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

Tommaso Scquizzato
Tommaso Scquizzato

Tommaso Scquizzato is a researcher in the fields of cardiac arrest and resuscitation science at the Center for Intensive Care and Anesthesiology of San Raffaele Hospital in Milan, Italy. He is the Social Media Editor of Resuscitation, member of the Social Media Working Group of ILCOR, and member of the ERC BLS Science and Education Committee.

Articles: 35