What is the impact of COVID-19 on cardiovascular function?

Cardiovascular involvement in patients with the novel coronavirus disease (COVID-19) has been noted in some cases, but the effect of COVID-19 on myocardial function and on the outcomes after treatment of cardiac and related illnesses is not well established, according to a study.

“While some information is available, further studies are imperative for a more cohesive understanding of the cardiac pathophysiology in COVID‐19 patients to promote more informed treatment and better clinical outcomes,” the researchers said.

Existing body of literature was reviewed for papers in the English language dealing with the cardiac implications of COVID-19.

Many COVID-19 patients with pre-existing cardiovascular disease were treated in intensive care unit settings and had higher rates of mortality than those without. In some studies, cardiac presentations for COVID-19, including acute pericarditis and left ventricular dysfunction, were more likely to be recorded rather than respiratory conditions. Some patients showed signs of acute myocardial injury, with correspondingly increased serum troponin I levels. [J Card Surg 2020;doi:10.1111/jocs.14538]

On the other hand, data were lacking in terms of myocardial protection during cardiac surgery for COVID-19 patients.

“Although some insights have been garnered in the study of cardiovascular diseases for these patients, these insights remain fragmented and have yet to cement clear guidelines for actionable clinical practice,” the researchers said.

Of note, cardiac injury in patients with COVID-19 could have been triggered by the virus itself. Viral infections usually cause infectious myocarditis. There is also evidence suggesting that common infections trigger acute coronary events and strokes. [Circ Res 2016;118:496‐514; Curr Opin Neurol 2007;20:51‐57; N Engl J Med 2004;351:2611‐2618]

In light of this, researchers tried to determine the mechanisms of COVID-19–mediated cardiac injury. One explanation was that the virus infects host cells through angiotensin-converting enzyme 2 (ACE2) receptors, potentially leading to pneumonia, acute myocardial injury and chronic cardiovascular damage. [Nat Rev Cardiol 2020;17:259-260]

ACE2 receptors are membrane-bound aminopeptidases that are important in the cardiovascular and immune systems and are highly expressed in the heart and lungs. In addition, these receptors have been confirmed to be the functional receptors for COVID-19. [Cell 2020;181:271-280.e8]

“These findings indicate that myocardial injury caused in COVID‐19 might be ACE2-related,” the researchers said. “Given this mechanism of action, there has been substantial discussion and controversy on the use of antihypertensive ACE inhibitors in COVID‐19‐infected patients.”

Nonetheless, the American Heart Association maintained that the use of ACE inhibitors remains safe in patients with myocardial infections, heart failure or hypertension. [https://professional.heart.org/professional/ScienceNews/UCM_505836_HFSAACCAHAstatement-addresses-concerns-re-using-RAAS-antagonists-in-COVID.jsp]

Other review articles have supported this guideline, stating that withdrawal of renin-angiotensin-aldosterone system inhibitors in COVID-19 patients may be harmful. [Eur Heart J 2020;doi:10.1093/eurheartj/ehaa235; New Engl J Med 2020;doi:10.1056/NEJMsr2005760]

“Based on what has been discovered and hypothesized about cardiac involvement in COVID‐19, there is a need for autopsies and rigorous gross, histological cardiac assessments, and more basic research into the effects of COVID‐19 on myocardial function and other associated clinical conditions such as diabetes,” the researchers said.

“Such analyses could further elucidate the mechanisms that seem to be at play in COVID‐19‐mediated heart dysregulation and injury,” they added.