Takotsubo Syndrome Presenting as MINOCA in a Patient with Hypertrophic Cardiomyopathy and Pre-Existing Advanced Conduction Disease: Diagnostic and Therapeutic Challenges
DOI:
https://doi.org/10.18502/rhythm.v21i4.23097Keywords:
Takotsubo Syndrome (TTS); Hypertrophic Cardiomyopathy (HCM); Atrioventricular Block; Left Ventricular Outflow Tract ObstructionAbstract
Background: Takotsubo syndrome (TTS) may mimic acute myocardial infarction and occasionally occurs in patients with hypertrophic cardiomyopathy (HCM), creating important diagnostic and therapeutic challenges.
Case Summary: A 76-year-old man with diabetes mellitus, hypertension, smoking history, HCM, and prior coronary angioplasty presented with chest pain and anterior ST-segment elevation. Transthoracic echocardiography demonstrated severe left ventricular systolic dysfunction with apical hypokinesia, whereas coronary angiography showed no obstructive culprit lesion, consistent with myocardial infarction with non-obstructive coronary arteries (MINOCA). During hospitalization, the patient developed worsening dyspnea, tachycardia, and hypotension. Repeat echocardiography demonstrated persistent severe left ventricular dysfunction and hypertrophy of the mid-anteroseptal wall suggestive of dynamic obstructive physiology in the setting of HCM. Because β-blocker therapy was considered necessary for hemodynamic stabilization in a patient with previously documented high-grade atrioventricular block and bifascicular block, a temporary transvenous pacemaker was implanted before initiation of β-blockade. Cardiac magnetic resonance imaging demonstrated extensive apical edema with limited late gadolinium enhancement, supporting TTS rather than ischemic myocardial infarction or myocarditis superimposed on underlying HCM. Owing to preexisting conduction disease, the patient ultimately underwent implantable cardioverter-defibrillator placement. One month later, complete recovery of ventricular systolic function was observed.
Discussion: This case highlights the complex interaction between TTS and HCM and emphasizes the importance of distinguishing preexisting conduction disease from arrhythmias directly attributable to TTS.