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Myocardial Ischemia and Necrosis in Patients with Cerebral Infarction

Jesper Khédri Jensen


For the past 60 years electrocardiographic evidence of myocardial ischemia has been reported in patients with stroke. In addition, different cardiac markers have been found elevated in patients with stroke. The majority of the earlier studies have been in patients with intracranial haemorrhages, which only account for approximately 15% of stroke cases. The aetiology of the majority of stroke cases (ischemic stroke) is arteriosclerosis. In addition, cardiovascular mortality is dominating the long-term follow-up in this type of patients. The purpose of this thesis was to identify the prevalence of ischemia-like electrocardiographic changes and myocardial necrosis during an acute ischemic stroke.of TnT.

A total of 250 consecutive patients admitted with the diagnosis of a definite acute ischemic stroke and no evidence of prior or present ischemic heart disease were included. All patients were clinically evaluated and a structured interview was conducted. Additionally, all patients had serial 12-lead resting ECGs obtained on a daily basis during the first 6 days of the ischemic stroke. Furthermore, cardiac biomarkers of troponin T, CK-MB and NT-proBNP were obtained. Two days after admission 24-hour Holter ST-segment monitoring was performed. Myocardial perfusion scintigraphy was performed in patients with TnT levels =0.10 μg/L and in comparable control patients without elevation of TnT.

The prevalence of ischemia-like ECG changes (ST-T changes) was 15% and in the majority of the patients the changes appeared 2 to 3 days after admission. No differences in stroke severity or localisation between patients with or without the ECG changes were found. The ST-T changes did not appear to be associated with an adverse short-term clinical outcome. The prevalence of the ST-T changes did not seem to be different from what would be expected in the general population. Elevated levels of troponin T (>0.03 μg/L) and CK-MB (=10 μg/L) were observed in 10 % and 9% of the patients, respectively. The probable cause of troponin elevation was most frequently heart- and/or renal failure. Only a minority (3%) were identified with an acute silent myocardial infarction. The patients with elevated troponin T levels were older and the stroke was more severe. Perfusion abnormalities during at rest myocardial perfusion imaging were not more frequent or pronounced in patients with levels of TnT =0.10 μg/L than in the control group. In addition, the highest concentrations of troponin and CK-MB were observed initially suggesting that the patients might have had a silent myocardial infarction in the days before the cerebrovascular event.When present, elevation of troponin T seems to be useful in identifying patients who are at increased risk of dying. NT-proBNP seems to be released during an acute ischemic stroke with a peak concentration the day after onset of symptoms. The variation of the marker is considerable, but it seems that a single measurement in the acute phase is sufficient to identify patients with increased short term mortality. Patients with evidence of myocardial ischemia in their resting 12-lead ECG or during Holter monitoring had higher levels of NT-proBNP than those without. This observation might indicate that the ECG changes represent true myocardial ischemia.

Based on the data from our study, it seems that the heart is not damaged by an acute ischemic stroke. Our observations indicate that when cardiac involvement occurs the underlying mechanism is probably not neuro-mediated. Well-known causes such as heart- and renal failure are much more likely explanations. However, recognition of myocardial damage in acute ischemic stroke patients is important, because it is associated with an impaired prognosis.