Our findings suggest that COVID-19 infection may lead to persistent endothelial dysfunction and hypercoagulability, portending increased severity of coronary artery ectasia and coronary thrombosis even after recovery from the initial infection.
Our study provides evidence of SARS-CoV-2 presence in human coronary vasculature and demonstrates viral tropism for vascular lesion macrophages in individuals with severe COVID-19. We found evidence of SARS-CoV-2 replication in all analyzed human autopsy coronaries regardless of their pathological classification, although viral replication was highest in PIT coronary lesions—early-stage lesions that progress to more advanced atherosclerotic plaques.
Our data conclusively demonstrate that SARS-CoV-2 is capable of infecting and replicating in macrophages within the coronary vasculature of patients with COVID-19.
Patients with severe COVID-19 requiring mechanical ventilation are 16 times more likely to develop ventricular tachycardia within six months compared to their peers without severe infection, according to research presented at EHRA 2023, a scientific congress of the European Society of Cardiology (ESC). Risks of other heart rhythm disorders were also elevated.
- 45.29 incidents of any prespecified cardiovascular outcome
- 23.48 incidents of major adverse cardiovascular events (MACEs), including myocardial infarction, stroke, and all-cause mortality
- 19.86 incidents of dysrhythmias, including 10.74 incidents of atrial fibrillation
- 12.72 incidents of other cardiovascular disorders including 11.61 incidents of heart failure and 3.56 incidents of nonischemic cardiomyopathy
- 9.88 incidents of thromboembolic disorders, including 5.47 incidents of pulmonary embolism and 4.18 incidents of deep vein thrombosis
- 7.28 incidents of ischemic heart disease including 5.35 incidents of acute coronary disease, 2.91 incidents of myocardial infarction, and 2.5 incidents of angina
- 5.48 incidents of cerebrovascular disorders, including 4.03 incidents of stroke
- 1.23 incidents of inflammatory disease of the heart or pericardium, including 0.98 incidents of pericarditis and 0.31 incidents of myocarditis
The excess death, defined as the difference between the observed and the predicted mortality rates, was most pronounced for the youngest (25–44 years) aged decedents, ranging from 23% to 34% for the youngest compared to 13%–18% for the oldest age groups.
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.
- COVID-19 infection has both intermediate and long-term consequences for the cardiovascular system.
- In acute infection, troponin elevation is more commonly a consequence of indirect cardiac injury from critical illness and multi-organ dysfunction than direct viral damage to the heart.
- In resolved infection, special attention should be paid to athletes at-risk for exercise-induced arrythmias, as well as survivors with residual cardiopulmonary symptoms.
Here, we conducted a comprehensive analysis of the cytopathic effects of SARS-CoV-2 in hiPSC-derived cardiac cells to model viral infection of the heart. Cytopathic effects were particularly notable in CMs, which manifested a distinctive pattern of myofibrillar fragmentation into individual sarcomeric units and a loss of nuclear DNA staining from intact cell bodies. Unexpectedly, these cytopathic effects occurred independent of the presence of actively replicating SARS-CoV-2 virus, suggesting a broader spectrum of adverse consequences than initially assumed.