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Covid-19: A Double Threat to Takotsubo Cardiomyopathy and Spontaneous Coronary Artery Dissection? Publisher Pubmed



Shojaei F1 ; Habibi Z2 ; Goudarzi S1 ; Firouzabadi FD3 ; Montazerin SM1 ; Najafi H1 ; Kahe F1 ; Momenzadeh K4 ; Mir M1 ; Khan F5 ; Jamil U6 ; Jamil A6 ; Lee JJ7 ; Chi G1
Authors
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Authors Affiliations
  1. 1. Division of Cardiovascular Medicine, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States
  2. 2. Global Studies Institute, Universite de Geneve, Geneva, Switzerland
  3. 3. Endocrinology and Metabolism Research Center, Vali-Asr Hospital, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  4. 4. Department of Orthopedic Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, 02215, MA, United States
  5. 5. Division of Cardiology, Department of Medicine, University of Nebraska Medical Center, Omaha, NE, United States
  6. 6. Department of Medicine, OSF Healthcare, St. Francis Medical Center, Peoria, IL, United States
  7. 7. Baim Institute for Clinical Research, Boston, MA, United States

Source: Medical Hypotheses Published:2021


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. © 2020 Elsevier Ltd