Apical Ballooning (Takotsubo Cardiomyopathy) in Mid-Ventricular Obstructive Hypertrophic Cardiomyopathy: A case report

Abstract Background The conventional view holds that left ventricular (LV) apical ballooning due to stress cardiomyopathy is caused by a hyperadrenergic state related to emotional or physical stress. However, some suggest ballooning also occurs in obstructive hypertrophic cardiomyopathy (HCM) when latent obstruction becomes severe. Nearly all cases of apical ballooning in HCM were reported in patients with LV outflow tract obstruction. Herein, we present a case due to mid-ventricular obstruction. Case Summary A 52 year old woman presented with dyspnea and chest pain. She denied any recent emotional or physical stress. Physical examination was notable for a grade 2/6 systolic murmur along the left sternal border. The peak high sensitivity troponin level was 315 ng/l (normal 6 ng/l). Coronary angiography was unremarkable. Echocardiography revealed LV apical ballooning with severely reduced LV ejection fraction. In addition, there was severe septal hypertrophy with mid-cavity obstruction. Continuous wave Doppler interrogation across the obstruction revealed a bifid (“lobster claw”) configuration with a characteristic abrupt early systolic drop in flow velocity. The patient was treated with beta-blockers. Follow-up examination revealed resolution of apical ballooning. Discussion Apical ballooning in our patient with HCM we believe resulted from severe afterload mismatch (produced by mid-cavity obstruction) and supply-demand ischemia, as well as the limited contractile reserve that characterizes myopathic muscle. This is supported by the rapid decline in early systolic flow velocity seen with Doppler interrogation (lobster claw configuration) across the obstruction.