Heart failure (HF) is a growing public health concern, with an increasing incidence among younger populations. Traditionally, HF was considered a condition primarily affecting the elderly, but of late, emerging evidence hints at a rapidly rising HF incidence in youth in the past 2 decades. HF in youth has been linked to a complex interaction between emerging risk factors, such as metabolic syndrome, environmental exposures, genetic predispositions, and lifestyle behaviors. This review examines these evolving determinants, including substance abuse, autoimmune diseases, and the long-term cardiovascular effects of coronavirus disease 2019, which disproportionately affect younger individuals. Through a comprehensive analysis, the study highlights the importance of early detection, targeted prevention strategies, and multidisciplinary management approaches to address this alarming trend. Promoting awareness and integrating age-specific interventions could significantly reduce the burden of HF and improve long-term outcomes among younger populations.

Many patients diagnosed with COVID-19 have persistent cardiovascular symptoms, but whether this represents a true cardiac process is unclear. This study assessed whether symptoms associated with long COVID among patients referred for cardiovascular evaluation are associated with objective abnormalities on cardiac testing to explain their clinical presentation.

A retrospective cohort study of 40,462 unique patients diagnosed with COVID-19 at our tertiary referral was conducted and identified 363 patients with persistent cardiovascular symptoms a minimum of 4 weeks after polymerase chain reaction confirmed COVID-19 infection. Patients had no cardiovascular symptoms prior to COVID-19 infection. Each patient was referred for cardiovascular evaluation at a tertiary referral center. The incidence and etiology of abnormalities on cardiovascular testing among patients with long COVID symptoms are reported here. The cohort was subsequently divided into 3 categories based on the dominant circulating severe acute respiratory syndrome coronavirus 2 variant at the time of initial infection for further analysis.

Among 40,462 unique patients diagnosed with COVID-19 at our tertiary referral center from April 2020 to March 2022, 363 (0.9%) patients with long COVID were evaluated by Cardiology for possible cardiac sequelae from COVID and formed the main study cohort. Of these, 229 (63%) were vaccinated and 47 (12.9%) had severe initial infection, receiving inpatient treatment for COVID prior to developing long COVID symptoms. Symptoms were associated with a cardiac cause in 85 (23.4%), of which 52 (14.3%) were attributed to COVID; 39 (10.7%) with new cardiac disease from COVID, and 13 (3.6%) to worsening of pre-existing cardiac disease after COVID infection. The median troponin change in 45 patients with troponin measurements within 4 weeks of acute infection was +4 ng/dL (9 to 13 ng/dL). Among the total cohort with long COVID, 83.7% were diagnosed during the pre-Delta phase, 13.2% during the Delta phase, and 3.1% during the Omicron phase of the pandemic. There were 6 cases of myocarditis, 11 rhythm disorders, 8 cases of pericarditis, 5 suspected cases of endothelial dysfunction, and 33 cases of autonomic dysfunction.

This pragmatic retrospective cohort study suggests that patients with long COVID referred for cardiovascular evaluation infrequently have new, objective cardiovascular disease to explain their clinical presentation. A multidisciplinary, patient-centered approach is warranted for symptom management along with conservative use of diagnostic testing.

The purpose of this systematic review is to evaluate the original peer-reviewed studies on athletes who developed myocarditis after coronavirus disease (COVID-19) infection or after COVID-19 mRNA vaccination. Both entities likely have an immunologic component. We discuss elite, professional, college, and adolescent athletes. The athletes are generally young and healthy, representing a distinctive population group that differs from the general population. This review includes diagnosis of myocarditis, incidence, complications, prognosis, and return-to-play guidance for sports medicine clinicians and coaches.

We surveyed the PUBMED, Embase, and Web of Science databases for the relevant peer-reviewed articles in the English language published from the onset of the pandemic until April 2023. Included were original observational studies and case series. Excluded were individual case reports and a small series with incomplete data. The resulting search yielded 30 original articles.

Reported myocardial abnormalities in athletes were rare after COVID-19 infection and even less frequent after COVID-19 mRNA vaccination. True incidence, however, may be higher because of under-reporting and frequent asymptomatic presentation. Male gender was prevalent for both manifestations; postvaccination myocarditis occurrence was the highest after the second vaccine dose. Diagnostic and return-to-play algorithms were developed and should be adopted and followed.

The risk of myocarditis from COVID-19 infection and COVID-19 mRNA vaccination is very low. The long-term prognosis and evolution of the observed cardiac magnetic resonance abnormalities are currently unknown. Although inferences can be made from the published data, COVID-19 and postvaccine myocarditis in athletes may represent only a small fraction of the true incidence of those who have been affected worldwide and not evaluated.

Background: Myocarditis is a serious disease that has drawn increasing attention due to its association with COVID-19 and vaccination. This study investigates the epidemiology of myocarditis beyond the COVID-19 pandemic, including its incidence and outcomes over time. Methods: We analyzed the population-wide retrospective data from the Admitted-Patient-Data-Collection database of patients admitted to hospitals in New South Wales (NSW), Australia, with a diagnosis of myocarditis from 2001 to 2022. The incidence of myocarditis, changing classification of myocarditis over time, and complications of myocarditis over time were all calculated. Results: There were 4071 patients diagnosed with their first episode of myocarditis, with a median age of 42 years old, and 66% were male. The incidence of myocarditis in NSW has tripled over 20-years to 8.3 per-100,000-persons by 2022. Reactive myocarditis (i.e., myocarditis within 30-days of a respiratory or digestive illness) accounted for 38% of first presentations of myocarditis. Post COVID-19 myocarditis, a subset of reactive myocarditis, accounted for 42% of myocarditis admissions since the onset of the COVID-19 pandemic in Australia. Eight percent of patients had a background history of malignancy, and 6% had a history of autoimmune disease. In-hospital mortality was 4.5% during the entire study period but has been falling by 11% per year. During follow up, most readmissions for myocarditis occurred within 6-months; with 5.1% recurrence at 6-months compared to only 6.7% at 5-years. Conclusions: Myocarditis is an important condition with increasing incidence in Australia and with markedly changing characteristics in the pandemic and post pandemic era.

COVID-19 is a new infectious disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS CoV-2). Since the outbreak in December 2019, it has caused an unprecedented world pandemic, leading to a global human health crisis. Although SARS CoV-2 mainly affects the lungs, causing interstitial pneumonia and severe acute respiratory distress syndrome, a number of patients often have extensive clinical manifestations, such as gastrointestinal symptoms, cardiovascular damage and renal dysfunction.

This review article discusses the pathogenic mechanisms of cardiovascular damage in COVID-19 patients and provides some useful suggestions for future clinical diagnosis, treatment and prevention.

An English-language literature search was conducted in PubMed and Web of Science databases up to 12th April, 2024 for the terms "COVID-19", "SARS CoV-2", "cardiovascular damage", "myocardial injury", "myocarditis", "hypertension", "arrhythmia", "heart failure" and "coronary heart disease", especially update articles in 2023 and 2024. Salient medical literatures regarding the cardiovascular damage of COVID-19 were selected, extracted and synthesized.

The most common cardiovascular damage was myocarditis and pericarditis, hypertension, arrhythmia, myocardial injury and heart failure, coronary heart disease, stress cardiomyopathy, ischemic stroke, blood coagulation abnormalities, and dyslipidemia. Two important pathogenic mechanisms of the cardiovascular damage may be direct viral cytotoxicity as well as indirect hyperimmune responses of the body to SARS CoV-2 infection.

Cardiovascular damage in COVID-19 patients is common and portends a worse prognosis. Although the underlying pathophysiological mechanisms of cardiovascular damage related to COVID-19 are not completely clear, two important pathogenic mechanisms of cardiovascular damage may be the direct damage of the SARSCoV-2 infection and the indirect hyperimmune responses.

In this study, we aimed to identify the causes, predictors and gender disparities of 30-day and 90-day cardiovascular readmissions after COVID-19-related hospitalisations using National Readmission Database (NRD) 2020.

We used the NRD from 2020 to identify hospitalised adults with a principal diagnosis of COVID-19 infection.

We included subjects who were readmitted within 30 days and 90 days after index admission. We excluded subjects with elective and traumatic admissions. We used a multivariate Cox regression model to identify independent predictors of readmission.

Our outcomes were inpatient mortality, 30-day and 90-day cardiovascular readmission rates following COVID-19 infection.

During the study period, there were 1 024 492 index hospitalisations with a primary diagnosis of COVID-19 infection in the 2020 NRD database, 644 903 (62.9%) were included for 30-day readmission analysis, and 418 122 (40.8%) were included for 90-day readmission analysis. Of patients involved in the 30-day analysis, 7140 (1.1%) patients had a readmission within 30 days; of patients involved in the 90-day analysis, 8379 (2.0%) had a readmission within 90 days due to primarily cardiovascular causes. Cox regression analysis revealed that the female sex (aHR 0.89; 95% CI 0.82 to 0.95; p=0.001) was associated with a lower hazard of 30-day cardiovascular readmissions; however, congestive heart failure (aHR 2.45; 95% CI 2.2 to 2.72; p<0.001), arrhythmias (aHR 2.45; 95% CI 2.2 to 2.72; p<0.001) and valvular disease (aHR 2.45; 95% CI 2.2 to 2.72; p<0.001) had a higher hazard. The most common causes of cardiovascular readmissions were heart failure (34.3%), deep vein thrombosis/pulmonary embolism (22.5%) and atrial fibrillation (9.5%).

Our study demonstrates that male gender, heart failure, arrhythmias and valvular disease carry higher hazards of 30-day and 90-day cardiovascular readmissions. Identifying risk factors and common causes of readmission may assist with lowering the burden of cardiovascular disease in patients with COVID-19 infection.

Data regarding the risk of incident pericarditis in coronavirus disease 2019 (COVID-19) recovered patients are lacking. We determined the risk of incident pericarditis after COVID-19 infection by performing a systematic review and meta-analysis of available data.

Following the PRISMA guidelines, we searched MEDLINE and Scopus to locate all articles published up to 11 February 2023 reporting the risk of incident pericarditis in patients who had recovered from COVID-19 infection compared to noninfected patients (controls) defined as those who did not experience the disease over the same follow-up period. Pericarditis risk was evaluated using the Mantel-Haenszel random effects models with hazard ratio (HR) as the effect measure with 95% confidence interval (CI) while heterogeneity was assessed using Higgins I2 statistic.

Overall, 16 412 495 patients (mean age 55.1 years, 76.8% males), of whom 1 225 715 had COVID-19 infection, were included. Over a mean follow-up of 9.6 months, pericarditis occurred in 3.40 (95% CI: 3.39-3.41) out of 1000 patients who survived COVID-19 infection compared with 0.82 (95% CI: 0.80-0.83) out of 1000 control patients. Recovered COVID-19 patients presented a higher risk of incident pericarditis (HR: 1.95, 95% CI: 1.56-2.43, I2 : 71.1%) compared with controls. Meta-regression analysis showed a significant direct relationship for the risk of incident pericarditis using HT ( P  = 0.02) and male sex ( P  = 0.02) as moderators, while an indirect association was observed when age ( P  = 0.01) and the follow-up length ( P  = 0.02) were adopted as moderating variables.

Recovered COVID-19 patients have a higher risk of pericarditis compared with patients from the general population.

Cardiovascular disorders are significantly associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Herein, we describe a case of myopericarditis and subsequent transient constrictive pericarditis after coronavirus disease 2019 (COVID-19). Three weeks following a mild SARS-CoV-2 illness, a 53-year-old woman was referred to the hospital with acute pleuritic chest pain, which was not attributable to any known cause and was only temporarily relieved. The pain persisted for the next few weeks until her second COVID-19 infection, which occurred 5 months after her first affliction. This time, Transthoracic echocardiography (TTE) revealed mild pericardial effusion, and cardiac magnetic resonance imaging (CMR) confirmed myopericarditis, leading to the administration of anti-inflammatory therapy for the patient. Despite a relative resolution of symptoms, her second CMR performed 8 months later revealed active perimyocarditis with transient constrictive pericarditis (CP). Additionally, fluorescent antinuclear antibody (FANA) and antimitochondrial Ab M2 (AMA) were tested positive for the first time. Thereafter, the patient was started on concurrent anti-inflammatory and immunosuppressant therapies, which were effective after 3 months. The transient CP was resolved, and there was no sign of active pericarditis on her last echocardiography. Acute pericarditis and its subsequent constrictive pericarditis are infrequent adverse outcomes of COVID-19. The unique feature of this case is the uncertainty regarding the underlying reason for cardiac complications, whether it is the first presentation of systemic lupus erythematosus (SLE) or viral-induced myopericarditis followed by a consequent transient CP.

Concerns remain regarding the rare cardiovascular adverse events, myocarditis and pericarditis (myo/pericarditis), particularly in younger individuals following mRNA COVID-19 vaccination. Our study aimed to comprehensively assess potential safety signals related to these cardiac events following the primary and booster doses, with a specific focus on younger populations, including children as young as 6 months of age. Using the Vaccine Adverse Events Reporting System (VAERS), the United States national passive surveillance system, we conducted a retrospective pharmacovigilance study analyzing spontaneous reports of myo/pericarditis. We employed both frequentist and Bayesian methods and conducted subgroup analyses by age, sex, and vaccine dose. We observed a higher reporting rate of myo/pericarditis following the primary vaccine series, particularly in males and mainly after the second dose. However, booster doses demonstrated a lower number of reported cases, with no significant signals detected after the fourth or fifth doses. In children and young adults, we observed notable age and sex differences in the reporting of myo/pericarditis cases. Males in the 12-17 and 18-24-year-old age groups had the highest number of cases, with significant signals for both males and females after the second dose. We also identified an increased reporting for a spectrum of cardiovascular symptoms such as chest pain and dyspnea, which increased with age, and were reported more frequently than myo/pericarditis. The present study identified signals of myo/pericarditis and related cardiovascular symptoms after mRNA COVID-19 vaccination, especially among children and adolescents. These findings underline the importance for continued vaccine surveillance and the need for further studies to confirm these results and to determine their clinical implications in public health decision-making, especially for younger populations.

There is a strong coordinated effort by vaccination groups all over the world to put an end to the current crisis of COVID-19. Now sufficient data are available to analyse and compare some results to explore the aftereffects of vaccination. Some influence variables on transmissions of the disease were discussed e.g., mass vaccination, lockdown and seasonality. Most studies covered here are up to the beginning of July 2022, while some analyses focused on the earlier period of mass vaccination. Well established, simple statistical techniques to evaluate results were presented those used open data sources of authoritative bodies. Some comparisons between vaccinated vs. unvaccinated were also discussed based on data from UK Government Health Security Agency (UHSA). In terms of mass vaccination, adverse reactions after vaccination received attention, as health and safety issues of the general public are of prime importance. Apart from direct side effects, the secondary effect of mass vaccination needs attention too. After the initiation of the vaccination programme, almost all countries experienced a sudden surge in transmission and most countries had to impose strict lockdown measures. Many countries, with a low prevalence of disease, suddenly showed a steep jump and some countries even followed a synchronized pattern between the rate of transmissions and the variation of vaccine doses. Time series analyses and bar diagram presentations were able to capture those features. In that context, fast mutation of the virus and new variants after mass vaccination and possible mechanisms/consequences were also attended. To understand the effect of seasonality, similarities between COVID-19 and the seasonal Flu are discussed for Europe and US to gain useful insight. Using time series analyses and spatial plots of regional temperature composites we showed, like Flu, seasonality played a dominant role in transmissions of COVID-19 in the Europe. Regulations of vaccine dose and policy implication were explored too. From 22^nd December 2021, global vaccine doses were reduced substantially, which followed a dramatic reduction in cases and thereafter deaths with around one month's lag between each. As strong dependency on seasonality is noticed in certain countries and observing that regulation of vaccine doses has roles in modulating the transmission with certain lags, globally as well as regionally, our results have policy implications for the management of COVID. Debating, questioning and criticism are always the foundation of great science and the major pillars of its progress. Following that objective, it is an effort to explore pragmatically, supported by scientific analyses, areas relating to the effectiveness of the COVID-19 vaccine and the exit strategy via the pathway of vaccination.

COVID-19 has become the first modern-day pandemic of historic proportion, affecting >600 million individuals worldwide and causing >6.5 million deaths. While acute infection has had devastating consequences, postacute sequelae of SARS-CoV-2 infection appears to be a pandemic of its own, impacting up to one-third of survivors and often causing symptoms suggestive of cardiovascular phenomena. This review will highlight the suspected pathophysiology of postacute sequelae of SARS-CoV-2, its influence on the cardiovascular system, and potential treatment strategies.

While coronavirus disease 2019 (COVID-19) infection rates have declined, and mortality outcomes have improved with vaccines, targeted antiviral therapies, and improved care practices over the course of the pandemic, post-acute sequelae of SARS CoV-2 infection (PASC, also referred to as "long COVID") has emerged as a significant concern, even among individuals who appear to have fully recovered from their initial infection. Acute COVID-19 infection is associated with myocarditis and cardiomyopathies, but the prevalence and presentation of post-infectious myocarditis are unclear. We provide a narrative review of post-COVID myocarditis, including symptoms and signs, physical exam findings, diagnosis, and treatment strategies. Post-COVID myocarditis has a wide range of presentations, from very mild symptoms to severe ones that can include sudden cardiac death. Several studies have noted what appears to be a bimodal distribution of affected patients, with individuals under age 16 (particularly males) most affected, followed by those over age 50. The gold standard of diagnosis for myocarditis is endomyocardial biopsy and cardiac magnetic resonance imaging with a confirmed diagnosis of COVID-19. However, if these are not available, other studies such as electrocardiogram, echocardiography, and inflammatory markers can guide clinicians to diagnose post-COVID myocarditis when appropriate. Treatment is largely supportive and may include oxygen therapy, intravenous hydration, diuretics, steroids, and antivirals. Post-COVID myocarditis is rare but important to recognize as more patients present with this condition in the inpatient setting.

Each injection of any known vaccine results in a strong expression of pro-inflammatory cytokines. This is the result of the innate immune system activation, without which no adaptive response to the injection of vaccines is possible. Unfortunately, the degree of inflammation produced by COVID-19 mRNA vaccines is variable, probably depending on genetic background and previous immune experiences, which through epigenetic modifications could have made the innate immune system of each individual tolerant or reactive to subsequent immune stimulations.We hypothesize that we can move from a limited pro-inflammatory condition to conditions of increasing expression of pro-inflammatory cytokines that can culminate in multisystem hyperinflammatory syndromes following COVID-19 mRNA vaccines (MIS-V). We have graphically represented this idea in a hypothetical inflammatory pyramid (IP) and we have correlated the time factor to the degree of inflammation produced after the injection of vaccines. Furthermore, we have placed the clinical manifestations within this hypothetical IP, correlating them to the degree of inflammation produced. Surprisingly, excluding the possible presence of an early MIS-V, the time factor and the complexity of clinical manifestations are correlated to the increasing degree of inflammation: symptoms, heart disease and syndromes (MIS-V).

The long COVID-19 syndrome has been recently described and some reports have suggested that acute pericarditis represents important manifestation of long COVID-19 syndrome. The aim of this study was to identify the prevalence and clinical characteristics of patients with long COVID-19, presenting with acute pericarditis.

We retrospectively included 180 patients (median age 47 years, 62% female) previously diagnosed with COVID-19, exhibiting persistence or new-onset symptoms ≥12 weeks from a negative naso-pharyngeal SARS CoV2 swamp test. The original diagnosis of COVID-19 infection was determined by a positive swab. All patients had undergone a thorough physical examination. Patients with suspected heart involvement were referred to a complete cardiovascular evaluation. Echocardiography was performed based on clinical need and diagnosis of acute pericarditis was achieved according to current guidelines.

Among the study population, shortness of breath/fatigue was reported in 52%, chest pain/discomfort in 34% and heart palpitations/arrhythmias in 37%. Diagnosis of acute pericarditis was made in 39 patients (22%). Mild-to-moderate pericardial effusion was reported in 12, while thickened and bright pericardial layers with small effusions (< 5 mm) with or without comet tails arising from the pericardium (pericardial B-lines) in 27. Heart palpitations/arrhythmias (OR:3.748, p = 0.0030), and autoimmune disease and allergic disorders (OR:4.147, p = 0.0073) were independently related to the diagnosis of acute pericarditis, with a borderline contribution of less likelihood of hospitalization during COVID-19 (OR: 0.100, p = 0.0512).

Our findings suggest a high prevalence of acute pericarditis in patients with long COVID-19 syndrome. Autoimmune and allergic disorders, and palpitations/arrhythmias were frequently associated with pericardial disease.

Myocarditis, diagnosed by symptoms and troponin elevation, has been well-described with COVID-19 infection, as well as shortly after COVID-19 vaccination. The literature has characterized the outcomes of myocarditis following COVID-19 infection and vaccination, but clinicopathologic, hemodynamic, and pathologic features following fulminant myocarditis have not been well-characterized. We aimed to compare clinical and pathological features of fulminant myocarditis requiring hemodynamic support with vasopressors/inotropes and mechanical circulatory support (MCS), in these two conditions.

We analyzed the literature on fulminant myocarditis and cardiogenic shock associated with COVID-19 and COVID-19 vaccination and systematically reviewed all cases and case series where individual patient data were presented. We searched PubMed, EMBASE, and Google Scholar for "COVID", "COVID-19", and "coronavirus" in combination with "vaccine", "fulminant myocarditis", "acute heart failure", and "cardiogenic shock". The Student's t-test was used for continuous variables and the χ2 statistic was used for categorical variables. For non-normal data distributions, the Wilcoxon Rank Sum Test was used for statistical comparisons.

We identified 73 cases and 27 cases of fulminant myocarditis associated with COVID-19 infection (COVID-19 FM) and COVID-19 vaccination (COVID-19 vaccine FM), respectively. Fever, shortness of breath, and chest pain were common presentations, but shortness of breath and pulmonary infiltrates were more often present in COVID-19 FM. Tachycardia, hypotension, leukocytosis, and lactic acidosis were seen in both cohorts, but patients with COVID-19 FM were more tachycardic and hypotensive. Histologically, lymphocytic myocarditis dominated both subsets, with some cases of eosinophilic myocarditis in both cohorts. Cellular necrosis was seen in 44.0% and 47.8% of COVID-19 FM and COVID-19 vaccine FM, respectively. Vasopressors and inotropes were used in 69.9% of COVID-19 FM and in 63.0% of the COVID-19 vaccine FM. Cardiac arrest was observed more in COVID-19 FM (p = 0.008). Venoarterial extracorporeal membrane oxygenation (VA-ECMO) support for cardiogenic shock was also used more commonly in the COVID-19 fulminant myocarditis group (p = 0.0293). Reported mortality was similar (27.7%) and 27.8%, respectively) but was likely worse for COVID-19 FM as the outcome was still unknown in 11% of cases.

In the first series to retrospectively assess fulminant myocarditis associated with COVID-19 infection versus COVID-19 vaccination, we found that both conditions had a similarly high mortality rate, while COVID-19 FM had a more malignant course with more symptoms on presentation, more profound hemodynamic decompensation (higher heart rate, lower blood pressure), more cardiac arrests, and higher temporary MCS requirements including VA-ECMO. In terms of pathology, there was no difference in most biopsies/autopsies that demonstrated lymphocytic infiltrates and some eosinophilic or mixed infiltrates. There was no predominance of young males in COVID-19 vaccine FM cases, with male patients representing only 40.9% of the cohort.

Coronavirus disease 2019 (COVID-19) is a viral infection with the novel severe acute respiratory distress syndrome corona virus 2 (SARS-CoV-2). Until now, more than 670 million people have suffered from COVID-19 worldwide, and roughly 7 million death cases were attributed to COVID-19. Recent evidence suggests an interplay between COVID-19 and cardiovascular disease (CVD). COVID-19 may serve as a yet underappreciated CVD risk modifier, including risk factors such as diabetes mellitus or arterial hypertension. In addition, recent data suggest that previous COVID-19 may increase the risk for many entities of CVD to an extent similarly observed for traditional cardiovascular (CV) risk factors. Furthermore, increased CVD incidence and worse clinical outcomes in individuals with preexisting CVD have been observed for myocarditis, acute coronary syndrome, heart failure (HF), thromboembolic complications, and arrhythmias. Direct and indirect mechanisms have been proposed by which COVID-19 may impact CVD and CV risk, including viral entry into CV tissue or by the induction of a massive systemic inflammatory response. In the current review, we provide an overview of the literature reporting an interaction between COVID-19 and CVD, review potential mechanisms underlying this interaction, and discuss preventive and treatment strategies and their interference with CVD that were evaluated since the onset of the COVID-19 pandemic.

Myocarditis is considered a serious adverse event after COVID-19 infection. The risk and severity of myocarditis after COVID-19 disease decreased significantly in the vaccinated population. We present a case of cardiac magnetic resonance proven fulminant myocarditis following COVID-19 disease in a young female who was previously vaccinated with 2 doses of the BIBP (Sinopharm) vaccine.

A 29-year-old female was referred to the hospital with acute chest pain, dyspnea, and nausea. Her electrocardiogram revealed ST-segment elevation in anterolateral leads with reciprocal changes in inferior leads. She was primarily diagnosed with ST-elevation myocardial infarction following spontaneous coronary artery dissection (SCAD) according to her age and gender. Her coronary angiography was normal. RT-PCR nasopharyngeal swab was positive for SARS-COV-2 infection. According to her history and excluding coronary artery diseases, she was clinically diagnosed with myocarditis and received corticosteroids, IVIG, and colchicine. She was discharged in a favorable condition after 11 days of hospitalization. Cardiac magnetic resonance imaging confirmed the diagnosis of myocarditis according to the updated lake Louise criteria. On her 4-month follow-up, she was asymptomatic, and her echocardiography showed improvement in biventricular function.

The diagnosis of myocarditis caused by COVID-19 infection may be challenging as the symptoms of myocarditis, and COVID-19 disease may overlap. It should be considered when patients have acute chest pain, palpitation, elevated cardiac biomarkers, and new abnormalities in ECG or echocardiography. Cardiac MRI is a non-invasive gold standard modality for diagnosing and follow-up of myocarditis and should be used in clinically suspected myocarditis. The long-term course of myocarditis following COVID-19 disease is still unclear, but some evidence suggests it may have a favorable mid-term outcome.

The coronavirus disease 2019 (COVID-19) has been a challenge for the whole world since the beginning of 2020, and COVID-19 vaccines were considered crucial for disease eradication. Instead of producing classic vaccines, some companies pointed to develop products that mainly function by inducing, into the host, the production of the antigenic protein of SARS-CoV-2 called Spike, injecting an instruction based on RNA or a DNA sequence. Here, we aim to give an overview of the safety profile and the actual known adverse effects of these products in relationship with their mechanism of action. We discuss the use and safety of these products in at-risk people, especially those with autoimmune diseases or with previously reported myocarditis, but also in the general population. We debate the real necessity of administering these products with unclear long-term effects to at-risk people with autoimmune conditions, as well as to healthy people, at the time of omicron variants. This, considering the existence of therapeutic interventions, much more clearly assessed at present compared to the past, and the relatively lower aggressive nature of the new viral variants.

(1) Background: Emerging data indicate that the ongoing COVID-19 pandemic may result in long-term cardiovascular complications, among which long COVID-19 myocarditis seems to be one of the most dangerous. Clinical presentation of cardiac inflammation ranges from almost asymptomatic to life-threatening conditions, including heart failure (HF) in different stages. (2) Methods: This is a retrospective case-series study that includes three adults with different clinical presentations of heart failure on grounds of myocarditis after initial COVID-19 infection. (3) Results: All patients had new-onset symptomatic HF of various severity: from a moderately reduced left ventricular ejection fraction in one patient to significantly reduced fractions in the remaining two. Moreover, complex ventricular arrhythmias were present in one case. All patients had confirmed past myocarditis in cardiac magnetic resonance. With optimal medical treatment, cardiac function improved, and the symptoms subsided in all cases. (4) Conclusions: In COVID-19 patients, long COVID myocarditis may be one of the severe complications of this acute disease. The heterogeneity in clinical symptoms and a paucity of specific diagnostic procedures expose the patient to the significant risk of misdiagnosing and further HF development.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) mRNA vaccine-induced myocarditis is a rare but well-documented complication in young males. The increased incidence of sudden death among athletes following vaccination has been reported and requires further investigation. Whether the risk of myocarditis, a known major cause of sudden death in young male athletes, also increases after coronavirus disease 2019 (COVID-19) infection is unknown. The severity and implications of these critical adverse effects require a thorough analysis to elucidate their key triggering mechanisms. The present review aimed to evaluate whether there is a justification to hypothesize that catecholamines in a "hypercatecholaminergic" state are the key trigger of SARS-CoV-2 mRNA vaccine-induced myocarditis and related outcomes and whether similar risks are also present following COVID-19 infection. A thorough, structured scoping review of the literature was performed to build the hypothesis through three pillars: detection of myocarditis risk, potential alterations and abnormalities identified after SARS-CoV-2 mRNA vaccination or COVID-19 infection and consequent events, and physiological characteristics of the most affected population. The following terms were searched in indexed and non-indexed peer review articles and recent preprints (<12 months): agent, "SARS-CoV-2" or "COVID-19"; event, "myocarditis" or "sudden death(s)" or "myocarditis+sudden death(s)" or "cardiac event(s)"; underlying cause, "mRNA" or "spike protein" or "infection" or "vaccine"; proposed trigger, "catecholamine(s)" or "adrenaline" or "epinephrine" or "noradrenaline" or "norepinephrine" or "testosterone"; and affected population, "young male(s)" or "athlete(s)." The rationale and data that supported the hypothesis were as follows: SARS-CoV-2 mRNA vaccine-induced myocarditis primarily affected young males, while the risk was not observed following COVID-19 infection; independent autopsies or biopsies of patients who presented post-SARS-CoV-2 mRNA vaccine myocarditis in different geographical regions enabled the conclusion that a primary hypercatecholaminergic state was the key trigger of these events; SARS-CoV-2 mRNA was densely present, and SARS-CoV-2 spike protein was progressively produced in adrenal medulla chromaffin cells, which are responsible for catecholamine production; the dihydroxyphenylalanine decarboxylase enzyme that converts dopamine into noradrenaline was overexpressed in the presence of SARS-CoV-2 mRNA, leading to enhanced noradrenaline activity; catecholamine responses were physiologically higher in young adults and males than in other populations; catecholamine responses and resting catecholamine production were higher in male athletes than in non-athletes; catecholamine responses to stress and its sensitivity were enhanced in the presence of androgens; and catecholamine expressions in young male athletes were already high at baseline, were higher following vaccination, and were higher than those in non-vaccinated athletes. The epidemiological, autopsy, molecular, and physiological findings unanimously and strongly suggest that a hypercatecholaminergic state is the critical trigger of the rare cases of myocarditis due to components from SARS-CoV-2, potentially increasing sudden deaths among elite male athletes.