A current review of COVID-19 for the cardiovascular specialist

Abstract

Although coronavirus disease 2019 predominantly disrupts the respiratory system, there is accumulating experience that the disease, particularly in its more severe manifestations, also affects the cardiovascular system. Cardiovascular risk factors and chronic cardiovascular conditions are prevalent among patients affected by COVID-19 and associated with adverse outcomes. However, whether pre-existing cardiovascular disease is an independent determinant of higher mortality risk with COVID-19 remains uncertain. Acute cardiac injury, manifest by increased blood levels of cardiac troponin, electrocardiographic abnormalities, or myocardial dysfunction, occurs in up to~60% of hospitalized patients with severe COVID-19. Potential contributors to acute cardiac injury in the setting of COVID-19 include (1) acute changes in myocardial demand and supply due to tachycardia, hypotension, and hypoxemia resulting in type 2 myocardial infarction; (2) acute coronary syndrome due to acute atherothrombosis in a virally induced thrombotic and inflammatory milieu; (3) microvascular dysfunction due to diffuse microthrombi or vascular injury; (4) stress-related cardiomyopathy (Takotsubo syndrome); (5) nonischemic myocardial injury due to a hyperinflammatory cytokine storm; or (6) direct viral cardiomyocyte toxicity and myocarditis. Diffuse thrombosis is emerging as an important contributor to adverse outcomes in patients with COVID-19. Practitioners should be vigilant for cardiovascular complications of COVID-19. Monitoring may include serial cardiac troponin and natriuretic peptides, along with fibrinogen, D-dimer, and inflammatory biomarkers. Management decisions should rely on the clinical assessment for the probability of ongoing myocardial ischemia, as well as alternative nonischemic causes of injury, integrating the level of suspicion for COVID-19. (Am Heart J 2020;226:29-44.) Coronavirus disease 2019 (COVID-19) has affected more than 2 million individuals worldwide. 1 Although COVID-19 predominantly disrupts the respiratory system, there is accumulating experience that the disease, particularly in its more severe manifestations, also affects the cardiovascular system. [2][3][4] Therefore, an understanding of how COVID-19 may influence the cardiovascular system is important for both cardiovascular practitioners and researchers. This review synthesizes the clinical evidence published to date on the cardiovascular complications of COVID-19, emerging perspectives on their pathophysiology, and evolving best practices for clinical management.

Racial Disparities-Associated COVID-19 Mortality among Minority Populations in the US

“…In addition, SARS-CoV-2 RNA was detected in heart tissue from 35% of patients who died during the SARS-CoV-2 outbreak in Toronto [65]. A cytokine storm and calcium-dependent apoptosis of cardiomyocytes are among other mechanism that could link CVD and COVID-19 [66] (Figure 3). ACE2-related signaling pathways also may have a role in heart injury.…”

Rationale for the use of N ‐acetylcysteine in both prevention and adjuvant therapy of COVID‐19

“…Different pathogenic disturbances are involved, such as acute changes in myocardial demand and supply due to tachycardia, hypotension, and hypoxemia resulting in type 2 myocardial infarction; acute coronary syndrome due to acute atherothrombosis in a virally induced thrombotic and inflammatory milieu; microvascular dysfunction due to diffuse microthrombi or vascular injury; stress-related cardiomyopathy (Takotsubo syndrome); direct viral cardiomyocyte toxicity and myocarditis. 3 All of these complications reflect inflammatory reactions stimulated by the viral infection.…”

Reduction in environmental noise during COVID‐19 pandemic and cardiovascular disease: A mystery for further investigation

“…Further evidence suggests that troponin and other cardiac enzymes reflecting, either myocarditis or myocardial infarction, are increased during the infection, and some of these patients have confirmed electrocardiographic findings 15,16 . Different pathophysiological mechanisms have been proposed from changes in myocardial demand to direct cardiac toxicity 17 . Stress is also a possible explanation taking into account the significant increase in the incidence of stress cardiomyopathy during the COVID‐19 pandemic 18 …”