Takotsubo cardiomyopathy after midodrine therapy.

A fter 7 days of oral midodrine therapy for symptomatic idiopathic hypotension, a 74-year-old woman presented with angina at a local hospital. Her vital signs were normal, and physical examination revealed nothing unusual. Results of chest radiography, a complete blood count, and a chemistry profile, including cardiac troponin T and creatine kinase, were normal. An electrocardiogram revealed ST-segment elevation of less than 1 mm in leads II, III, and aVF. The patient was given aspirin, intravenous nitroglycerin, and heparin. Urgent coronary angiography revealed minor luminal irregularities with no evidence of plaque rupture or thrombus. Left ventriculography revealed an estimated ejection fraction of 0.40, akinesis of the mid and distal left ventricle, and normal systolic function of the basal segments (Fig. 1). Troponin T measurement was subsequently positive. The diagnosis of takotsubo cardiomyopathy was made. The patient reported no recent emotional stress or illnesses. Midodrine was suspected as the trigger of the cardiomyopathy because of its a1 agonist properties, and this therapy was discontinued. A transthoracic echocardiogram 2 weeks after the patient’s hospital discharge showed complete recovery of left ventricular systolic function.