Recognizing COVID-19–related myocarditis: The possible pathophysiology and proposed guideline for diagnosis and management

Abstract

Human coronavirus-associated myocarditis is known, and a number of coronavirus disease 19 (COVID-19)-related myocarditis cases have been reported. The pathophysiology of COVID-19-related myocarditis is thought to be a combination of direct viral injury and cardiac damage due to the host's immune response. COVID-19 myocarditis diagnosis should be guided by insights from previous coronavirus and other myocarditis experience. The clinical findings include changes in electrocardiogram and cardiac biomarkers, and impaired cardiac function. When cardiac magnetic resonance imaging is not feasible, cardiac computed tomographic angiography with delayed myocardial imaging may serve to exclude significant coronary artery disease and identify myocardial inflammatory patterns. Because many COVID-19 patients have cardiovascular comorbidities, myocardial infarction should be considered. If the diagnosis remains uncertain, an endomyocardial biopsy may help identify active cardiac infection through viral genome amplification and possibly refine the treatment risks of systemic immunosuppression. Arrhythmias are not uncommon in COVID-19 patients, but the pathophysiology is still speculative. Nevertheless, clinicians should be vigilant to provide prompt monitoring and treatment. The longterm impact of COVID-19 myocarditis, including the majority of mild cases, remains unknown.

ACE2 and TMPRSS2 Potential Involvement in Genetic Susceptibility to SARS-COV-2 in Cancer Patients

“…It is indeed believed that multiorgan failure in the advanced stages of COVID-19 is the result of an uncontrolled proliferation and activation of the immune system with a supraphysiological release of IL-1, IL-6, and TNF-α resulting in witnessing a cytokine release syndrome. In addition, COVID-19 patients present with diarrhea in 2% to 50% of cases 30 , might show cardiac complications up to fibrillations, myocarditis, and heart arrest 31 , and are likely related to high ACE2 expression in the intestine and the heart, respectively. Importantly, patients with diarrhea remain positive for SARS-CoV-2 in the feces up to 12 days after disease onset, with a considerable fraction of individuals still negative if tested in the respiratory tract 32 .…”

An impaired natriuretic peptide hormone system may play a role in COVID‐19 severity in vulnerable populations

“…29,30 There is also evidence that a natriuretic peptide treatment approach has the potential to attenuate the coagulopathy associated with COVID-19, [30][31][32] and the cardioprotective effects of natriuretic peptides 33 may attenuate COVID-19 myocarditis and acute cardiovascular syndrome. 34,35 Limiting progression of the disease to this stage could have a profound impact on number of deaths since most patients who require mechanical ventilation die (88.1% in NYC cohort, 1 93% in Wuhan study 30 ). This treatment approach may be most beneficial for COVID-19 patients who have dysregulated natriuretic peptide signaling, including African Americans, obese patients, and elderly patients, who appear to be most vulnerable to COVID-19.…”

Findings on the relationship between cardiovascular disease and coronavirus disease 2019: a systematic review

“…This raises the possibility of secondary cardiac injury related to an increase in oxygen demand caused by sepsis in subclinical coronary artery disease. Sepsis would lead to ischemia resulting in type 2 acute myocardial infarction [25]. This sequence of events may contribute to the elucidation of the ndings of study 3 (Table 1), which included 113 patients who died as a result of the COVID-19, among which 100% had sepsis and 49% had heart failure.…”

“…When a set of cytokines is considered, the predictive value for cardiac complications increases, since it is known that cytokines work together leading to a complex in ammatory response [33]. IL-6 participates in the activation of T lymphocytes and the cytotoxicity of these cells leads to an intense in ammatory response that can damage the heart muscle [34]. The T-lymphocytes present a cardiotropism by an interaction between the heart-produced hepatocyte growth factor (HGF) and c-Met, the HGF receptor on naïve T-cells [35].…”