COVID-19 and Acute Myocardial Injury and Infarction: Related Mechanisms and Emerging Challenges

Abstract

In the era of the coronavirus disease 2019 (COVID-19) pandemic, acute cardiac injury (ACI), as reflected by elevated cardiac troponin above the 99th percentile, has been observed in 8%-62% of patients with COVID-19 infection with highest incidence and mortality recorded in patients with severe infection. Apart from the clinically and electrocardiographically discernible causes of ACI, such as acute myocardial infarction (MI), other cardiac causes need to be considered such as myocarditis, Takotsubo syndrome, and direct injury from COVID-19, together with noncardiac conditions, such as pulmonary embolism, critical illness, and sepsis. Acute coronary syndromes (ACS) with normal or near-normal coronary arteries (ACS-NNOCA) appear to have a higher prevalence in both COVID-19 positive and negative patients in the pandemic compared to the pre-pandemic era. Echocardiography, coronary angiography, chest computed tomography and/or cardiac magnetic resonance imaging may render a correct diagnosis, obviating the need for endomyocardial biopsy. Importantly, a significant delay has been recorded in patients with ACS seeking advice for their symptoms, while their routine care has been sharply disrupted with fewer urgent coronary angiographies and/or primary percutaneous coronary interventions performed in the case of ST-elevation MI (STEMI) with an inappropriate shift toward thrombolysis, all contributing to a higher complication rate in these patients. Thus, new challenges have emerged in rendering a diagnosis and delivering treatment in patients with ACI/ACS in the pandemic era. These issues, the various mechanisms involved in the development of ACI/ACS, and relevant current guidelines are herein reviewed.

A Real Pandora’s Box in Pandemic Times: A Narrative Review on the Acute Cardiac Injury Due to COVID-19

“…Essentially, vasodilation represents the main pathophysiological mechanism of the response of the cardiovascular system to sepsis. In addition, hypotension is the natural consequence of vasodilation, which can even progress to hemodynamic collapse, thus inducing or aggravating coronary hypoperfusion with subsequent acute myocardial injury through a reduced O 2 supply [ 60 ]. At the same time, in the context of sepsis, reflex tachycardia increases the myocardial oxygen demand.…”

Non-invasive coronary imaging in patients with COVID-19: A narrative review

“…Moreover, in addition to type 1 and type 2 MI, in COVID-19 patients there has been an increased incidence of MINOCA (myocardial infarction with non-obstructive coronary arteries) [24] which includes plaque (causing <50% stenosis) rupture or erosion, coronary embolism and dissection, and coronary artery spasm. From a clinical point of view, differential diagnosis between different causes of ACS and acute cardiac injury in patients with COVID-19 can be difficult [25] , [26] . In this setting, after excluding type 1 MI with coronary angiography demonstrating a culprit lesion, non-invasive cardiac imaging represents a useful diagnostic tool.…”

Myocardial Infarction With Non-obstructive Coronary Arteries: Risk Factors and Associated Comorbidities

“…Moreover, infections may promote platelet activation and endothelial dysfunction, increase metabolic demand, and induce hypoxaemia and hypotension ( 46 ). During the coronavirus disease 2019 (COVID-19) pandemic, new challenges arose in the diagnosis and treatment of patients with acute myocardial injury or ACSs ( 47 ). Whereas severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection primarily affects the lungs, a heightened risk of thromboembolism has widely been reported ( 48 ).…”

“…Accordingly, MINOCA has been increasingly described in COVID-19 patients, due to various mechanisms. First, increased sympathetic activation associated with viral infection may promote ACSs in patients with pre-existing CAD ( 47 ). Similarly, cytokine storm may lead to coronary plaque instability as well as initiation and perpetuation of a pro-thrombotic milieu.…”

“…Finally, significant hypoxia in course of viral pneumonia may not only trigger coronary plaque rupture and thrombosis, but also cause type 2 MI because of reduced oxygen supply. This deleterious pathogenic ensemble seems to be responsible for ACSs in COVID-19 ( 47 ). In addition, myocarditis, TTS, and acute heart failure are important aetiologies of myocardial injury in COVID-19, albeit non-cardiac conditions should also be considered.…”