Page 88 - Cardiac abnormalities after aneurysmal subarachnoid hemorrhage

Chapter 6
one control patient. Sensitivity analyses showed no difference in the number of inflammatory cells or myocytolysis in patients with- or without proven aneurysm.
Discussion
In the present autopsy study we documented an influx of neutrophil granulocytes, lymphocytes and macrophages into the myocardium of patients who died following SAH. In some this coincided with myocytolysis and thrombi in intramyocardial arteries. According to the Dallas criteria this finding suggests that patients with SAH have a borderline myocarditis and some have a myocarditis.
Although other studies have reported on myocardial cellular infiltration and myocytolysis after SAH, classification of the inflammatory cells is not described before and we could not find previous studies establishing myocarditis after SAH. Most studies focused on the myocardial cell damage after SAH, only a few studies used immunohistochemical staining methods which were not specific for the type of cell.
There is overwhelming evidence from clinical and experimental studies that catecholaminergic stress after acute cerebral lesions causes myocardial cell damage.3, 9-16 However, influx of inflammatory cells in the myocardium was not investigated. Intramyocardial catecholamine release by sympathetic nerve endings has been suggested as the primary source of the catecholamines, since experimental SAH studies showed no myocardial damage following SAH in sympathectomized baboons, while extensive myocardial damage was documented in adrenalectomized dogs.17 This hypothesis is supported by the finding that cardiomyocytolysis after SAH is more prevalent in the direct surrounding of the sympathetic nerve terminals.18
We found evidence of thrombi in the intramyocardial arteries. It is known that
myocarditis may cause vasospasm which may cause the formation of thrombi.
Thrombi might cause obstruction of the microarteries thus causing myocardial
infarction.19, 20 Several other studies reported patchy subendocardial infarction after
SAH, suggesting that thrombi, and likely myocarditis, were present in these cases as well.6, 12, 21
The clinical relevance of our study is that treatment of cardiac abnormalities after SAH may improve outcome as they are associated with poor outcome independent of other clinical parameters.22 Our finding that myocarditis with microvascular thrombosis occurs in patients who die from SAH, has some potential clinical
86