Is there evidence linking COVID-19 vaccines to cardiovascular fatalities?

Answer from top 10 papers

The question of whether COVID-19 vaccines cause cardiovascular fatalities is addressed with varying perspectives across the literature. While there is no direct claim in the provided papers that COVID-19 vaccines cause cardiovascular fatalities, there are discussions of cardiovascular complications associated with both COVID-19 infection and vaccination. Beavis et al. (2022) outlines the potential mechanisms of myocardial damage in COVID-19 patients, emphasizing the importance of understanding cardiovascular damage to reduce mortality rates (Beavis et al., 2022). Sakai et al. (2022) and Zhao et al. (2020) also discuss the cardiovascular complications related to COVID-19, noting that patients with pre-existing cardiovascular diseases (CVDs) have an increased risk of severe outcomes (Sakai et al., 2022; Zhao et al., 2020).
Interestingly, Sakai et al. (2022) and Hussain et al. (2023) mention adverse events following vaccination, including cardiovascular issues, but these are not explicitly linked to fatalities (Hussain et al., 2023; Sakai et al., 2022). Hussain et al. (2023) suggests that vaccination may reduce the severity of SARS-CoV-2 infection in vulnerable patients with cardiovascular comorbidities (Hussain et al., 2023). Additionally, Kumar (2020) presents a case of subacute thyroiditis following vaccination, which is an inflammatory condition but not a direct cardiovascular event or fatality (Kumar, 2020).
In summary, while cardiovascular complications are a concern in the context of COVID-19, the reviewed papers do not provide evidence that directly links COVID-19 vaccines to cardiovascular fatalities. Instead, they highlight the importance of monitoring for cardiovascular issues in patients with COVID-19 and suggest that vaccination may offer protective benefits, particularly in vulnerable populations with pre-existing conditions (Beavis et al., 2022; Hussain et al., 2023; Sakai et al., 2022; Zhao et al., 2020). It is crucial to differentiate between cardiovascular complications and fatalities, and the papers reviewed do not establish a causal relationship between COVID-19 vaccines and cardiovascular fatalities.

Source Papers

Coronavirus disease 2019 and cardiovascular disease.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus behind the coronavirus disease 2019 (COVID-19) pandemic, is a type of RNA virus that is nonsegmented. Cardiovascular diseases (CVDs) increase the mortality risk of patients. In this review article, we overview the existing evidence regarding the potential mechanisms of myocardial damage in coronavirus disease 2019 (COVID-19) patients. Having a comprehensive knowledge of the cardiovascular damage caused by SARS-CoV-2 and its underlying mechanisms is essential for providing prompt and efficient treatment, ultimately leading to a reduction in mortality rates. Severe COVID-19 causes acute respiratory distress syndrome and shock in patients. In addition, awareness regarding COVID-19 cardiovascular manifestations has increased, including the adverse impact on prognosis with cardiovascular involvement. Angiotensin-converting enzyme 2 receptor may play a role in acute myocardial injury caused by SARS-CoV-2 infection. COVID-19 patients experiencing heart failure may have their condition exacerbated by various contributing factors and mechanisms. Increased oxygen demand, myocarditis, stress cardiomyopathy, elevated pulmonary pressures, and venous thrombosis are potential health issues. The combination of these factors may lead to COVID-19-related cardiogenic shock, resulting in acute systolic heart failure. Extracorporeal membrane oxygenation (ECMO) and left ventricular assist devices (LVADs) are treatment options when inotropic support fails for effective circulatory support. To ensure effective COVID-19-related cardiovascular disease (CVD) surveillance, it is crucial to closely monitor the future host adaptation, viral evolution, and transmissibility of SARS-CoV-2, given the virus's pandemic potential.

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Open Access
SARS-CoV-2 vaccine-related cutaneous manifestations: a systematic review.

To date, over 250 million people have been reportedly infected by COVID‐19 disease, which has spread across the globe and led to approximately 5.1 million fatalities. To prevent both COVID‐19 and viral transmission, DNA‐based/RNA‐based vaccines, non‐replicating viral vector vaccines, and inactivated vaccines have been recently developed. However, a precise clinical and histological characterization of SARS‐CoV‐2 vaccine‐related dermatological manifestations is still lacking. A systematic review of 229 articles was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta‐Analyses (PRISMA) guidelines, in order to provide an extensive overview of SARS‐CoV‐2 vaccine‐related skin manifestations. Data on demographics, number of reported cases with cutaneous involvement, vaccine, and rash type (morphology) were extracted from articles and summarized. A total of 5941 SARS‐CoV‐2 vaccine‐related dermatological manifestations were gathered. Local injection‐site reactions were the most frequently observed, followed by rash/unspecified cutaneous eruption, urticarial rashes, angioedema, herpes zoster, morbilliform/maculopapular/erythematous macular eruption, pityriasis rosea and pityriasis rosea‐like eruptions, and other less common dermatological manifestations. Flares of pre‐existing dermatological conditions were also reported. Cutaneous adverse reactions following SARS‐CoV‐2 vaccine administration seem to be heterogeneous, rather infrequent, and not life‐threatening. Vaccinated patients should be monitored for skin manifestations, and dermatological evaluation should be offered, when needed.

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Open Access
Efficacy of Parainfluenza Virus 5 (PIV5)-vectored Intranasal COVID-19 Vaccine as a Single Dose Vaccine and as a Booster against SARS-CoV-2 Variants.

Immunization with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccines has greatly reduced coronavirus disease 2019 (COVID-19)-related deaths and hospitalizations, but waning immunity and the emergence of variants capable of immune escape indicate the need for novel SARS-CoV-2 vaccines. An intranasal parainfluenza virus 5 (PIV5)-vectored COVID-19 vaccine CVXGA1 has been proven efficacious in animal models and blocks contact transmission of SARS-CoV-2 in ferrets. CVXGA1 vaccine is currently in human clinical trials in the United States. This work investigates the immunogenicity and efficacy of CVXGA1 and other PIV5-vectored vaccines expressing additional antigen SARS-CoV-2 nucleoprotein (N) or SARS-CoV-2 variant spike (S) proteins of beta, delta, gamma, and omicron variants against homologous and heterologous challenges in hamsters. A single intranasal dose of CVXGA1 induces neutralizing antibodies against SARS-CoV-2 WA1 (ancestral), delta variant, and omicron variant and protects against both homologous and heterologous virus challenges. Compared to mRNA COVID-19 vaccine, neutralizing antibody titers induced by CVXGA1 were well-maintained over time. When administered as a boost following two doses of a mRNA COVID-19 vaccine, PIV5-vectored vaccines expressing the S protein from WA1 (CVXGA1), delta, or omicron variants generate higher levels of cross-reactive neutralizing antibodies compared to three doses of a mRNA vaccine. In addition to the S protein, the N protein provides added protection as assessed by the highest body weight gain post-challenge infection. Our data indicates that PIV5-vectored COVID-19 vaccines, such as CVXGA1, can serve as booster vaccines against emerging variants.

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Open Access
ODP516 Subacute Thyroiditis due to SARS-CoV-2 Vaccine

Abstract Background Coronavirus disease 2019 (COVID-19) is a disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that resulted in a pandemic in 2019, causing systemic complications including endocrine system diseases. Subacute thyroiditis (SAT) of COVID-19 infection is believed to be due to direct virus entry into cells and cell destruction, cellular dysfunction due to inflammation and immune/antibody-mediated hormonal dysfunction. Here we present a case of SAT after the SARS-CoV-2 vaccine (Pfizer-BioNTech). Clinical Case A 39-year-old male healthcare worker presented with four weeks history of symptoms: fullness of the anterior neck, odynophagia, enlarged cervical lymph nodes, palpitations, anxiety and weight loss. Onset of symptoms was two days the second dose of Pfizer-BioNTech vaccine. There was no recent history of upper respiratory system infection or COVID-19 infection. Vital signs and physical exam findings were unavailable, as it was a telephone encounter. Initial workup was significant for a TSH of 0. 020 uIU/mL (n 0.45-5.330 uIU/mL), free T4 of 2.42 ng/mL (n 0.45-1.80 ng/mL) and total T3 225.4 pg/mL (n 87-179 pg/mL). There was no evidence of leukocytosis. Ultrasound of the thyroid gland was unremarkable for nodules or hyperemia. Autoimmune thyroid disease was ruled out with negative levels of thyroid stimulating immunoglobulin, thyroid receptor antibody and anti-microsomal antibody. Thyroid scintigraphy was significant for abnormally low uptake, consistent with SAT. Clinical and biochemical improvements (TSH 4.193 uIU/mL; free T4 0.98 ng/dL) were seen after 5 months. Conclusion Subacute thyroiditis (SAT) is an acute inflammatory disorder of the thyroid usually related to a viral infection. It was described in total of 27 patients of COVID-19 infection (3) . There are only a handful of cases related to COVID-19 vaccine and most of them are due to the inactivated vaccine (1,2) . To our knowledge, there are only three documented cases of subacute thyroiditis after receiving the Pfizer mRNA vaccine (1) . The pathophysiology in generating an autoimmune response is believed to be due to molecular mimicry and cross recognition between the coronavirus spike protein targeted with the mRNA vaccine and healthy thyroid cell antigens (1,2) . Clinicians should be alert and consider the possibility of SARS-CoV-2 vaccine as an etiology when evaluating patients for subacute thyroiditis.

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Open Access
Complications of SARS-CoV-2 Infection During Cardiac Rehabilitation: A Case Series.

Vaccination strongly reduces the risk of hospitalization and death due to coronavirus disease 2019 (COVID-19). However, the severity of the acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection and the degree of protection exerted over time by vaccination remains to be fully elucidated among hospitalized comorbid and vulnerable patients with SARS-CoV-2 infection. We report a case series of nine hospitalized vulnerable patients who developed a SARS-CoV-2 infection during a cardiac rehabilitation inpatient program. Age ranged from 50 to 81years. All but one patient had received at least three doses of anti-COVID-19 vaccine more than 4months before the cardiac event. Indications for cardiac rehabilitation included acute coronary syndromes, congestive heart failure, heart valve surgery, and coronary artery bypass graft. After the confirmed diagnosis of SARS-CoV-2 infection, all patients developed symptoms. Eight patients developed at least one SARS-CoV-2-related complication, including a significant increase in high-sensitivity troponin I levels, new-onset hypoxemia, persistent atrial fibrillation, non-sustained ventricular tachycardia and recurrent sinus arrest, pericardial effusion, and a persistent increase in blood pressure. Almost all patients developed complications which, however, did not evolve towards more severe expressions of the disease. These data suggest that even in this new phase of the pandemic, vaccination may exert a potential role to reduce the risk of progression towards more severe disease of SARS-CoV-2 infection in vulnerable patients with cardiovascular comorbidities.

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Open Access
Neutralizing antibodies and T-cell responses to inactivated SARS-CoV-2 vaccine in COVID-19 convalescents one and a half years after infection

Vaccines have been considered the most promising solution for ending the coronavirus disease 2019 (COVID-19) pandemic. Information regarding neutralizing antibodies (NAbs) and T-cell immune response in inactivated SARS-CoV-2 vaccine-immunized COVID-19 convalescent patients were either only available for a short time after illness recovered or not available at all (T-cell immunity). We evaluated SARS-CoV-2 NAbs and cellular immune responses to the SARS-CoV-2 inactivated vaccine in convalescent patients who recovered from infection for about one and a half years. We found that compared to before vaccination, SARS-CoV-2 NAbs and specific T-cell responses were significantly boosted by the inactivated vaccine in convalescent patients, which confirmed the pre-existing adaptive immunity in SARS-CoV-2 infected people. We observed that NAbs and IFN-γ-secreting T-cell response elicited by a single vaccine dose in subjects with prior COVID-19 infection were higher than after two doses of vaccine in SARS-CoV-2 naïve subjects. Both humoral and cellular immune responses elicited by one and two doses of inactivated vaccine were comparable in COVID-19-recovered persons. In conclusion, inactivated COVID-19 vaccine induced robust NAbs and T-cell responses to SARS-CoV-2 in COVID-19 convalescent patients and immune responses after one dose were equal to that after receiving two doses, which highlighted that robust humoral and cellular immune response can be reactivated by the inactivated vaccine in SARS-CoV-2 convalescent patients.

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Open Access