Page 83 - Cardiac abnormalities after aneurysmal subarachnoid hemorrhage

Myocarditis in patients with subarachnoid hemorrhage: a histopathological study
Introduction
Cardiac dysfunction following subarachnoid hemorrhage (SAH), such as ECG changes, wall motion abnormalities and troponin release, occurs frequently and is associated with poor prognosis.1 The massive sympathetic activation following the SAH leads to a catecholamine release in the myocardium which is thought to cause these cardiac abnormalities.2 On a cellular level, catecholamine release has been associated with myocardial damage.2-6 Literature is limited and early pathology studies that reported on myocardial cellular infiltration and myocytolysis following SAH, using immunohistochemical staining7 , did not classify the inflammatory response nor did they specify the types of inflammatory cells in the heart. According to the Dallas criteria, myocardial infiltration of inflammatory cells and myocytolysis qualifies as a myocarditis.8 Myocarditis after SAH has never been established but is a plausible explanation in the pathway from catecholamine release; it may explain the cardiac abnormalities and may have important clinical implications for treatment and prognosis. Therefore, the objectives of the present study were to characterize the infiltration of inflammatory cells in the heart after SAH compared to controls, to investigate whether this cellular infiltration meets criteria for the diagnosis myocarditis and to search for other myocarditis stigmata such as myocytolysis and intra-arterial thrombi.
Methods
Patients’ Selection 6 Myocardium of patients who died from SAH between 1994 and 2004 was obtained
from the departments of Pathology of the VU University Medical Center Amsterdam,
the Netherlands and the Erasmus Medical Center Rotterdam, the Netherlands. The
pathology databases were searched for cases in which SAH was documented as cause of death, as indicated by the clinician requesting autopsy, in concomitance with the presence of subarachnoid blood documented in the autopsy report. As a control group, myocardium of oncologic patients without cardiac involvement of the disease whom did not receive cardiotoxic chemotherapy or radiotherapy in the cardiac region was obtained. Control patients who died from a neurological disease or potentially suffered from an underlying disease associated with cardiac inflammation, e.g. sepsis, were excluded. The study was approved by and performed according to the guidelines
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