The presence of troponin elevation in high catecholamine states such as in ischemic stroke has been confirmed. But, the etiology of increased troponin levels in acute stroke patients is still incompletely understood. Jensen et al. studied acute ischemic stroke patients with no overt coronary heart disease. Their findings suggested that etiologies other than an acute coronary syndrome, such as congestive heart failure and renal failure were responsible for the observed elevated troponin levels [11].
Also, it has been suggested that cardiac injury in acute stroke patients is caused by patchy subendocardial hemorrhage or swollen myocytes surrounding the epicardial nerves (myocytolysis) [12]. Jespersen et al. suggested that increased catecholamine release in the myocardium, that likely to originate from the insular cortex, could lead to an excessive release of intracellular calcium ions which can cause myocyte dysfunction and impairment of cardiac function due to the perfusion disturbance at the level of capillaries caused by an enhanced platelet aggregation [13].
Barber et al. found an association between elevated troponin and epinephrine in ischemic stroke patients [14]. Christensen et al. found an association between elevated troponin and cortisol [15]. These findings may suggest a link between the sympathetic nervous system and myocardial cell damage after ischemic stroke.
In this study, we investigated the prognostic significance of troponin elevation for poor short-term outcome after intravenous thrombolysis with recombinant tissue plasminogen activator in acute ischemic stroke patients.
In the current study, an elevated serum level of T-I ≥ 0.01 μg/L was observed in 18% of patients (group 1), and 82% had average normal serum troponin-I level at admission (group 2). Comparison between both groups showed that group 1 had older age, higher incidence of diabetes mellitus, previous stroke, and atrial fibrillation which was statistically significant (P = 0.02, 0.01, 0.003, and 0.04 respectively). Regarding group 1, we found a statistical significant decrease in high-density lipoprotein cholesterol (P = 0.02) and a statistical significant increase of admission NIHSS score (P = 0.01).
In the same line with our results, Faigle and colleagues [3] reported that patients with measured troponin were more likely to have a history of atrial fibrillation and higher NIHSS scores at presentation.
Regarding the neurological outcome, we found that the frequency of major neurological improvement (good outcome) was significantly higher in group 2. Also, death (poor outcome) was significantly higher in group 1. But as regard disability (poor outcome), there was no statistical significant difference between both groups. In the present study, poor outcomes in group 1 were significantly associated with older age groups, diabetes mellitus, atrial fibrillation, elevated serum troponin-I level at admission, and admission NIHSS score. In the same line with our results, Bray and colleagues [16] reported that older thrombolyzed ischemic stroke patients are more likely to have poor outcomes when compared to younger patients.
Also, our results corroborate the findings of Nikneshan and colleagues [17]; they showed that thrombolyzed stroke patients with diabetes have poorer outcomes compared with patients without diabetes. Atrial fibrillation may worsen the clinical outcomes of patients with acute ischemic stroke after thrombolysis. Those patients have increased risk of mortality and less favorable outcome compared to patients without atrial fibrillation [18].
Moreover, thrombolyzed stroke patients with measured troponin had history of atrial fibrillation, and higher NIHSS at presentation that resulted in poor outcome [3]. Stroke can induce stress on the patient’s heart causing troponin to be elevated and this might be an indication of a lower cardiac tolerance caused by the acute stroke [1]. This may be one explanation for the relationship between elevated T-I and a poor short-term outcome found in the present study, and for this reason, physicians should be more careful when dealing with these patients.
In the current study, the most significant risk factors of poor outcome in group 1 were elevated serum troponin-I level at admission, higher NIHSS score on admission, and diabetes mellitus. Our results are supported by that of Faigle and colleagues [3] who found that troponin elevation in thrombolyzed stroke patients is associated with a significant increase in mortality and critical care needs in white but not black patients. Also, this is in accordance with two previous studies [19, 20].
Mehta and colleagues [19] reported that NIHSS at admission > 15, diabetes, and blood sugar > 250 mg/dL, were the significant predictors of the poor outcomes after intravenous thrombolysis for acute ischemic stroke. Liu and colleagues [20] reported that older ages, NIHSS score > 20, and serum glucose on admission > 9.0 mmol/L were independent predictors of poor outcome (hemorrhage) after thrombolysis in their patients.
The association of high serum levels of both of troponin I and glucose in acute cerebrovascular stroke is not yet understood, regardless of that the role of high serum glucose was built up as a hazard factor for platelet-dependent clot formation in coronary illness patients, so coagulation changes might be the ascribed etiology [21]. Moreover, hyperglycemia happens after injury to the central autonomic centers and as a reaction to the release of stress hormones such as cortisol and noradrenaline [22].