doi: 10.1161/01.STR.0000117566.64450.DD
(Stroke. 2004;35:552.)
© 2004 American Heart Association, Inc.
Original Contributions |
Editorial Comment—Myocardial Damage in Patients With Subarachnoid Hemorrhage
Division of Cardiology, Columbia University College of Physicians & Surgeons, New York, NY
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.8–10 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 increase in plasma concentration is noted within 5 minutes after SAH induction in dogs.11 However, it is not clear if it is increased plasma catecholamine, locally released catecholamine, or both that lead to the pattern of myocardial necrosis seen in SAH patients.
In our patients, myocardial necrosis is reflected by enzyme release such as CPK-MB and troponin I. Recent studies indicate that 
40% of patients with SAH demonstrate increased serum markers for myocardial necrosis. Presumably, these are the patients in whom characteristic histological lesions are seen. However, since ECG changes in SAH are largely neurally mediated and myocardial lesions tend to be small and patchy, elevated enzymes can occur in the absence of ECG changes. On the other hand, functional testing of the heart, such as by echocardiogram, is a more accurate method to assess the effect of SAH on ventricular function, and using this method approximately 10% of patients with SAH demonstrate left ventricular (LV) wall motion abnormalities; a subset of these patients will have irreversible myocardial damage, but most regain LV function in several weeks.
The article by Tung et al12 confirms that a commonly and widely used neurological grade on admission predicts myocardial damage as measured by cardiac enzyme release. This study is notable in that it consists of a large number of consecutive patients from a single center, minimizing potential bias seen in multicenter studies. Unlike some of the previous reports, this report did not demonstrate catecholamine level to be related to the degree of cardiac enzyme release. However, the number of subjects considered for this analysis was small (50 of 233), and sample collection took place at a considerable time interval after the onset of a bleed, which will affect the catecholamine levels.
Tung et al also confirm the importance of gender in myocardial injury seen in patients with SAH. This was suggested by Mayer et al, who showed abnormal LV function to be more common in women with SAH, and by Sato et al, who demonstrated that women tended to have LV wall motion abnormalities more frequently compared with men.13,14 The reasons for this are unclear. Lambert et al demonstrated higher catecholamine spillover from cerebrospinal fluid to plasma in women after SAH, indicating that the catecholamine release may be different for men and women.15 There are also known to be differences between the autonomic nervous systems of men and women, possibly contributing to a difference in sympathetic nervous activation in women with SAH compared to men.16,17
Tung et al noted that increased heart rate and ventricular mass were independent predictors of myocardial enzyme release, suggesting that increased oxygen demand in patients with SAH is associated with myocardial damage. Additionally, phenylephrine dose was independently associated with myocardial enzyme release, suggesting that it either caused reduced oxygen delivery to the myocardial tissue or acted synergistically with existing catecholamines to increase the myocardial damage.
As indicated by Tung et al, the causal factors for myocardial damage in patients with SAH are many and include not only aspects of autonomic nervous function and the effect of catecholamines but also factors affecting myocardial oxygen demand and the effect of medications administered in the course of treatment. It is with studies such as this one by Tung et al that we hope to gain knowledge to potentially reduce mortality from cardiac causes in patients with SAH.
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11. Masuda T, Sato K, Yamamoto S, Matsuyama N, Shimohama T, Matsunaga A, Obuchi S, Shiba Y, Shimizu S, Izumi T. Sympathetic nervous activity and myocardial damage immediately after subarachnoid hemorrhage in a unique animal model. Stroke. 2002; 33: 1671–1676.
12. Tung P, Kopelnik A, Banki N, Ong K, Ko N, Lawton MT, Gress D, Drew B, Foster E, Parmley W, Zaroff J. Predictors of neurocardiogenic injury after subarachnoid hemorrhage. Stroke. 2004; 35: 548–553.
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16. Dart AM, Du XJ, Kingwell BA. Gender, sex hormones and autonomic nervous control of the cardiovascular system. Cardiovasc Res. 2002; 53: 678–687.
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