Abstract
In order to clarify the pathogenesis of electrocardiographic changes in cerebrovascular accidents, the electrocardiograms and laboratory data before and after the stroke were compared in 18 autopsy proven intracranial hemorrhages and in 29 cerebral infarctions of the aged. Coronary stenosis and sites as well as sizes of cerebral lesions were also investigated in each group.
The electrocardiographic changes after the stroke were observed in 88.9% of intracranial hemorrhages and 89.7% of cerebral infarctions. The ST-T changes were found in 61.0% and in 69.0% respectively, the severe ischemic changes being of high incidence in cerebral infarction. Various arrhythmias were found in 55.6% in intracranial hemorrhage and in 41.4% in cerebral infarction. Appearance of atrial fibrillation on storke was exclusively observed in cerebral infarction, in 10.3%. The extrasystoles were frequently seen in intracranial hemorrhage, supraventricular origin in 22.1%, and ventricular origin in 11.1%, while the extrasystoles were seen in cerebral infarction in 10.3% and in 3.4% respectively.
Significant increase in hematocrit was observed in stroke and the elevation was more prominent in cerebral infarction; in cases with ischemic ST-T changes the increase being by 2.44±0.56% in intracranial hemorrhage and by 6.04±1.74% in cerebral infarction. This suggested that the ischemic ST-T changes were attributable to the elevation of hematocrit which induced the disturbance in coronary microcirculation.
The systolic blood pressure increased by 52.5±8.9mmHg in intracranial hemorrhage, and blood pressure reached over 200mmHg regardless of the pattern of the electrocardiographic changes. The cerebral infarction revealed small increase in systolic blood pressure by 8.7±10.4mmHg, indicating that the elevation of blood pressure per se could not be the cause of the electrocardiographic changes.
The severity of the coronary stenosis was similar in various types of electrocardiographic changes in both cerebral hemorrhage and infarction. This indicated that the ischemic ST-T changes were not derivied from the stenosis of the large coronary arteries. The myocardial infarction was associated in intracranial hemorrhage by 5.6%, while this association was 50.0% in cerebral infarction.
The ischemic ST-T changes were relatively frequent in lateral type of cerebral hemorrhage, while the infarction of medial cerebral artery revealed various types of electrocardiographic changes. The sizes of cerebral lesions showed no relations to the ischemic ST-T changes.
The ischemic ST-T changes observed in intracranial hemorrhage and infarction were probably induced by the elevation of hematocrit which led to the disturbance of coronary microcirculation. The site and size of cerebral lesions, coronary stenosis, elevation of blood pressure failed to correlated with the electrocardiographic changes.
