-exposure controls

To further examine the robustness of our approach, we developed and tested a pair of negative-exposure controls. We hypothesized that receipt of influenza vaccination in odd-numbered and even-numbered calendar days between 1 March 2020 and 15 January 2021 would be associated with similar risks of the pre-specified cardiovascular outcomes examined in this analysis. We, therefore, tested the associations between receipt of influenza vaccine in even-numbered (n = 571,291) versus odd-numbered (n = 605,453) calendar days and the pre-specified cardiovascular outcomes. We used the same data sources, cohort design, analytical approach (including covariate specification and weighting method) and outcomes. The results suggest that receipt of influenza vaccination in odd-numbered calendar days versus even-numbered calendar days was not significantly associated with any of the pre-specified cardiovascular outcomes (Supplementary Table 26).


In this study involving 153,760 people with COVID-19, 5,637,647 contemporary controls and 5,859,411 historical controls—which, altogether, correspond to 12,095,836 person-years of follow-up—we provide evidence that, beyond the first 30 d of infection, people with COVID-19 exhibited increased risks and 12-month burdens of incident cardiovascular diseases, including cerebrovascular disorders, dysrhythmias, inflammatory heart disease, ischemic heart disease, heart failure, thromboembolic disease and other cardiac disorders. The risks were evident regardless of age, race, sex and other cardiovascular risk factors, including obesity, hypertension, diabetes, chronic kidney disease and hyperlipidemia; they were also evident in people without any cardiovascular disease before exposure to COVID-19, providing evidence that these risks might manifest even in people at low risk of cardiovascular disease. Our analyses of the risks and burdens of cardiovascular outcomes across care settings of the acute infection reveal two key findings: (1) that the risks and associated burdens were evident among those who were not hospitalized during the acute phase of the disease—this group represents the majority of people with COVID-19; and (2) that the risks and associated burdens exhibited a graded increase across the severity spectrum of the acute phase of COVID-19 (from non-hospitalized to hospitalized individuals to those admitted to intensive care). The risks and associated burdens were consistent in analyses considering the contemporary control group and, separately, the historical control group as the referent category. The difference-in-differences analyses, which are designed to further investigate the causality of study findings, show that the increased risks of post-acute COVID-19 cardiovascular outcomes are attributable sequelae to COVID-19 itself. The results were robust to challenge in multiple sensitivity analyses. Application of a positive-outcome control yielded results consistent with established knowledge; and testing of a battery of negative-outcome controls and negative-exposure controls yielded results consistent with a priori expectations. Taken together, our results show that 1-year risks and burdens of cardiovascular diseases among those who survive the acute phase of COVID-19 are substantial and span several cardiovascular disorders. Care strategies of people who survived the acute episode of COVID-19 should include attention to cardiovascular health and disease.

The broader implications of these findings are clear. Cardiovascular complications have been described in the acute phase of COVID-19 (refs. 6,7,8). Our study shows that the risk of incident cardiovascular disease extends well beyond the acute phase of COVID-19. First, the findings emphasize the need for continued optimization of strategies for primary prevention of SARS-CoV-2 infections; that is, the best way to prevent Long COVID and its myriad complications, including the risk of serious cardiovascular sequelae, is to prevent SARS-CoV-2 infection in the first place. Second, given the large and growing number of people with COVID-19 (more than 72 million people in the United States, more than 16 million people in the United Kingdom and more than 355 million people globally), the risks and 12-month burdens of cardiovascular diseases reported here might translate into a large number of potentially affected people around the world. Governments and health systems around the world should be prepared to deal with the likely significant contribution of the COVID-19 pandemic to a rise in the burden of cardiovascular diseases. Because of the chronic nature of these conditions, they will likely have long-lasting consequences for patients and health systems and also have broad implications on economic productivity and life expectancy. Addressing the challenges posed by Long COVID will require a much-needed, but so far lacking, urgent and coordinated long-term global response strategy9,10.

The mechanism or mechanisms that underlie the association between COVID-19 and development of cardiovascular diseases in the post-acute phase of the disease are not entirely clear11,12. Putative mechanisms include lingering damage from direct viral invasion of cardiomyocytes and subsequent cell death, endothelial cell infection and endotheliitis, transcriptional alteration of multiple cell types in heart tissue, complement activation and complement-mediated coagulopathy and microangiopathy, downregulation of ACE2 and dysregulation of the renin–angiotensin–aldosterone system, autonomic dysfunction, elevated levels of pro-inflammatory cytokines and activation of TGF-β signaling through the Smad pathway to induce subsequent fibrosis and scarring of cardiac tissue11,13,14,15,16,17. An aberrant persistent hyperactivated immune response, autoimmunity or persistence of the virus in immune-privileged sites has also been cited as putative explanations of extrapulmonary (including cardiovascular) post-acute sequelae of COVID-19 (refs. 11,13,14,18). Integration of the SARS-CoV-2 genome into DNA of infected human cells, which might then be expressed as chimeric transcripts fusing viral with cellular sequences, has also been hypothesized as a putative mechanism for continued activation of the immune-inflammatory-procoagulant cascade19,20. These mechanistic pathways might explain the range of post-acute COVID-19 cardiovascular sequelae investigated in this report. A deeper understanding of the biologic mechanisms will be needed to inform development of prevention and treatment strategies of the cardiovascular manifestations among people with COVID-19.

Our analyses censoring participants at time of vaccination and controlling for vaccination as a time-varying covariate show that the increased risk of myocarditis and pericarditis reported in this study is significant in people who were not vaccinated and is evident regardless of vaccination status.

This study has several strengths. We used the vast and rich national healthcare databases of the US Department of Veterans Affairs to build a large cohort of people with COVID-19. We designed the study cohort to investigate incident cardiovascular disease in the post-acute phase of the disease. We pre-specified a comprehensive list of cardiovascular outcomes. We examined the associations using two large control groups: a contemporary and a historical control; this approach allowed us to deduce that the associations between COVID-19 and risks of cardiovascular outcomes are not related to the broader temporal changes between the pre-pandemic and the pandemic eras but, rather, are related to exposure to COVID-19 itself. Our modeling approach included specification of 19 pre-defined variables selected based on established knowledge and 100 algorithmically selected variables from high-dimensional data domains, including diagnostic codes, prescription records and laboratory test results. We evaluated the associations across care settings of the acute infection. Our difference-in-differences approach further enhances the causal interpretation of study results. We challenged the robustness of results in multiple sensitivity analyses and successfully tested positive-outcome and negative-outcome controls and negative-exposure controls. We provided estimates of risk on both the ratio scale (HRs) and the absolute scale (burden per 1,000 persons at 12 months); the latter also reflects the contribution of baseline risk and provides an estimate of potential harm that is more easily explainable to the public than risk reported on the ratio scale (for example, HR).

This study has several limitations. The demographic composition of our cohort (majority White and male) might limit the generalizability of study findings. We used the electronic healthcare databases of the US Department of Veterans Affairs to conduct this study, and, although we used validated outcome definitions and took care to adjust the analyses for a large set of pre-defined and algorithmically selected variables, we cannot completely rule out misclassification bias and residual confounding. It is possible that some people might have had COVID-19 but were not tested for it; these people would have been enrolled in the control group and, if present in large numbers, might have biased the results toward the null. Our datasets do not include information on causes of death. Finally, as the pandemic, with all its dynamic features, continues to progress, as the virus continues to mutate and as new variants emerge, as treatment strategies of acute and post-acute COVID-19 evolve and as vaccine uptake improves, it is possible that the epidemiology of cardiovascular manifestations in COVID-19 might also change over time21.

In summary, using a national cohort of people with COVID-19, we show that risk and 12-month burden of incident cardiovascular disease are substantial and span several cardiovascular disease categories (ischemic and non-ischemic heart disease, dysrhythmias and others). The risks and burdens of cardiovascular disease were evident even among those whose acute COVID-19 did not necessitate hospitalization. Care pathways of people who survived the acute episode of COVID-19 should include attention to cardiovascular health and disease.



We used the electronic healthcare databases of the US Department of Veterans Affairs to conduct this study. The VHA, within the US Department of Veterans Affairs, provides healthcare to discharged veterans of the US armed forces. It operates the largest nationally integrated healthcare system in the United States, with 1,255 healthcare facilities (including 170 VA Medical Centers and 1,074 outpatient sites) located across the United States. All veterans who are enrolled with the VHA have access to the comprehensive medical benefits package of the VA (which includes preventative and health maintenance, outpatient care, inpatient hospital care, prescriptions, mental healthcare, home healthcare, primary care, specialty care, geriatric and extended care, medical equipment and prosthetics). The VA electronic healthcare databases are updated daily.


A flowchart of cohort construction is provided in Fig. 1. Of 6,241,346 participants who encountered the VHA in 2019, 162,690 participants who had a positive COVID-19 test between 1 March 2020 and 15 January 2021 were selected into the COVID-19 group. To examine post-acute outcomes, we then selected participants from the COVID-19 group who were alive 30 d after the date of the positive COVID-19 test (n = 153,760). The date of the COVID-19-positive test served as T0 for the COVID-19 group.

A contemporary control group of people with no evidence of SARS-CoV-2 infection was constructed from those who had encountered the VHA in 2019 (n = 6,241,346). Of those who were still alive by 1 March 2020 (n = 5,960,737), 5,806,977 participants were not in the COVID-19 group and were selected into the contemporary control group. To ensure that this contemporary control group had a similar follow-up time as the COVID-19 group, we randomly assigned T0 in the contemporary control group based on the distribution of T0 in the COVID-19 group so that the proportion of people enrolled on a certain date would be the same in both the contemporary and COVID-19 groups. Of 5,658,938 participants alive at the assigned T0, 5,637,647 participants in the contemporary control group were alive 30 d after T0. In the COVID-19 and contemporary control groups, 31 October 2021 was the end of follow-up.

To examine the associations between COVID-19 and cardiovascular outcomes compared to those who did not experience the pandemic, a historical control group was constructed from 6,461,205 participants who used the VHA in 2017. Of the 6,150,594 participants who were alive on 1 March 2018, 6,008,499 participants did not enroll into the COVID-19 group and were further selected into the historical control group. To ensure that this historical control group had a similar follow-up time as the COVID-19 group, we randomly assigned T0 in the historical control group with a similar distribution as T0 minus 2 years (730 d) in the COVID-19 group. Of 5,875,818 historical control participants alive at assigned T0, 5,859,411 were alive 30 d after T0. In the historical control group, end of follow-up was set as 31 October 2019.

Data sources

Electronic health records from the VA Corporate Data Warehouse (CDW) were used in this study. Demographic information was collected from the CDW Patient domain. The CDW Outpatient Encounters domain provided clinical information pertaining to outpatient encounters, whereas the CDW Inpatient Encounters domain provided clinical information during hospitalization. Medication information was obtained from the CDW Outpatient Pharmacy and CDW Bar Code Medication Administration domains. The CDW Laboratory Results domain provided laboratory test information, and the COVID-19 Shared Data Resource provided information on COVID-19. Additionally, the Area Deprivation index (ADI), which is a composite measure of income, education, employment and housing, was used as a summary measure of contextual disadvantage at participants’ residential locations22.

Pre-specified outcomes

The pre-specified outcomes were selected based on our previous work on the systematic characterization of Long COVID1,23. Incident cardiovascular outcomes in the post-acute phase of COVID-19 were assessed in the follow-up period between 30 d after T0 until the end of follow-up in those without history of the outcome in the year before T0. Each cardiovascular outcome was defined based on validated diagnostic codes. We also aggregated individual outcomes in a related category of composite outcome (for example, stroke and TIA were aggregated to cerebrovascular disease). We also specified two additional composite outcomes: (1) MACE was a composite outcome of all-cause mortality, myocardial infarction and stroke; and (2) the composite of any cardiovascular outcome was defined as the first incident occurrence of any of the cardiovascular outcomes investigated in this study.


To adjust for the difference in baseline characteristics between groups, we considered both pre-defined and algorithmically selected high-dimensional covariates assessed within 1 year before T0. Pre-defined variables were selected based on prior knowledge1,7,24,25. The pre-defined covariates included age, race (White, Black and Other), sex, ADI, body mass index, smoking status (current, former and never) and healthcare use parameters, including the use number of outpatient and inpatient encounters and use of long-term care. We additionally specified several comorbidities as pre-defined variables, including cancer, chronic kidney disease, chronic lung disease, dementia, diabetes, dysautonomia, hyperlipidemia and hypertension. Additionally, we adjusted for estimated glomerular filtration rate and systolic and diastolic blood pressure. Missing values were accounted for by conditional mean imputation based on value within the group26. Continuous variables were transformed into restricted cubic spline functions to account for potential non-linear relationships.

In addition to pre-defined covariates, we further algorithmically selected additional potential confounders from data domains, including diagnoses, medications and laboratory tests27. To accomplish this, we gathered all patient encounter, prescription and laboratory data and classified the information into 540 diagnostic categories, 543 medication classes and 62 laboratory test abnormalities. For the diagnoses, medications and laboratory abnormalities that occurred in at least 100 participants within each group, univariate relative risk between the variable and exposure was calculated, and the top 100 variables with the strongest relative risk were selected28. The process of algorithmically selecting the high-dimensional covariates was independently conducted for each outcome-specific cohort in each comparison (for example, the COVID-19 versus contemporary control analyses to examine incident heart failure and the COVID-19 versus historical control analyses to examine incident heart failure).

All pre-defined and algorithmically selected covariates were used in the models.

Statistical analyses

Baseline characteristics of the COVID-19 and contemporary and historical control groups, along with standardized mean difference between groups, were described.

We then estimated the risks, burdens and excess burdens of incident cardiovascular outcomes for COVID-19 compared to the contemporary control group and, separately, compared to the historical control group, after adjusting for differences in baseline characteristics through inverse probability weighting. To estimate the risk of each incident cardiovascular outcome, we built a subcohort of participants without a history of the outcome being examined (that is, the risk of incident heart failure was estimated within a subcohort of participants without history of heart failure in the year before enrollment). In each subcohort, a propensity score for each individual was estimated as the probability of belonging to the VHA users group in 2019 (target population) based on both pre-defined and algorithmically selected high-dimensional variables. This propensity score was then used to calculate the inverse probability weight as the probability of belonging in the target population divided by 1 − the probability of being in the target population. Covariate balance after application of weights was assessed by standardized mean differences.

HRs of incident cardiovascular outcomes between the COVID-19 and contemporary cohorts and the COVID-19 and historical cohorts were estimated from cause-specific hazard models where death was considered as a competing risk, and the inverse probability weights were applied. Burden per 1,000 participants at 12 months of follow-up and the excess burden based on the differences between COVID-19 and control groups were estimated.

We conducted analyses in subgroups by age, race, sex, obesity, smoking, hypertension, diabetes, chronic kidney disease, hyperlipidemia and cardiovascular disease. And, separately, we undertook analyses in a cohort without history of any cardiovascular outcomes before cohort enrollment.

We then developed causal difference-in-differences analyses to estimate the adjusted incident rate ratios of all cardiovascular outcomes in the pre-COVID-19 and post-COVID-19 exposure period relative to both contemporary and historical controls29,30,31,32. To enhance the interpretability of difference-in-difference analyses, the pre-exposure period was defined as with same follow-up time as the post-exposure period, and the incident rate ratio for the pre-exposure period was examined within those without history of the outcome within 1 year before the period. Incident rate ratios for all groups in the pre-exposure and post- exposure periods were weighted toward the common target population (VHA users in 2019) based on pre-exposure characteristics. The adjusted incident rate ratios in the pre-exposure and post-exposure periods were then compared. Difference-in-differences analyses were also conducted in mutually exclusive groups according to care setting of the acute phase of the disease. We also evaluated the associations between COVID-19 and risks of post-acute cardiovascular sequelae in mutually exclusive groups according to care setting of the acute phase of the disease (that is, whether people were non-hospitalized, hospitalized or admitted into the intensive care unit during the first 30 d of infection). Inverse probability weights were estimated for each care setting group using the approach outlined in the previous paragraph. Cause-specific hazard models with inverse probability weighting were then applied, and HRs, burdens and excess burdens were reported.

We conducted multiple sensitivity analyses to test the robustness of our study results. (1) To capture additional potential confounders, we expanded our inclusion of high-dimensional variables from the top 100 to the top 300 when constructing the inverse probability weight. (2) We then modified our adjustment strategy by using only pre-defined variables when constructing the inverse probability weight (not including the 100 high-dimensional covariates used in the primary analyses). Finally, (3) we alternatively applied a doubly robust approach, where both covariates and the inverse probability weights were applied to the survival models, to estimate the associations33.

COVID-19 is associated with an increased risk of fatigue in the post-acute phase of the disease, which is generally considered as a signature post-acute sequela34. To test whether our approach would reproduce known associations, we, therefore, examined the association between COVID-19 and fatigue as a positive outcome control. Reproducing this known association (using our data, cohort design and analytic strategy) would provide some measure of assurance that our approach yields result consistent with a priori expectations.

We also subjected our approach to the application of a battery of negative-outcome controls where no prior knowledge supports the existence of a causal association between the exposure and the risks of negative-outcome controls35. The negative-outcome controls included hypertrichosis, melanoma in situ, sickle cell trait, perforation of the tympanic membrane, malignant neoplasm of the tongue, B cell lymphoma and Hodgkin’s lymphoma. We also developed and tested a pair of negative-exposure controls (defined as exposure to influenza vaccine in odd-numbered or even-numbered calendar days between 1 March 2020 and 15 January 2021). Our pre-test expectation was that there would be no differences in risk of any of the pre-specified cardiovascular outcomes examined in this analysis between those who received influenza vaccine in odd-numbered versus even-numbered calendar days. The successful application of negative controls might reduce concern about the presence of spurious biases related to cohort building, study design, covariate selection, analytic approaches, outcome ascertainment, residual confounding and other sources of latent biases.

Estimation of variance when weightings were applied was accomplished by using robust sandwich variance estimators. In all analyses, a 95% confidence interval that excluded unity was considered evidence of statistical significance. This study was approved by the institutional review board of the VA St. Louis Health Care System (protocol number 1606333), which granted a waiver of informed consent. Analyses were conducted using SAS Enterprise Guide version 8.2 (SAS Institute), and results were visualized using R version 4.04.

Ethical approval

This research project was reviewed and approved by the institutional review board of the VA St. Louis Health Care System (protocol number 1606333).

Reporting Summary

Further information on research design is available in the Nature Research Reporting Summary linked to this article.

Data availability

The data that support the findings of this study are available from the US Department of Veterans Affairs. VA data are made freely available to researchers behind the VA firewall with an approved VA study protocol. For more information, visit or contact the VA Information Resource Center at

Code availability

SAS codes are available at and


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This study used data from the VA COVID-19 Shared Data Resource. This research was funded by the US Department of Veterans Affairs (to Z.A.-A.) and two American Society of Nephrology and KidneyCure fellowship awards (to Y.X. and B.B.). The contents do not represent the views of the US Department of Veterans Affairs or the US government.

1000 Peer Reviewed Studies Questioning Covid-19 Vaccine Safety

Peer Reviewed Medical Papers Submitted To Various Medical Journals, Evidencing A Multitude Of Adverse Events In Covid-19 Vaccine Recipients.

The list includes studies published as of January 20, 2022 concerning the potential adverse reaction from COVID-19 vaccines, such as myocarditis, thrombosis, thrombocytopenia, vasculitis, cardiac, Bell’s Palsy, immune-mediated disease, and many more.

  1. Myocarditis after mRNA vaccination against SARS-CoV-2, a case series:
  2. Myocarditis after immunization with COVID-19 mRNA vaccines in members of the US military. This article reports that in “23 male patients, including 22 previously healthy military members, myocarditis was identified within 4 days after receipt of the vaccine”:
  3. Association of myocarditis with the BNT162b2 messenger RNA COVID-19 vaccine in a case series of children:
  4. Acute symptomatic myocarditis in seven adolescents after Pfizer-BioNTech COVID-19 vaccination:
  5. Myocarditis and pericarditis after vaccination with COVID-19 mRNA: practical considerations for care providers:
  6. Myocarditis, pericarditis and cardiomyopathy after COVID-19 vaccination:
  7. Myocarditis with COVID-19 mRNA vaccines:
  8. Myocarditis and pericarditis after COVID-19 vaccination:
  9. Myocarditis temporally associated with COVID-19 vaccination:
  10. COVID-19 Vaccination Associated with Myocarditis in Adolescents:
  11. Acute myocarditis after administration of BNT162b2 vaccine against COVID-19:
  12. Temporal association between COVID-19 vaccine Ad26.COV2.S and acute myocarditis: case report and review of the literature:
  13. COVID-19 vaccine-induced myocarditis: a case report with review of the literature:
  14. Potential association between COVID-19 vaccine and myocarditis: clinical and CMR findings:
  15. Recurrence of acute myocarditis temporally associated with receipt of coronavirus mRNA disease vaccine 2019 (COVID-19) in a male adolescent:
  16. Fulminant myocarditis and systemic hyper inflammation temporally associated with BNT162b2 COVID-19 mRNA vaccination in two patients:
  17. Acute myocarditis after administration of BNT162b2 vaccine:
  18. Lymphohistocytic myocarditis after vaccination with COVID-19 Ad26.COV2.S viral vector:
  19. Myocarditis following vaccination with BNT162b2 in a healthy male:
  20. Acute myocarditis after Comirnaty (Pfizer) vaccination in a healthy male with previous SARS-CoV-2 infection:
  21. Acute myocarditis after vaccination with SARS-CoV-2 mRNA-1273 mRNA:
  22. Acute myocarditis after SARS-CoV-2 vaccination in a 24-year-old man:
  23. A series of patients with myocarditis after vaccination against SARS-CoV-2 with mRNA-1279 and BNT162b2:
  24. COVID-19 mRNA vaccination and myocarditis:
  25. COVID-19 vaccine and myocarditis:
  26. Epidemiology and clinical features of myocarditis/pericarditis before the introduction of COVID-19 mRNA vaccine in Korean children: a multicenter study e/en/covidwho-1360706.
  27. COVID-19 vaccines and myocarditis:
  28. Myocarditis and other cardiovascular complications of COVID-19 mRNA-based COVID-19 vaccines
  29. Myocarditis and other cardiovascular complications of COVID-19 mRNA-based COVID-19 vaccines
  30. Myocarditis, pericarditis, and cardiomyopathy after COVID-19 vaccination:
  31. Myocarditis with covid-19 mRNA vaccines:
  32. Association of myocarditis with COVID-19 mRNA vaccine in children: vid-19-vaccine-in-children/
  33. Association of myocarditis with COVID-19 messenger RNA vaccine BNT162b2 in a case series of children:
  34. Myocarditis after immunization with COVID-19 mRNA vaccines in members of the U.S. military:
  35. Myocarditis occurring after immunization with COVID-19 mRNA-based COVID-19 vaccines:
  36. Myocarditis following immunization with Covid-19 mRNA:
  37. Patients with acute myocarditis after vaccination withCOVID-19 mRNA:
  38. Myocarditis associated with vaccination with COVID-19 mRNA:
  39. Symptomatic Acute Myocarditis in 7 Adolescents after Pfizer-BioNTech COVID-19 Vaccination:
  40. Cardiovascular magnetic resonance imaging findings in young adult patients with acute myocarditis after COVID-19 mRNA vaccination: a case series:
  41. Clinical Guidance for Young People with Myocarditis and Pericarditis after Vaccination with COVID-19 mRNA:
  42. Cardiac imaging of acute myocarditis after vaccination with COVID-19 mRNA:
  43. Case report: acute myocarditis after second dose of mRNA-1273 SARS-CoV-2 mRNA vaccine:
  44. Myocarditis / pericarditis associated with COVID-19 vaccine:
  45. The new COVID-19 mRNA vaccine platform and myocarditis: clues to the possible underlying mechanism:
  46. Myocarditis associated with COVID-19 vaccination: echocardiographic, cardiac tomography, and magnetic resonance imaging findings:
  47. In-depth evaluation of a case of presumed myocarditis after the second dose of COVID-19 mRNA vaccine:
  48. Occurrence of acute infarct-like myocarditis after COVID-19 vaccination: just an accidental coincidence or rather a vaccination-associated autoimmune myocarditis?:

This list is not meant to be all inclusive of all peer-reviewed potential harms from mRNA vaccines. To access any of the 1,000 Vaccine Harms published in Medical journals Click The Link Below:


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Myocarditis following mRNA vaccination against SARS-CoV-2, a case series

Authors:William W.KingaMatthew R.PetersenaRalph M.MatarbJeffery B.BudwegaLydaCuervo PardocJohn W.Petersenb

American Heart Journal Plus: Cardiology Research and Practice Volume 8, August 2021, 100042



mRNA COVID-19 vaccines have emerged as a new form of vaccination that has proven to be highly safe and effective against COVID-19 vaccination. Rare adverse events including myocarditis have been reported in the literature.


Data were gathered from the electronic medical record of four patients personally treated by the authors.


Four patients, ages 20 to 30, presented with myocarditis characterized by chest pain, elevations in troponin-I and C-reactive protein, and negative viral serologies two to four days following mRNA vaccine administration. One had a cardiac MRI showing delayed gadolinium enhancement in a subpericardial pattern. All experienced symptom resolution by the following day, and the two who have returned for follow-up had normal troponin-I and CRP values.


Along with previously reported instances, these cases raise suspicion for a possible link between mRNA vaccines and myocarditis.


COVID-19MyopericarditisMyocarditisPericarditismRNA vaccine

1. Introduction

In 2020 SARS-CoV-2 spread across the globe, inducing hypoxic respiratory failure, acute respiratory distress syndrome, hypercoagulability, and severe systemic inflammation. Cardiovascular manifestations of COVID-19, the disease caused by SARS-CoV-2, include myocardial infarction, transient systolic and diastolic dysfunction, and myocarditis. Both preexisting cardiovascular disease and COVID-induced myocarditis are associated with higher mortality.

Myopericarditis refers to simultaneous myocarditis and pericarditis, inflammatory conditions of the myocardium and pericardium, respectively. Characteristic symptoms and objective findings raise suspicion for myocarditis. Symptoms include chest pain, dyspnea on exertion, palpitations, and unexplained cardiogenic shock. Objective findings include arrhythmias, conduction delays, troponin-I elevations, and functional or structural abnormalities on cardiac imaging. Often cardiac magnetic resonance imaging (CMR) demonstrates characteristic late gadolinium enhancement, supporting this diagnosis. However, definitive diagnosis requires endomyocardial biopsy, the sensitivity of which is low due to the focal and transient nature of infiltrates. Pericarditis is diagnosed by the presence of two or more of the following: pleuritic chest pain, pericardial friction rub, new pericardial effusion, and ECG changes including down-sloping PR depression and diffuse ST elevations.

In early 2020, researchers developed vaccines against SARS-CoV-2 utilizing a novel vaccination strategy of inoculating liposome-encapsulated recombinant mRNA encoding the SARS-CoV-2 spike protein. Phase 3 multicenter randomized controlled trials showed 94–95% efficacy in prevention of severe COVID-19 [1][2]. In the Moderna trial, 1.5% of vaccine recipients and 1.3% of placebo recipients reported grade 3 adverse reactions, side effects altering daily activity. Similar numbers were reported in the Pfizer trial, with 1.2% of vaccine recipients and 0.7% of placebo recipients reporting severe adverse events. In both trials the most common systemic reactions were fatigue, headache, muscle pain, and chills. These effects occurred most frequently after the second dose and in participants in the youngest age group. They resolved on average 2–3 days post-vaccine. Neither study reported major cardiovascular adverse events, including myocarditis [1][2]. Due to the efficacy and safety demonstrated in these clinical trials, the Food and Drug Administration granted emergency use authorization to both mRNA vaccines in December 2020.

2. Case 1

A 23-year-old woman presented with chest pain 5 days after receiving her second dose of the Moderna vaccine. She had an ECG (Fig. 1) with down-sloping PR depressions and diffuse ST elevations, as well as a troponin of 14,045 pg/mL and an elevated CRP (Table 1). Her troponin peaked the following day. Coxsackie, HCV, CMV, and EBV serologies were all negative. Transthoracic echocardiography (TTE) demonstrated a left ventricular ejection fraction (LVEF) of 55 to 60%, with basal inferior and basal inferolateral hypokinesis. CMR (Fig. 2Fig. 3Fig. 4) revealed late gadolinium enhancement involving the basal inferior, basal to mid inferolateral, mid anterolateral, apical lateral, apical septal, and apical inferior wall segments in a subepicardial distribution pattern, consistent with myocarditis. Her symptoms resolved quickly, and her CRP declined to 11 mg/L by the third day of her hospitalization. She was discharged on hospital day 3. She presented to clinic for follow-up two weeks after discharge, where her CRP had declined to 0.8 mg/L and she had no residual symptoms.

Fig. 1

Table 1. Summary of clinical findings. All patients presented 2 to 5 days following their 2nd vaccine dose with troponin and CRP elevation, and the viral serologies that were tested were negative. ECG and TTE abnormalities may be compared as well.

Case numberAge and sexVaccine makerDays from 2nd vaccine dose to presentationPeak troponin-I (pg/mL)CRP (mg/L)Viral serologiesaECG abnormalitiesTTE findings
123FModerna516,26341NegativeDown-sloping PR depressions, diffuse ST elevationsLVEF 55–60%, basal inferior and basal inferolateral hypokinesis
220MModerna2>27,00088NegativeDown-sloping PR depressions, diffuse ST elevationsLVEF 45%, apical septal hypokinesis
329MModerna4680214Down-sloping PR depressions, diffuse ST elevationsLVEF 55%, no regional wall motion abnormalities
430MPfizer42518129NegativeT-wave inversions in lateral leadsLVEF 65–70%, no regional wall motion abnormalities

CRP: C-reactive protein.

ECG: electrocardiogram.

TTE: transthoracic echocardiogram.

LVEF: left ventricular ejection fraction.a

Coxsackie virus, EBV, CMV.

Fig. 2
Fig. 3
Fig. 4

3. Case 2

A 20-year-old man presented with a 2-day history of progressive chest pain, 2 days after receiving his second dose of the Moderna vaccine. His symptoms started with a viral prodrome approximately ten days prior to the onset of his chest pain. His ECG had down-sloping PR depressions and diffuse ST elevations; his troponin-I was 22,638 and CRP was markedly elevated (Table 1). Troponin-I peaked the following day. Viral serologies for HIV, hepatitis B and C viruses, coxsackie virus type b, and EBV were all undetectable. TTE revealed a LVEF of 45% with moderate hypokinesis of the apex and apical septum. Outpatient CMR remains pending. His chest pain resolved the following day. He was discharged on hospital day 3. He presented to clinic eleven days after discharge, where he his troponin had normalized to 0.03 ng/dL, and his CRP to 2.5 mg/L.

4. Case 3

A 29-year-old man presented with chest pain 4 days after receiving his second dose of the Moderna vaccine. His ECG had diffuse ST elevations with no PR depressions; initial troponin-I was 3785 pg/mL and CRP was notably elevated (Table 1). Troponin-I peaked the next day. TTE revealed and EF of 55% with no regional wall motion abnormalities. He did not undergo CMR or viral serology testing. An autoimmune workup showed an anti-nuclear antibody titer of 1:80 in a speckled pattern and negative double stranded DNA, rheumatoid factor, ribonucleic protein IgG, scleroderma-70, anti–Sjögren’s-syndrome-related antigen A, and anti-Smith autoantibodies were negative. His chest pain resolved on the first day of his hospitalization, and he was discharged the following day.

5. Case 4

A 30-year-old man presented on with chest pain 4 days after receiving his second dose of the Pfizer vaccine. ECG was notable only for T-wave inversions in the lateral leads that resolved on follow-up ECG. Troponin-I was 2447 pg/mL and CRP was notably elevated (Table 1). Troponin-I peaked the next day. EBV, CMV, and coxsackie serologies were all negative. CMR was not performed. TTE was unremarkable with normal LVEF and no regional wall motion abnormalities. His symptoms resolved on first day of hospitalization, and he was discharged on hospital day 3.

6. Discussion

This is among the first series to report multiple cases of myocarditis in adults following vaccination against SARS-CoV-2. All four patients were young, between 20 and 30. All presented with chest pain two to five days after their second vaccine dose. All had significantly elevated troponin-I levels. Though one had a viral prodrome, all had negative serologies. None reported prior COVID-19 infection. None had stigmata of autoimmune disease, and the one who underwent a rheumatologic workup while hospitalized had unremarkable autoimmune serologies. Reassuringly, the two patients who have returned for follow up in the weeks following discharge had normalized CRP values and denied symptom recurrence.

Myocarditis is most often caused by direct viral injury or by autoimmune mechanisms but has been sporadically linked to vaccination. Over 50 cases had been reported to the Department of Defense Smallpox Vaccination Program [3]. Myopericarditis has also been reported soon after vaccines against anthrax, haemophilus influenzae type b, hepatitis B virus, inactivated influenza, and live attenuated zoster vaccines [4].

Neither clinical trial reported adverse cardiac events including myocarditis [1][2]. As vaccination rates increase among younger patients, however, several cases of post-vaccine myocarditis are being reported in adolescents and young adults [5][6][7]. In addition to these anecdotes, a multinational cohort study analyzed electronic health record databases and found the incidence of myocarditis and pericarditis among vaccine recipients aged 18 to 35 to be approximately 0.016% for women and 0.037% for men [8]. The CDC has since warned clinicians to be wary of post-vaccine myocarditis in teens and young adults [9]. It remains unclear why younger patients are more prone to develop this adverse effect. A possible explanation could be related to the stronger immune response in younger patients, which can also explain the higher prevalence of side effects to the vaccines in this patient population [10].

While certainly a pattern worth exploring, this case series has numerous limitations, including a small sample size, variation in workup and treatment strategies, and retrospective analysis insufficient to establish causality. Nevertheless, the odds of incidental seronegative viral myocarditis occurring in four patients presenting to a single medical center within days of vaccine administration would be long. The authors would encourage further investigation and reporting of potential cases of post-vaccine myocarditis. The authors seek not to frustrate vaccination efforts, but rather to prepare patients and providers for a rare but potential adverse effect. Furthermore, the authors hope the dramatic improvement in all four patients will reassure those who do suffer from myocarditis following vaccination.

Declaration of competing interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.


The authors would like to recognize Drs. R David Anderson, MD and Joshua Latner, MD who diagnosed and treated the first case.


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