Cardiac involvement in COVID-19 patients

• Definition of cardiac involvement in COVID19 is challenging: SARS-CoV-2 infection has multifaceted effects
• From a clinical point of view, cardiac involvement during COVID19 may present a wide spectrum of severity, ranging from subclinical myocardial injury to well-defined clinical entities
• Three clinical scenarios may be encountered:
  1. Primary cardiac involvement
     • It may be a consequence of direct viral damage (hypothesized) to the endothelium and (presumably) to the myocardium causing viral myocarditis
     • The possible link between the respiratory syndrome and the pleomorphic cardiovascular manifestations associated with COVID-19 could be the ACE-2 (membrane-bound enzyme that serves as a cell-entry receptor for SARS-CoV-2)
       • expressed in lung alveolar epithelial cells, enterocytes of the small intestine, arterial smooth muscle cells, and endothelial cells
     • myocardial infection by coronavirus is possible: in an autopsy series, SARS-CoV ribonucleic acid was found in 35% of sampled hearts, along with macrophage infiltration and myocardial damage
     • currently, no cases of SARS-CoV-2 nucleic acid isolation from myocardial specimens have been described
     • several cases have reported on the occurrence of severe myocarditis in COVID-19 + patients causing severe LV dysfunction recovering following medical therapy
     • other possible differential diagnoses make it difficult diagnosis of SARS-CoV-2-related myocarditis
  2. Secondary cardiac involvement
     • indirect myocardial damage during SARS-CoV-2 infection
     • Cytokine storm –> inflammatory myocarditis
     • Oxygen supply-demand imbalance –> Type 2 MI
     • Inflammatory prothrombotic state and atherosclerotic plaque instability –> Type 1 MI
     • Inflammatory prothrombotic state –> VTE and acute PE
     • Lung inflammation, hypoxic vasoconstriction, high-PEEP mechanical ventilation, pulmonary thromboembolism –> RV increased afterload
  3. Worsening of previous cardiovascular diseases
     • High prevalence of patients with pre-existing cardiovascular comorbidities in nonsurvivor cohorts: patients with HF are more vulnerable to hemodynamic decompensation during viral infections
     • Infection-related metabolic demand and cytokine storm –> heart failure exacerbation
     • Hypoxia, cytokine storm, drug side effects (QT interval prolongation from hydroxychloroquine and azithromycin alone or in combination with antiarrhythmic drugs) –> arrhythmias

References

Agricola E, Beneduce A, Esposito A, et al. Heart and Lung Multimodality Imaging in COVID-19. JACC Cardiovasc Imaging. 2020;13(8):1792-1808. doi:10.1016/j.jcmg.2020.05.017