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(Stroke. 2004;35:552.)
© 2004 American Heart Association, Inc.
Original Contributions |
Division of Cardiology, Columbia University College of Physicians & Surgeons, New York, NY
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Cardiac effects of intracranial hemorrhage were initially described in 1903 by Cushing, who noted alterations in blood pressure and cardiac rhythm in such patients.1 However, since ECG was not available at that time, it was not until 1947 that Byer et al described ECG changes in a patient with subarachnoid hemorrhage (SAH).2 Later, a series of experiments described the effect of hypothalamic stimulation on ECG morphology and rhythm indicating that myocardial damage need not be present for ECG changes to occur.3,4 Indeed, some form of ECG changes are noted in almost all patients with SAH.5 Up to 10% of the patients with SAH are noted to have a potentially lethal arrhythmia such as ventricular tachycardia and fibrillation, and it has been suggested that this may account for some of the mortality in patients not reaching medical care with SAH.
A series of autopsy studies in patients with SAH demonstrated petechial subendocardial hemorrhage, and histologically, myocardial cell cytoplasm with dense eosinophilic transverse bands.6,7 This occurred not only in patients with SAH with ECG changes but also in those without such changes. Similar lesions could be created in experimental animals by stimulation of the stellate ganglion and infusion of catecholamines, and clinically this was seen in patients with a pheochromocytoma.810 Such evidence suggests that myocardial damage in patients with SAH is likely an effect of increased catecholamines on the myocardial cells rather than due to preexisting coronary artery disease. Increase in catecholamine level can be significant, and experimentally up to a 30-fold
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