COVID-19: A double threat to takotsubo cardiomyopathy and spontaneous coronary artery dissection?. (January 2021)

• Record Type: Journal Article
• Authors: Shojaei, Fahimehalsadat; Habibi, Zahra; Goudarzi, Sogand; Firouzabadi, Fatemeh Dehghani; Montazerin, Sahar Memar; Najafi, Homa; Kahe, Farima; Momenzadeh, Kaveh; Mir, Mahshid; Khan, Faris; Jamil, Umer; Jamil, Adeel; Lee, Jane J.; Chi, Gerald
• Is Part Of: Medical hypotheses. Volume 146(2021)
• Publication Date: 2021-01
• Subjects: ACS acute coronary syndrome -- COVID-19 coronavirus disease 2019 -- SCAD spontaneous coronary artery dissection -- TTC takotsubo cardiomyopathy; COVID-19 -- Takotsubo cardiomyopathy -- Spontaneous coronary artery dissection -- Stress cardiomyopathy -- Acute coronary syndrome; Medicine -- Periodicals; Medicine -- Periodicals; Médecine -- Périodiques; Medicine; Periodicals; 610
• DOI: 10.1016/j.mehy.2020.110410
• Languages: English
• ISSNs: 0306-9877

Abstract

Abstract: Coronavirus disease 2019 (COVID-19) is an ongoing pandemic that has affected millions of individuals worldwide. Prior studies suggest that COVID-19 may be associated with an increased risk for various cardiovascular disorders, such as myocardial injury, arrhythmia, acute coronary syndrome, and venous thromboembolism. Early reports of non-COVID-19 patients have described the concurrence of takotsubo cardiomyopathy (TTC) and spontaneous coronary artery dissection (SCAD). However, the interplay between COVID-19, TTC and SCAD has not been well established. We herein propose two sets of two-hit hypotheses for the development of SCAD and TTC in the context of COVID-19. The first two-hit hypothesis explains the development of SCAD, in which TTC-associated formation of vulnerable coronary substrate serves as the first hit (predisposing factor), and COVID-19-associated inflammation and vascular disruption serves as the second hit (precipitating factor). The second two-hit hypothesis is proposed to explain the development of TTC, in which SCAD-associated formation of vulnerable myocardial substrate serves as the first hit, and COVID-19-associated sympathetic overactivity serves as the second hit. Under this conceptual framework, COVID-19 poses a double threat for the development of SCAD (among patients with underlying TTC) as well as TTC (among patients with underlying SCAD), thereby forming a reciprocal causation. This hypothesis provides a rationale for the joint assessment of TTC and SCAD in COVID-19 patients with pertinent cardiovascular manifestations.