Focal Myocardial Necrosis in Cases of Increased Intracranial Pressure

Abstract

Small areas of myocardial necrosis were found in 36 of 100 patients dying secondary to central nervous system disease, such as subarachnoid hemorrhage, parenchymal intracerebral hemorrhage, encephalomalacia, and various brain tumors. The myocardial lesions were observed with increasing frequency in the following disorders: subarachnoid hemorrhage, parenchymal intracerebral hemorrhage, encephalomalacia, and brain tumors. The main factor in the pathogenesis of these myocardial lesions appears to represent neurohumoral mechanisms with a hyperactivity of the sympathetic nervous system. These findings may be important for human cardiac transplantation.

Use of the peak troponin value to differentiate myocardial infarction from reversible neurogenic left ventricular dysfunction associated with aneurysmal subarachnoid hemorrhage

“…7,34,36,65 Focal areas of myofibrillar and fuchsinophilic degeneration are also noted in the subendocardium of the left ventricle. 13,27,29 It has previously been demonstrated that more severe grades of SAH are associated with cTn elevations, and a cTn leak in this setting may be associated with myocardial dysfunction. 51 Ay,et al,4 demonstrated that CK-MB but not cTn is elevated following stroke and they suggested that elevated CK-MB combined with normal levels of cTnT may not be a biological marker for myocytolysis.…”

Sympathetic Nervous Activity and Myocardial Damage Immediately After Subarachnoid Hemorrhage in a Unique Animal Model

“…6 Recently, some clinical studies have shown wall motion abnormalities of the left ventricle that developed in the acute phase of SAH, and myocytolysis or contraction band of the myocardium was observed at the autopsy of those patients. [7][8][9] Although several investigators have suggested that myocardial dysfunction associated with pathological damage is related to the development of ECG abnormalities and pulmonary edema in patients with SAH, 10 the precise mechanisms underlying myocardial damage, presenting as a complication of SAH, are still unknown.…”

Improvement of hypoxia during early surgery for ruptured intracranial aneurysm: a retrospective evaluation

“…Although the cause of hypoxia is unclear, neurogenic pulmonary edema (NPE) is one of the conditions related to hypoxia. The following are considered to be possible causes of NPE: pulmonary capillary hyperpermeability neurally evoked by a disorder of the central nervous system and/or elevation of intracranial pressure [6][7][8], hydrostatic pulmonary edema evoked by centralization of the circulatory blood after release of large amounts of cathecolamines [8][9][10], and cardiogenic pulmonary edema caused by myocardial impairment as a result of release of large amounts of cathecolamines [11]. Although hypoxia tends to occur more in comatose patients than in conscious patients, we occasionally see hypoxia in patients with relatively good consciousness [12], as described in this study.…”