key: cord-0796245-993832jd
authors: Finsterer, Josef
title: SARS-CoV-2-associated Takotsubo is not necessarily triggered by the infection
date: 2020-07-25
journal: Int J Cardiol Heart Vasc
DOI: 10.1016/j.ijcha.2020.100606
sha: 70b4a9738d8a68841cc50e63307b3773c564ce0e
doc_id: 796245
cord_uid: 993832jd

nan

Letter to the Editor With interest we read the article by Sattar et al. about a 67 years old female with diabetes and arterial hypertension developing Takotsubo syndrome (TTS) after having been infected with SARS-CoV-2 since 2 weeks prior [1] . TTS was complicated by tachycardious atrial fibrillation requiring anticoagulation and amiodarone [1] . We have the following comments and concerns. A shortcoming of the study is that no coronary angiography had been carried out. Diagnosing TTS according to the Mayo Clinic criteria requires exclusion of coronary heart disease [2] . TTS may be complicated by heart failure [2] , ventricular arrhythmias [2] , or sudden cardiac death [3] . Why was a patient with symptomatic SARS-CoV-2 infection and TTS discharged to home isolation? Due to their increased risk to acquire cardiac complications, TTS patients require close surveillance until resolution of the dysfunction.

and myocarditis may be misdiagnosed as TTS [4] , we should know if the patient underwent cardiac MRI with contrast medium or endo-myocardial biopsy to rule out myocarditis. On cardiac MRI myocarditis may present as edema (pseudohypertrophy) [4] or contrast enhancement [4] . On endomyocardial biopsy myocarditis may present with diffuse infiltration of the myocardium with T-lymphocytes in the absence of any scars [4] . Characteristically, myocarditis in SARS-CoV-2 infected patients is virusnegative [4] . TTS is usually triggered by physical or emotional stress [5] . We should know the trigger of TTS. Which was the psychosocial stress the patient was exposed to? In case TTS was triggered by emotional stress it is not justified to suggest that the SARS-CoV-2 infection was the trigger, as indicated in the title. Double anti-thrombotic treatment (acetyl-salicylic acid (ASS) plus clopidogrel) is not a standard treatment for TTS. We should know why this regimen was chosen in the absence of symptomatic or per-symptomatic atherosclerosis. We should know if the patient received a triple therapy of ribaroxaban, ASS, and clopidogrel or if clopidogrel and ASS were replaced by rivaroxaban. If the patient received a triple therapy, its indication should be discussed. In summary, the interesting report has some shortcomings and would profit from supplementary data. Application of a triple therapy to patients with TTS should be well considered.

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