Cardiac inflammation in COVID-19: Lessons from heart failure

LIFE SCIENCES

卷:260

Review

Unudurthi, Sathya D.¹  Luthra, Priya²  Bose, Rajendran J. C.¹  McCarthy, Jason R.¹  Kontaridis, Maria Irene^1,3,4 

[1] Masonic Med Res Inst, Dept Biomed Res & Translat Med, Utica, NY USA

[2] Trudeau Inst, Saranac Lake, NY USA

[3] Harvard Med Sch, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA

[4] Harvard Med Sch, Beth Israel Deaconess Med Ctr, Dept Med, Div Cardiol, Boston, MA 02115 USA

关键词: SARS-Cov2;    COVID-19;    Cytokine storm;    Heart failure;    Myocarditis;    Immunopathology;    Neutrophils;    Monocytes;    Macrophages;    Myofibroblasts;   

DOI  :  10.1016/j.lfs.2020.118482

来源: Elsevier

【 摘 要 】

Cardiovascular disease (CVD) is the most common co-morbidity associated with COVID-19 and the fatality rate in COVID-19 patients with CVD is higher compared to other comorbidities, such as hypertension and diabetes. Preliminary data suggest that COVID-19 may also cause or worsen cardiac injury in infected patients through multiple mechanisms such as 'cytokine storm', endotheliosis, thrombosis, lymphocytopenia etc. Autopsies of COVID-19 patients reveal an infiltration of inflammatory mononuclear cells in the myocardium, confirming the role of the immune system in mediating cardiovascular damage in response to COVID-19 infection and also suggesting potential causal mechanisms for the development of new cardiac pathologies and/or exacerbation of underlying CVDs in infected patients. In this review, we discuss the potential underlying molecular mechanisms that drive COVID-19-mediated cardiac damage, as well as the short term and expected long-term cardiovascular ramifications of COVID-19 infection in patients.

【 授权许可】

Free