evidence: SARS-CoV-2-induced endotheliitis and microvascular dysfunction are also relevant for the myocardium. The cytokine storm that is observed in severe COVID-19 (ref.72) is thought to result in vascular inflammation and atherosclerotic plaque instability, as well as in myocardial inflammation73,74,75,76,77,78. An acute COVID-19 cardiovascular syndrome can occur, which is characterized by an acute cardiac injury with cardiomyopathy, ventricular arrhythmias and haemodynamic instability in the absence of obstructive coronary artery disease75. The cause of this injury is uncertain but is suspected to be related to myocarditis, microvascular injury, systemic cytokine-mediated injury or stress-related cardiomyopathy. ACE2 is highly expressed in arterial and venous endothelial cells, pericytes and also in cardiomyocytes. Therefore, acute cellular injury of cardiomyocytes caused by SARS-CoV-2 through ACE2-mediated entry and subsequent viral replication is considered important76,77,78. These pathologies can result in clinical manifestation in patients with COVID-19, such as acute coronary syndrome, acute myocardial injury without obstructive coronary artery disease, arrhythmias, heart failure with or without cardiogenic shock, pericardial effusion and thromboembolic complications75. Whether COVID-19 primarily induces CVD or whether cardiovascular complications are predominantly a consequence of severe COVID-19 is still unsolved77. Most probably, both pathogenic courses are relevant for COVID-19. [...] Ponsford, M. J. et al. Cardiometabolic traits, sepsis, and severe COVID-19: a Mendelian randomization investigation. Circulation142, 1791–1793 (2020). Mendelian randomization analyses performed in this study show that a higher genetically proxied BMI was associated with increased risk of severe COVID-19.