to the editor: Takotsubo cardiomyopathy (also known as stress-induced cardiomyopathy or broken heart syndrome) is a transient condition that occurs most commonly in older women and is triggered by intense emotional or physical stress. It is characterized by transient akinesis or dyskinesis of the apical and midventricular segments of the left ventricle in association with regional wall motion abnormalities.

A 74-year-old black woman with a history of hypertension presented with complaints of weakness and chest pain a few days after the death of her husband whom she had been married to for 35 years. Her examination revealed a blood pressure of 186/88 mm Hg and tachycardia. Electrocardiography (ECG) showed ST-segment elevation in leads V₃ through V₆, and deep T-wave inversions in leads V₃ through V₆ and in leads II, III, and aVF. Cardiac enzyme levels were normal. Cardiac catheterization showed no coronary artery stenosis. However, left ventriculography showed apical ballooning in diastole and systole. Echocardiography showed an ejection fraction of 25 percent and ballooning of the left ventricle. The shape of the ventricle resembled that of an octopus trap (called “tako-tsubo” in Japanese), confirming the diagnosis of Takotsubo cardiomyopathy. The patient was treated with beta blockers, angiotensin-converting enzyme (ACE) inhibitors, and aspirin. Two weeks later, repeat echocardiography showed a normal ejection fraction and normal shape of the left ventricle. ECG showed complete resolution of the ST-segment elevation and absence of Q-wave formation.

Takotsubo cardiomyopathy is an increasingly reported syndrome characterized by reversible ballooning of the left ventricular apex in the absence of significant coronary artery disease. The clinical presentation is similar to myocardial ischemia with ECG changes of ST elevation and T-wave inversion but normal coronary angiography. The exact pathology is unclear, but a role for the sympathetic nervous system has been proposed. Management involves a combination of drugs that improve left ventricular systolic dysfunction (e.g., beta blockers, ACE inhibitors, diuretics), as necessary for volume overload. Because this condition is transient, long-term treatment is not required. The prognosis is good with complete left ventricular systolic function recovery typically occurring within weeks.^1–3