Importance The coronavirus disease 2019 (COVID-19) pandemic has resulted in severe psychological, social, and economic stress in people’s lives. It is not known whether the stress of the pandemic is associated with an increase in the incidence of stress cardiomyopathy. Objective To determine the incidence and outcomes of stress cardiomyopathy during the COVID-19 pandemic compared with before the pandemic. Design, Setting, and Participants This retrospective cohort study at cardiac catheterization laboratories with primary percutaneous coronary intervention capability at 2 hospitals in the Cleveland Clinic health system in Northeast Ohio examined the incidence of stress cardiomyopathy (also known asTakotsubo syndrome) in patients presenting with acute coronary syndrome who underwent coronary arteriography. Patients presenting during the COVID-19 pandemic, between March 1 and April 30, 2020, were compared with 4 control groups of patients with acute coronary syndrome presenting prior to the pandemic across 4 distinct timelines: March to April 2018, January to February 2019, March to April 2019, and January to February 2020. Data were analyzed in May 2020. Exposures Patients were divided into 5 groups based on the date of their clinical presentation in relation to the COVID-19 pandemic. Main Outcomes and Measures Incidence of stress cardiomyopathy. Results Among 1914 patient presenting with acute coronary syndrome, 1656 patients (median [interquartile range] age, 67 [59-74]; 1094 [66.1%] men) presented during the pre–COVID-19 period (390 patients in March-April 2018, 309 patients in January-February 2019, 679 patients in March-April 2019, and 278 patients in January-February 2020), and 258 patients (median [interquartile range] age, 67 [57-75]; 175 [67.8%] men) presented during the COVID-19 pandemic period (ie, March-April 2020). There was a significant increase in the incidence of stress cardiomyopathy during the COVID-19 period, with a total of 20 patients with stress cardiomyopathy (incidence proportion, 7.8%), compared with prepandemic timelines, which ranged from 5 to 12 patients with stress cardiomyopathy (incidence proportion range, 1.5%-1.8%). The rate ratio comparing the COVID-19 pandemic period to the combined prepandemic period was 4.58 (95% CI, 4.11-5.11;P  Conclusions and Relevance This study found that there was a significant increase in the incidence of stress cardiomyopathy during the COVID-19 pandemic when compared with prepandemic periods.

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Incidence of Stress Cardiomyopathy During the Coronavirus Disease 2019 Pandemic.

The initial mechanism for severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection is the binding of the virus to the membrane-bound form of ACE2, which is mainly expressed in the lung. Since the heart and the vessels also express ACE2, they both could become targets of the virus. However, at present the extent and importance of this potential involvement are unknown. Cardiac troponin levels are significantly higher in patients with more severe infections, patients admitted to intensive care units or in those who have died. In the setting of COVID-19, myocardial injury, defined by an increased troponin level, occurs especially due to non-ischaemic myocardial processes, including severe respiratory infection with hypoxia, sepsis, systemic inflammation, pulmonary thrombosis and embolism, cardiac adrenergic hyperstimulation during cytokine storm syndrome, and myocarditis. At present, there are limited reports on definite diagnosis of myocarditis caused by SARS-CoV-2 in humans and limited demonstration of the virus in the myocardium. In conclusion, although the heart and the vessels are potential targets in COVID-19, there is currently limited evidence on the direct infection of the myocardium by SARS-CoV-2. Additional pathological studies and autopsy series will be very helpful to clarify the potentiality of COVID-19 to directly infect the myocardium and cause myocarditis.

https://heart.bmj.com/content/heartjnl/106/15/1127.full.pdf

COVID-19 pandemic and troponin: indirect myocardial injury, myocardial inflammation or myocarditis?

Systematic review of COVID-19 related myocarditis: Insights on management and outcome.

Cardiovascular Implications of the COVID-19 Pandemic: A Global Perspective.

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is now a global pandemic with the highest number of affected individuals in the modern era. Not only is the infection inflicting significant morbidity and mortality, but there has also been a significant strain to the health care system and the economy. COVID-19 typically presents as viral pneumonia, occasionally leading to acute respiratory distress syndrome (ARDS) and death. However, emerging evidence suggests that it has a significant impact on the cardiovascular (CV) system by direct myocardial damage, severe systemic inflammatory response, hypoxia, right heart strain secondary to ARDS and lung injury, and plaque rupture secondary to inflammation. Primary cardiac manifestations include acute myocarditis, myocardial infarction, arrhythmia, and abnormal clotting. Several consensus documents have been released to help manage CV disease during this pandemic. In this review, we summarize key cardiac manifestations, their management, and future implications.

/pdf/covid-19-pandemic-cardiovascular-complications-and-future-47znstqbbz.pdf

COVID-19 Pandemic: Cardiovascular Complications and Future Implications.

A 67-year-old woman presented with upper respiratory symptoms and was diagnosed with coronavirus disease-2019 (COVID-19). She was found to have a large hemorrhagic pericardial effusion wit...

Penny L D'Souza

Papers

Cardiac Tamponade Secondary to COVID-19.