tetano
Editor, Senior Moderator
Curr Cardiol Rep. 2020 Apr 21;22(5):32. doi: 10.1007/s11886-020-01292-3.
Cardiovascular Complications in Patients with COVID-19: Consequences of Viral Toxicities and Host Immune Response.
Zhu H[SUP]1,[/SUP][SUP]2,[/SUP][SUP]3[/SUP], Rhee JW[SUP]1,[/SUP][SUP]2,[/SUP][SUP]3[/SUP], Cheng P[SUP]1,[/SUP][SUP]2,[/SUP][SUP]3[/SUP], Waliany S[SUP]1[/SUP], Chang A[SUP]1,[/SUP][SUP]4[/SUP], Witteles RM[SUP]1,[/SUP][SUP]3[/SUP], Maecker H[SUP]5,[/SUP][SUP]6[/SUP], Davis MM[SUP]5,[/SUP][SUP]6,[/SUP][SUP]7[/SUP], Nguyen PK[SUP]1,[/SUP][SUP]2,[/SUP][SUP]3[/SUP], Wu SM[SUP]8,[/SUP][SUP]9,[/SUP][SUP]10[/SUP].
Author information
Abstract
PURPOSE OF REVIEW:
Coronavirus disease of 2019 (COVID-19) is a cause of significant morbidity and mortality worldwide. While cardiac injury has been demonstrated in critically ill COVID-19 patients, the mechanism of injury remains unclear. Here, we review our current knowledge of the biology of SARS-CoV-2 and the potential mechanisms of myocardial injury due to viral toxicities and host immune responses.
RECENT FINDINGS:
A number of studies have reported an epidemiological association between history of cardiac disease and worsened outcome during COVID infection. Development of new onset myocardial injury during COVID-19 also increases mortality. While limited data exist, potential mechanisms of cardiac injury include direct viral entry through the angiotensin-converting enzyme 2 (ACE2) receptor and toxicity in host cells, hypoxia-related myocyte injury, and immune-mediated cytokine release syndrome. Potential treatments for reducing viral infection and excessive immune responses are also discussed. COVID patients with cardiac disease history or acquire new cardiac injury are at an increased risk for in-hospital morbidity and mortality. More studies are needed to address the mechanism of cardiotoxicity and the treatments that can minimize permanent damage to the cardiovascular system.
KEYWORDS:
COVID-19; Cardiac injury; Cardiovascular system; Cytokine storm; Immune response; SARS-CoV-2
PMID:32318865DOI:10.1007/s11886-020-01292-3
Cardiovascular Complications in Patients with COVID-19: Consequences of Viral Toxicities and Host Immune Response.
Zhu H[SUP]1,[/SUP][SUP]2,[/SUP][SUP]3[/SUP], Rhee JW[SUP]1,[/SUP][SUP]2,[/SUP][SUP]3[/SUP], Cheng P[SUP]1,[/SUP][SUP]2,[/SUP][SUP]3[/SUP], Waliany S[SUP]1[/SUP], Chang A[SUP]1,[/SUP][SUP]4[/SUP], Witteles RM[SUP]1,[/SUP][SUP]3[/SUP], Maecker H[SUP]5,[/SUP][SUP]6[/SUP], Davis MM[SUP]5,[/SUP][SUP]6,[/SUP][SUP]7[/SUP], Nguyen PK[SUP]1,[/SUP][SUP]2,[/SUP][SUP]3[/SUP], Wu SM[SUP]8,[/SUP][SUP]9,[/SUP][SUP]10[/SUP].
Author information
Abstract
PURPOSE OF REVIEW:
Coronavirus disease of 2019 (COVID-19) is a cause of significant morbidity and mortality worldwide. While cardiac injury has been demonstrated in critically ill COVID-19 patients, the mechanism of injury remains unclear. Here, we review our current knowledge of the biology of SARS-CoV-2 and the potential mechanisms of myocardial injury due to viral toxicities and host immune responses.
RECENT FINDINGS:
A number of studies have reported an epidemiological association between history of cardiac disease and worsened outcome during COVID infection. Development of new onset myocardial injury during COVID-19 also increases mortality. While limited data exist, potential mechanisms of cardiac injury include direct viral entry through the angiotensin-converting enzyme 2 (ACE2) receptor and toxicity in host cells, hypoxia-related myocyte injury, and immune-mediated cytokine release syndrome. Potential treatments for reducing viral infection and excessive immune responses are also discussed. COVID patients with cardiac disease history or acquire new cardiac injury are at an increased risk for in-hospital morbidity and mortality. More studies are needed to address the mechanism of cardiotoxicity and the treatments that can minimize permanent damage to the cardiovascular system.
KEYWORDS:
COVID-19; Cardiac injury; Cardiovascular system; Cytokine storm; Immune response; SARS-CoV-2
PMID:32318865DOI:10.1007/s11886-020-01292-3