Page 101 - Cardiac abnormalities after aneurysmal subarachnoid hemorrhage

artery disease, pathological studies31, 33-35 and coronary angiography32, 36-39 have repeatedly failed to demonstrate this form of injury in such patients. In contrast to the belief that neurogenic changes on ECGs reflect purely electrical phenomena, affected patients frequently show evidence of structural cardiac damage, such as subendocardial infarctions, contraction band necrosis and myofibrillar lesions. These were first reported in the early 1960’s after acute cerebral lesions.33, 35, 40-42 Focal myocardial necrosis was seen in animals after traumatic brain injury as early as the 1970s.43 Elrifai et al.44 performed electron microscopy on the myocardium of dogs with experimental SAH. Individual myocardial cell lesions with a swollen and loose appearance were described. The myocardial fibers appeared distorted and separated. Remarkably an unusual infiltration of fibroblasts and macrophages were present, indicating some form of inflammation. Several other authors describe the same microscopic finding.
Biochemical markers of myocardial damage are also frequently elevated and enzyme release seems to be related with the severity of the neurological injury.45 We found that troponins are frequently elevated, are associated with poor outcome and that positive troponins on admission predict the occurrence of left ventricular dysfunction during admission (Chapter 4). Furthermore, in Chapter 6 we describe myocarditis after aSAH. Data on troponins were lacking in that study, however it is plausible that the source of the troponins after aSAH is caused by an aseptic, catecholamine induced myocarditis. Clinical presentation of myocarditis consists of ECG changes, left ventricular dysfunction and positive troponins and this is similar to the changes observed after aSAH. Future studies are needed to elucidate not only the incidence and prevalence of this phenomenon, but also the identification of possible clinical predictive variables of myocardial damage and treatment options.
Etiology
Innervation of the heart 7 This thesis focusses on incidence and clinical relevance of cardiac abnormalities after
aSAH, but not on pathophysiology. However, some data are available on potential
etiologic factors. As already stated in the introduction of this thesis, Cushing46 first
reported that increased intracranial pressure due to cerebral tumors might lead to a substantial increase in blood pressure, a drop in heart rate, and slow irregular respiration. This is called the Cushing reflex. The Central Nervous System, consisting of a parasympathetic and a sympathetic pathway, innervates the heart through a
General Discussion
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