946 Takotsubo Syndrome Triggered by Reflex Syncope: A Potentially Fatal Complication of a Benign Condition

Abstract

Introduction Vasovagal syncope is traditionally considered a benign condition due to parasympathetic nervous system activation. Here is a case of reflex syncopal episodes that triggered recurrent Takotsubo Syndrome (TS) with life–threatening presentation. Report of a Case A 71-year-old female presented to the Emergency Department (ED) complaining with dyspnoea and chest pain developed half an hour after a vasovagal syncope. Her past medical history was consistent with arterial hypertension, dyslipidaemia, and well-tolerated reflex syncopal episodes since she was a child. At hospital admission, a 12-leads ECG showed T-wave inversion in anterior leads while transthoracic echocardiogram (TTE) showed hypokinesia of the mid-apical segments, reduced left ventricular ejection fraction (LVEF) [40%], and severe mitral regurgitation (MR). Blood tests revealed increased hs-troponin I values [peak value: 1500 ng/L]. A coronary angiography (CA) was thus performed in the suspect of NSTEMI, showing non obstructive coronary disease. A diagnosis of TS was eventually made with ECG normalisation and resolution of echocardiographic abnormalities at 6 month follow-up. Five years later, the patients presented to the ED because of a new syncopal episode followed by severe pulmonary oedema. Since the presence of electrocardiographic T-wave inversion, apical segments akinesia and elevated hs-troponin I were consistent with NSTEMI, a CA was performed revealing (again!) normal coronary vessels. A suspect of TS relapse was thus made. Three months after discharge, ECG and echocardiogram were normal and a syncope diagnostic work–up was suggested. A 24/h ambulatory blood pressure monitoring demonstrated normal pressure values and a tilt test confirmed the well-established history of reflex syncope showing a remarkable cardioinhibitory response. A pacemaker implant was thus indicated. Discussion TS is a heart syndrome characterized by transient contractile dysfunction historically related to catecholamine activation of alpha and beta receptors. While sympathetic system involvement in the development of TS is clearly established, new evidence is emerging about the vagal role in the etiopathogenesis of the disease. Although syncopal episodes could be related to TS, because of LVOT obstruction or major arrhythmias, according to our experience, TS may be triggered by vagal hypertonus [i.e., after vasovagal syncopal episodes]. In similar situation, the implantation of a pace-maker could be considered to prevent future dangerous complications related to recurrent reflex syncope even if well tolerated by the patients. Conclusion In our experience, recurrent episodes of TS appeared triggered by reflex syncope. A condition traditionally considered benign may instead have life-threatening consequences. Moreover, the role of parasympathetic and vagal tone in the development of TS needs further investigation that may lead to the design of new strategies of clinical diagnosis and management.