Substance abuse—or more likely, its abrupt cessation—was a likely trigger for an unusual cardiac syndrome. A 25-year-old woman was brought to the emergency department from home after a seizure episode. En route to the hospital, the patient lost consciousness, and the emergency medical team discovered that she was in torsades de pointes, which then progressed to ventricular fibrillation. The patient was defibrillated to sinus tachycardia with a monophasic waveform shock of 360 J. She was successfully resuscitated, regained consciousness, and denied any chest pain or shortness of breath. On further questioning, she denied any past history of arrhythmia or family history of sudden cardiac arrest or unexplained death.
Assessment
The patient admitted to daily heavy alcohol consumption, and 3 days before hospitalization, she had used cocaine. Her potassium and magnesium levels on admission were 3.2 mEq/L and 1.4 mg/dL, respectively. An electrocardiogram (ECG) performed 3 hours after resuscitation revealed a narrow complex sinus tachycardia with deep, inverted T waves in leads II, III, AVF, and V3-V6, and a remarkably prolonged QTc interval of more than 660 msec (Figure 1). She was not taking any medications known to prolong the QT interval.
Serial cardiac enzymes remained within the normal range. A chest X-ray and computed tomography of the head were normal. However, a transthoracic echocardiogram disclosed an anteroapical regional wall motion abnormality and a reduced left-ventricular ejection fraction of 35-40%. Coronary angiography was normal. Left ventriculography showed basal hyperkinesis with apical ballooning, a finding consistent with takotsubo cardiomyopathy. The condition also is known as stress cardiomyopathy, because it can be induced by short-term emotional or physiologic stress.
Diagnosis
Our patient’s diagnosis of takotsubo cardiomyopathy was based on the following criteria: transient hypokinesis, akinesis, or dyskinesis of the left ventricular apical and mid-ventricular segments; absence of obstructive coronary artery disease; ECG changes, either ST-segment elevation and/or T-wave inversion; and absence of head trauma, intracranial bleeding, pheochromocytoma, hypertrophic obstructive cardiomyopathy, or myocarditis.(1, 2)
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— Nishant Kalra, MD, Prashant Khetpal, MD, MPH, Vincent L. Sorrell, MD
This article was originally published in the August 2009 issue of The American Journal of Medicine.
