Coronary Implications of COVID-19

Abstract

Patients with SARS-CoV-2 infection carry an increased risk of cardiovascular disease encompassing various implications, including acute myocardial injury or infarction, myocarditis, heart failure, and arrhythmias. A growing volume of evidence correlates SARS-CoV-2 infection with myocardial injury, exposing patients to higher mortality risk. SARS-CoV-2 attacks the coronary arterial bed with various mechanisms including thrombosis/rupture of preexisting atherosclerotic plaque, de novo coronary thrombosis, endotheliitis, microvascular dysfunction, vasculitis, vasospasm, and ectasia/aneurysm formation. The angiotensin-converting enzyme 2 receptor plays pivotal role on the cardiovascular homeostasis and the unfolding of COVID-19. The activation of immune system, mediated by proinflammatory cytokines along with the dysregulation of the coagulation system, can pose an insult on the coronary artery, which usually manifests as an acute coronary syndrome (ACS). Electrocardiogram, echocardiography, cardiac biomarkers, and coronary angiography are essential tools to set the diagnosis. Revascularization is the first-line treatment in all patients with ACS and obstructed coronary arteries, whereas in type 2 myocardial infarction treatment of hypoxia, anemia and systemic inflammation are indicated. In patients presenting with coronary vasospasm, nitrates and calcium channel blockers are preferred, while treatment of coronary ectasia/aneurysm mandates the use of antiplatelets/anticoagulants, corticosteroids, immunoglobulin, and biologic agents. It is crucial to untangle the exact mechanisms of coronary involvement in COVID-19 in order to ensure timely diagnosis and appropriate treatment. We have reviewed the current literature and provide a detailed overview of the pathophysiology and clinical spectrum associated with coronary implications of SARS-COV-2 infection. Patients with SARS-CoV-2 infection carry an increased risk of cardiovascular disease encompassing various implications, including acute myocardial injury or infarction, myocarditis, heart failure, and arrhythmias. A growing volume of evidence correlates SARS-CoV-2 infection with myocardial injury, exposing patients to higher mortality risk. SARS-CoV-2 attacks the coronary arterial bed with various mechanisms including thrombosis/rupture of preexisting atherosclerotic plaque, de novo coronary thrombosis, endotheliitis, microvascular dysfunction, vasculitis, vasospasm, and ectasia/aneurysm formation. The angiotensin-converting enzyme 2 receptor plays pivotal role on the cardiovascular homeostasis and the unfolding of COVID-19. The activation of immune system, mediated by proinflammatory cytokines along with the dysregulation of the coagulation system, can pose an insult on the coronary artery, which usually manifests as an acute coronary syndrome (ACS). Electrocardiogram, echocardiography, cardiac biomarkers, and coronary angiography are essential tools to set the diagnosis. Revascularization is the first-line treatment in all patients with ACS and obstructed coronary arteries, whereas in type 2 myocardial infarction treatment of hypoxia, anemia and systemic inflammation are indicated. In patients presenting with coronary vasospasm, nitrates and calcium channel blockers are preferred, while treatment of coronary ectasia/aneurysm mandates the use of antiplatelets/anticoagulants, corticosteroids, immunoglobulin, and biologic agents. It is crucial to untangle the exact mechanisms of coronary involvement in COVID-19 in order to ensure timely diagnosis and appropriate treatment. We have reviewed the current literature and provide a detailed overview of the pathophysiology and clinical spectrum associated with coronary implications of SARS-COV-2 infection.

Keywords: Aneurysm; Atherothrombosis; COVID-19; Coronary artery; Endotheliitis; Microvascular dysfunction; Myocardial infarction; Myocardial injury; Vasculitis; Vasospasm.

Fig. 1.

Coronary implications of COVID-19: the spike protein of SARS-CoV-2 attacks the vascular cells via the ACE-2 receptor. The activation of proinflammatory cytokines and the renin-angiotensin-aldosterone system along with platelet aggregation cause thrombosis/rupture of preexisting atherosclerotic plaque, whereas de novo coronary thrombosis-endotheliitis is mediated by increased levels of interleukin (IL)-1b, IL-8 and TNF-a. IL-6 and matrix metalloproteinases play a pivotal role in the formation of coronary artery ectasia. Accumulation of reactive oxygen species and immune complexes cause microvascular dysfunction and vasculitis, respectively. Extensive catecholamine release coupled with nitric oxide depletion induce coronary vasospasm.

Fig. 2.

Treatment of COVID-19-related coronary complications. Percutaneous or surgical revascularization is indicated in patients with acute coronary syndromes and obstructed coronary arteries alongside optimal medical therapy. Coronary vasospasm responds to nitrates and calcium channel antagonists. In type 2 myocardial infarction, treatment of hypoxia, anemia, and systemic inflammation control is essential. Treatment of multisystem inflammatory syndrome in children (MIS-C) and adults (MIS-A) mandates the use of antiplatelets/anticoagulants, corticosteroids, immunoglobulin, and/or biologic agents.