P319 MID VENTRICULAR TAKOTSUBO SYNDROME IN A PATIENT WITH COVID 19 PNEUMONIA: A CASE REPORT

Abstract

Abstract Background Takotsubo Syndrome (TTS) is an acute and transient myocardial disfunction associated with chest pain, electrocardiographic changes and minimal myocardial enzymatic release mimicking acute myocardial infarction but without significant coronary artery disease. Physical or emotional stress play a central role in the pathogenesisof this cardiomyopathy. Several variants have been described including the classic type, reverse Takotsubo, midventricular type and focal type. Mid ventricular Takotsubo is characterized by circumferential mid–ventricular hypokinesia with hypercontractility of base and apex. This atypical variant is one of the most rare form that occurs in 15% of patients with Takotsubo syndrome. We report a Takotsubo case with mid–ventricular pattern in a postmenopausal woman with COVID–19 interstitial pneumonia. Clinical case A 56–year–old female patient was admitted to our intensive cardiac care unit for acute chest pain and dyspnea. In clinical history hypertension, dyslipidemia, anemia and schizophrenia were documented. COVID–19 molecular test was positive. CT scan showed multiple ground–glass opacities bilaterally. Hemodynamic parameters were normal but ECG showed ST–segment elevation and T waves inversion in the lateral precordial leads. Troponin–I was elevated and peaked at 1704 ng/mL. A transthoracic echocardiogram showed ballooning of the midventricular segments with hyperkinesis of the basal and apical segment. Coronary angiography showed normal coronaries. The patient was treated with beta–blockers and intravenous fluid infusion. After 10 days in hospital, echocardiography showed normalization of regional contractility and improvement of ejection fraction. The patient was discharged in good condition. Conclusions Recent studies have reported an increase in TTS incidence during the COVID–19 pandemic. SARS-CoV-2 infection induces physical and psychological stress in patients, which may lead to an increase in the risk of TTS development. The pathophysiology of COVID-19-induced TTS still remains unclear. The mortalityrate of TTS is higher (36.5%) in COVID–19 patients.