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Review
. 2021 Oct;97(1152):655-666.
doi: 10.1136/postgradmedj-2020-138284. Epub 2020 Sep 17.

COVID-19 and the heart: what we have learnt so far

Affiliations
Review

COVID-19 and the heart: what we have learnt so far

Kunal Bikram Shaha et al. Postgrad Med J. 2021 Oct.

Abstract

Since the outbreak of COVID-19 or coronavirus disease caused by severe acute respiratory syndrome coronavirus 2 from Wuhan, China, the cardiology fraternity's interest has been drawn towards the pandemic with a high case fatality rate of 10.5% and 6% in patients with heart disease and hypertension, respectively. One of the postulated mechanisms for this high fatality rate is the possible abundance of ACE type 2 receptor in the cardiovascular system that strongly binds with the spike protein of COVID-19 and helps internalise into the cell resulting in acute cardiac injury (ACI). More than 7% of cases with COVID-19 are reported to have this type of ACI. A tenfold rise in mortality has been observed in patients with COVID-19 who experience a rise in high-sensitivity (hs)-troponin. All most half of the patients who died of COVID-19 had a rise in hs-troponin. More than 15% of cases with COVID-19 experienced different types of arrhythmias. All these statistics denote how important cardiovascular pathology is in patients with COVID-19. Controversies of renin-angiotensin-aldosterone system inhibitors usage in patients with COVID-19 and meticulous handling of case with acute coronary syndrome categorically stresses cardiologists to bust the myths hovering around and set a standard guideline to counterfeit the fatality with timely diagnosis and treatment of COVID-19-induced ACI. In this review, we sought to summarise the current evidence of COVID-19-associated cardiac injury and suggest the implications for its proper diagnosis and treatment.

Keywords: Angiotensin receptor blocker; Arrhythmias; COVID-19; Carditis; SARS-Cov-2.

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Conflict of interest statement

Competing interests: None declared.

Figures

Figure 1
Figure 1
Three-step SARS-CoV-2 virus internalisation in host cell. SARS-CoV-2, severe acute respiratory syndrome coronavirus 2; TMPRSS2, type 2 transmembrane protease receptor.
Figure 2
Figure 2
Proposed multipronged attack by COVID-19 resulting in acute cardiac injury. DIC, disseminated intravascular coagulation.
Figure 3
Figure 3
(A) Putative mechanism of type 1 MI in COVID-19. (B) Putative mechanism of type 2 MI in COVID-19. MI, myocardial infarction.
Figure 4
Figure 4
SARS-CoV-2–induced ACE-mediated damage and role of ACEI/ARB in COVID-19. ACEI, ACE inhibitor; Ang I, angiotensin I; ARB, angiotensin receptor blocker; ATIR, angiotensin II type 1 receptor.
Figure 5
Figure 5
SARS-CoV-2 virology and possible therapeutic intervention. (A) Fusion. (B) Entocytosis. (C) Translation. (D) Proteolysis. (E) Translation and RNA replication. (F) Virion release. SARS-CoV-2, severe acute respiratory syndrome coronavirus 2.

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