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on October 18, 2007

Stroke. 2007
Published online before print October 18, 2007, doi: 10.1161/STROKEAHA.107.483578
A more recent version of this article appeared on December 1, 2007
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Right arrow Cerebral Aneurysm, AVM, & Subarachnoid hemorrhage

Submitted on January 24, 2007
Revised on May 9, 2007
Accepted on May 14, 2007

When the Worst Headache Becomes the Worst Heartache!

Abdul Hakeem MD*; Adam D. Marks MPH; Sabha Bhatti MD; and Su Min Chang MD

From the Divisions of Cardiovascular and Internal Medicine, Department of Medicine, University of Wisconsin Hospital and Clinics, Madison, Wisc.

* To whom correspondence should be addressed. E-mail: a.hakeem{at}hosp.wisc.edu.

Background and Purpose—Although a great deal of literature has been generated regarding left ventricular wall abnormalities, ECG changes and cardiac enzyme leaks associated with subarachnoid hemorrhage (SAH), there have been only a few reports of true transient left ventricular apical ballooning syndrome in patients with SAH. Several pathophysiological mechanisms have been proposed to explain the unusual features of this syndrome, such as multivessel coronary vasospasm, abnormalities in coronary microvascular function, and catecholamine-mediated cardiotoxicity.

Summary of Case—A previously healthy 64-year-old woman with no history of vascular disease was found unresponsive at home. She was taken to the emergency room where a CT head revealed an SAH due to a ruptured aneurysm of the posterior communicating artery. On admission, an ECG showed deeply inverted T-waves and QT prolongation, typical of SAH. Cardiac troponin was measured at 1.2 ng/mL, and later increased to 3.7 ng/mL. A transthoracic echocardiogram on the next day revealed a large left ventricular wall abnormality, characteristic of apical ballooning with an ejection fraction of 25% to 30%. The patient remained hemodynamically stable and was started on low dose {beta}-blocker and angiotensin-converting enzyme inhibitor. She had an uneventful cardiac recovery within 5 days at which time a repeat transthoracic echocardiogram revealed a normal ejection fraction with no wall motion abnormality.

Conclusions—This report adds to the growing list of "stressors" for Takotsubo cardiomyopathy. Clinicians should be aware of the existence and the typical clinical manifestations of this syndrome, which is increasingly recognized in various populations. In particular, neurologists should consider this syndrome in the differential diagnosis of ECG changes and apical wall motion abnormalities in patients with SAH. Prognosis is generally very good with full recovery in most patients; however, there may be increased morbidity associated in patients with SAH.


Key words: Broken Heart Syndrome • subarachnoid hemorrhage • Takotsubo cardiomyopathy