Letter by Finsterer Regarding Article, “COVID-19-Associated Stress (Takotsubo) Cardiomyopathy”

Abstract

HomeCirculation: Cardiovascular ImagingVol. 13, No. 10Letter by Finsterer Regarding Article, “COVID-19-Associated Stress (Takotsubo) Cardiomyopathy” Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBLetter by Finsterer Regarding Article, “COVID-19-Associated Stress (Takotsubo) Cardiomyopathy” Josef Finsterer, MD, PhD Josef FinstererJosef Finsterer https://orcid.org/0000-0003-2839-7305 Klinikum Landstrasse, Messerli Institute, Vienna, Austria. Search for more papers by this author Originally published23 Sep 2020https://doi.org/10.1161/CIRCIMAGING.120.011577Circulation: Cardiovascular Imaging. 2020;13:e011577To the Editor:With interest we read the article by Tsao et al1 about a 59-year-old obese but otherwise healthy woman who experienced a severe infection with severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) manifesting as coronavirus disease 2019 (COVID-19) and complicated by the development of Takotsubo syndrome (TTS), also known as stress cardiomyopathy or broken-heart syndrome. The patient recovered from TTS despite the severe COVID-19 infection.1 We have the following comments and concerns.We do not agree with the notion that “TTS associated with COVID-19 has not been well described.”1 A literature search brought to light that at least 37 cases with TTS in the setting of an acute SARS-CoV-2 infection, including the index case, have been reported. The first patient with TTS triggered by a SARS-CoV-2 infection was an 83-year-old Swiss woman described by Meyer et al.2 She had a history of arterial hypertension and developed acute chest pain together with dry cough 3 days before admission.2 Transthoracic echocardiography revealed apical ballooning with hyperkinetic basal segments.2 On hospital day 3, she was tested positive for SARS-CoV-2. She recovered completely within 10 days upon conventional heart failure therapy.2 The most recently presented case was published by Sattar et al.3In the vast majority of the patients with SARS-CoV-2 associated TTS, TTS developed after onset of the SARS-CoV-2 infection. Age ranged between 39 and 87 years. The distribution between genders was almost equal, and the majority of patients presented with the classical type of TTS. Only 2 patients each presented with the midventricular, respectively, basal type of TTS. Treatment for TTS was quite variable, but most patients received β-blockers, diuretics, heparin, or acetyl-salicylic acid. Ten patients recovered; 3 patients died; and in 20 patients, the outcome was not reported.Since the infection with SARS-CoV-2 may go along with myocarditis4 and myocarditis may be misinterpreted as TTS,4 we should know how myocarditis was ruled in the index patient. Particularly, we should know whether the patient underwent cardiac magnetic resonance imaging with contrast medium or endomyocardial biopsy to see whether there was myocardial inflammation or not. Myocarditis on cardiac magnetic resonance imaging may show up as edema (pseudohypertrophy)4 or enhancement with contrast medium.4 Acute myocarditis on endomyocardial biopsy may show up as diffuse infiltration of the myocardium with T lymphocytes in the absence of any scars.4 Myocarditis in SARS-CoV-2–infected patients is usually virus negative but characterized by T-cell infiltration.4Interestingly, the prevalence of TTS generally increased during the COVID-19 crisis.5 The median length of hospitalization of these patients was longer than that during the non-COVID period.5 However, mortality and rehospitalization rate were the same as that before the crisis.5In summary, TTS is a well-recognized complication of COVID-19. Clinical presentation, epidemiology, treatment, and outcome of SARS-CoV-2–associated TTS are similar to COVID-19–unrelated TTS. Workup for TTS in patients with COVID-19 is indicated if they develop symptoms and signs of a myocardial infarction or heart failure in addition to the pulmonary compromise.AcknowledgmentsDr Finsterer contributed to the design, literature search, discussion, first draft, and critical comments.DisclosuresNone.FootnotesThe opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.