COVID-19 and cardiovascular diseases

Abstract

Infection by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is responsible for the second pandemic of the XXI century after influenza A in 2009. As of mid-June 2020, more than 4,40,000 fatal cases of SARS-CoV-2-related disease (COVID-19) have occurred worldwide. Besides its prominent expression at the level of the respiratory apparatus, COVID-19 is also characterized by a substantial degree of cardiovascular involvement, both in terms of deterioration of pre-existing conditions, and as the effect of inflammation-facilitated acute events. They include ischemic/inflammatory heart disease, ventricular arrhythmias, conduction disturbances, thrombotic events at the level of the lungs, and systemic activation of the coagulation cascade, configuring the scenario of disseminated intravascular coagulation. Herein, we summarize the main COVID-19 features of relevance for the clinicians in the cardiovascular field. The rationale, concerns, and possible side effects of specific therapeutic measures, including anticoagulants, renin-angiotensin-aldosterone system inhibitors, and anti-inflammatory/antiviral medications applied to the treatment of COVID-19 are also discussed.

Keywords: COVID-19; Cardiovascular diseases; Coagulation; Electrocardiography; Renin-angiotensin-aldosterone system inhibitors.

Fig. 1

Chronic comorbidities among 3335 deceased COVID-19 patients in Italy as of June 4th, 2020. (A) Comorbidities by gender. (B) Proportion of patients with 0, 1, 2, or at least 3 comorbidities: 4.1%, 14.8%, 21.5%, and 59.7%, respectively. HTN, hypertension; DM2, diabetes mellitus type 2; IHD, ischemic heart disease; AF, atrial fibrillation; CKD, chronic kidney disease; COPD, chronic obstructive pulmonary disease; HF, heart failure.

Fig. 2

COVID-19: from viral aggression to systemic involvement. In the early phase, COVID-19 affects the sites of replication, primarily represented by the lungs: the immune system begins to generate antibodies and cytokines, while specific virus-dependent mechanisms limit the lymphocytic response. In a second phase, healing or worsening of the disease can occur. Specifically, a cytokine syndrome (“cytokine storm”) can develop, leading to a marked increase in the intensity of local and systemic inflammation, leading to multiorgan insufficiency. Hypercoagulation is a feature of both the early and the late stage of the disease, potentially leading to thrombosis and/or disseminated intravascular coagulation (DIC). The increase in the levels of angiotensin II (Ang II), caused by the binding of SARS-CoV-2 with ACE2, is present since the early stage and participates in the induction of damage. The figure is original from the author (CF).

Fig. 3

Effects of SARS-CoV-2 binding to angiotensin-converting enzyme (ACE) 2. ACE2, the functional receptor for SARS-CoV-2, converts angiotensin II (Ang II) into angiotensin (1–7) [Ang-(1–7)], which exerts vasodilator, anti-inflammatory effects. The binding of SARS-CoV-2 to the enzyme, facilitated by the type II transmembrane serine proteases (TMPRSS2), determines an unbalance in Ang II and Ang-(1–7), with a decrease in the latter. The figure is original from the authors.