الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Stroke remains a major cause of human mortality and morbidity. Cardiovascular and cerebrovascular diseases appear to be very frequently encountered now and responsible for great deal of morbidity. Inspite of our increasing understanding of the pathophysiology and epidemiology of cardiovascular diseases and stroke and continuing advances in diagnosis, prevention and treatment, the burden of the above said diseases is high.
Neurogenic influence on the heart is a newly well-known phenomenon with pathological proof of myocytolysis and electrophysiological proof of cardiac conduction abnormalities.
Although the etiology of increased troponin T in the setting of acute cerebro-vascular stroke has not been entirely elucidated, current research supports an exaggerated catecholamine release (likely originating in the right insular cortex as a result of increase intracranial pressure) leading to excessive release of intracellular calcium ions and subsequent reversible myocyte dysfunction. An alternate explanation is that the catecholamine surge acts as an uncontrolled severe myocardial stress test, which essentially reveals stable coronary plaques.
Biochemical markers especially troponins have recognized to play a successful role in diagnosis, risk stratification, prognostic values and guidance of treatment for cardiac complications of cerebral stroke.
The aim of the present work is to assess the level of troponin T in sera of acute stroke patients and its relation with stroke severity.
The study was carried out on two equal groups:
Group A: Included 25 patients presented with acute hemorrhagic cerebro-vascular stroke. They were subdivided as regard the serum troponin-T level into group A1 and group A2. Group A1 included acute hemorrhagic stroke patients with normal serum troponin-T. Group A2 included acute hemorrhagic stroke patients with elevated serum troponin-T.
Group B: Included 25 patients presented with acute ischemic cerebro-vascular stroke. They were subdivided as regard the serum troponin-T level into group B1 and group B2. Group B1 included acute ischemic stroke patients with normal serum troponin-T. Group B2 included acute ischemic stroke patients with elevated serum troponin-T.
• Thorough history taking with particular stress on history of focal neurological deficit, cardiac disease or surgery, diabetes mellitus, hypertension, smoking and drug history.
• Full physical, musculoskeletal and neurological examination after exclusion of patients with ischemic heart disease, heart failure, history of cardiac surgery and cardiac catheterization for non ischemic cause within one month and impaired renal function.
• Assessment of stroke severity by The Scandinavian Stroke Scale (SSS).
• Twelve lead electrocardiography (ECG) at the time of admission and 12 hours later.
• Computerized tomography (CT) on the brain.
• Follow up after three months to assess the outcome and mortality.
• Routine laboratory investigations.
• Serum troponin T and creatine kinase–myocardial band (CK-MB) level in all patients at the time of admission and five days later.
The results of our study can be summarized as follow:
• Severity of the stroke assessed by Scandinavian stroke scale was statistically significant higher in the hemorrhagic and ischemic groups patients with elevated serum troponin-T at the time of admission and 3 months later with a negative significant correlation between Scandinavian stroke scale on admission and serum troponin-T in hemorrhagic group with normal serum troponin –T and ischemic group with elevated serum troponin –T and there was no correlation in hemorrhagic group with elevated serum troponin T- and ischemic group with normal serum troponin-T, while there was no correlation between Scandinavian stroke scale on admission versus CKMB in the studied groups.
• Pathological ECG changes were statistically significant in both hemorrhagic and ischemic group with elevated serum troponin-T than groups with normal serum troponin-T level and the prevalence of pathological ECG findings was ST-T changes in 2 patients (11.8%) and T wave inversion in 3 patients (17.6%) in the hemorrhagic group with normal serum troponin-T. ST-T changes in 3 patients (37.5%), T wave inversion in 4 patients (50.0%) and atrial fibrillation in 1 patient (12.5%) in the hemorrhagic group with elevated serum troponin-T. ST-T changes in 2 patients (12.5%), T wave inversion in 2 patients (12.5%) and atrial fibrillation in 1 patient (6.3%) in the ischemic group with normal serum troponin-T. ST-T changes in 3 patients (33.3%), T wave inversion in 4 patients (44.4%) and atrial fibrillation in 2 patients 22.2% in the ischemic group group with elevated serum troponin-T.
• The size of the lesion was statistically significant higher in the hemorrhagic and ischemic groups with elevated serum troponin-T with a positive correlation between serum troponin-T on admission vs widest diameter in the studied groups, while there was no correlation between the sizes of the lesions versus CKMB in the studied groups.