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COVID-19 Infection: Matters of the Heart Image
Apr 20, 2021

COVID-19 Infection: Matters of the Heart

Ylenia A. Quiaoit Photo

Ylenia A. Quiaoit DNP, ACNP-BC

Though the respiratory tract is the main target of COVID-19, its potential impact on the cardiovascular (CV) system is a very serious matter, portending a higher degree of morbidity and mortality. Thus, it is important for clinicians to be cognizant of the CV complications in COVID-19. This post provides an overview of COVID-19–related CV complications.


Acute Myocardial Injury

Acute myocardial injury is the most common CV complication and a strong negative prognostic marker in patients with COVID-19. The pathophysiology of myocardial injury can be direct, via SARS-CoV-2 viral invasion of cardiomyocytes, or indirect, via overwhelming immune response leading to multiple organ dysfunction and/or via severe hypoxia from acute respiratory damage resulting in oxidative stress and increased cardiometabolic demand. Myocardial injury manifests itself by elevation of the troponin level.


Acute Myocarditis

The clinical spectrum of acute myocarditis has a wide and variable range of severity. Findings can range from mild chest pain, dyspnea, and fatigue, to more severe disorders such as biventricular failure, cardiogenic shock, arrhythmias, fulminant myocarditis, and sudden death. It is important to note that COVID-19–induced myocarditis can mimic acute coronary syndrome (ACS), with ST-segment elevation and abnormal (elevated) cardiac enzymes. Differentiating acute myocarditis from ACS can be challenging; thus, echocardiography and cardiology consultation are encouraged. Echocardiography can help evaluate the presence of focal wall motion dyskinesis or hypokinesis (more consistent with ACS); no wall motion defects or global wall motion dysfunction are more consistent with severe forms of COVID-19–related myocarditis.


Acute Myocardial Infarction or Acute Coronary Syndrome

Acute myocardial infarction (MI) or ACS in COVID-19 is attributed to plaque rupture and coronary thrombosis. The plaque rupture and coronary thrombosis occurring in patients with COVID-19 are consequences of inflammation and increases in shear stress, especially in patients with preexisting CV risks and a hypercoagulability state.


Acute Heart Failure and Cardiomyopathy

Acute heart failure (HF) can be common in patients with COVID-19; it can also be the primary presenting manifestation of the disease. Critically ill patients can develop sepsis-related cardiomyopathy with left ventricular dilatation and impaired systolic function. COVID-19 can also exacerbate underlying HF and lead to mixed shock syndrome (septic and cardiogenic). Stress cardiomyopathy can also occur due to generalized inflammatory response and sympathetic activation, leading to a more classic form of acute HF decompensation with elevated filling pressure and pulmonary edema.


Arrhythmias and Cardiac Arrest

Symptomatic and asymptomatic tachycardia are the most common arrhythmias in patients with COVID-19. Tachycardias occur in COVID-19 due to several causes, such as hypoperfusion, fever, and anxiety. The prevalence and severity of arrhythmia in COVID-19 is associated with other CV complications such as myocarditis, myocardial ischemia, shock, and hypoxia. If a patient with COVID-19 presents with arrhythmia and has elevated cardiac enzymes, then myocardial injury, myocarditis, and ACS must be considered. More lethal forms of arrhythmias—such as ventricular tachycardia, ventricular fibrillation, and asystole—can occur in severe COVID-19 cases.


Venous Thromboembolic Events

COVID-19 causes dysregulation of the coagulation process, producing a coagulopathy associated with hypercoagulability, manifested by venous and arterial thrombosis and multiorgan dysfunction. Mild thrombocytopenia; slight prolongation of the prothrombin time; high levels of D-dimer; and elevated levels of fibrinogen, factor VIII, and von Willebrand factor are characteristics of coagulopathy related to COVID -19.

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