Multiple electrocardiographic (ECG) abnormalities can be observed during the acute phase of ischemic stroke (IS), the most common of which are arrhythmias and repolarization abnormalities with QT interval prolongation and/or ST segment depression. These abnormalities may be transient or may indicate an existing cardiac disorder (1-4). Right-hemisphere stroke with insular involvement is an additional risk factor for cardiac complications of cerebral origin and also for sudden death during this period (5-7). Stimulation of the right insula increases blood pressure and heart rate, whereas stimulation of the left insula causes a decrease in blood pressure and bradycardia (8). Such abnormalities are often observed in patients despite the absence of any previous cardiac history and justify the necessity for ECG monitoring during the acute phase of stroke. The concentration of cardiac-specific troponin (cTn) may be helpful in identifying these disorders. It is a highly sensitive and specific marker of cardiomyocyte damage. Troponin I concentration begins to rise within the first 3 to 8 hours after the onset of chest pain, peaks at 18 to 24 hours and remains elevated for 4 to 7 days after infarction (9).

Studies that have examined the prognostic value of elevated cTn level and its association with a higher risk of death and further vascular events are of interest to cardiologists and other specialists (10-13). These studies emphasize the importance of the cTn concentration measurement to assess mortality risk in patients with internal and/or systemic diseases. The identification of mechanisms contributing to elevated cTnI concentrations in IS patients would enable the identification of patients at especially high risk for cardiac complications. As a result, appropriate treatment would be initiated earlier, resulting in a better prognosis.

The goals of this study were: to assess the influence of elevated cTnI concentration in patients with IS on the course of stroke and survival prognosis; to characterize the potential relationship between cTnI concentration and other factors influencing the course of stroke, and to identify any correlations between lesion location in the central nervous system (CNS) and elevations in cTnI concentrations following IS.

This was a hospital-based, prospective, observational, case-control study conducted at the Department of Neurology and Epileptology, Medical Centre of Postgraduate Education, Warsaw, Poland. The study was approved by the Medical Centre of Postgraduate Education Ethics Committee. Two hundred and sixty-one of acute stroke patients were consecutive admitted to the Department between March 2003 and June 2005. Inclusion criteria included: time from stroke onset less than 72 hours, age less than 85 years, stable coronary artery disease (CAD), without history of myocardial infarction (MI) in the four weeks prior to study entry. The study group consisted of 128 women (49%) and 133 men (51%) with IS who were transferred from the Emergency Room directly to the Department. The study group was divided into subgroups according to their cTnI concentration and patient death or survival. The first subgroup consisted of subjects with IS who demonstrated or did not demonstrate elevated cTnI concentrations on admission. Whereas the second subgroup consisted of patients who died or survived throughout the observation period. For each patient, the study period lasted six months starting from the onset of stroke symptoms. At one and six months after IS, the neurological status was re-evaluated or the death of the patient was registered. Patients who failed to show up for follow-up appointments were telephoned at home, and data concerning their health and course of disease were obtained. When it was otherwise impossible to obtain these data, we asked the Warsaw Registrar’s Office for help in identifying patients who died during the study period. Additional tests were carried out in accordance with the European Stroke Initiative guidelines (14). A computed tomographic (CT) imaging study was performed to confirm IS by excluding other reasons for the observed neurological deficits. A standard 12-lead ECG was also recorded routinely on admission. The cTnI concentration was measured once in a blood sample collected on admission, using the AxSYM Troponin-I and AxSYM Troponin-I ADV (starting in October 2004) tests (Abbott Laboratories). Because it was impossible to linearly convert “earlier” cTnI concentrations to “more modern” ones, two ranges were defined with the following nominal values: 0 = cTnI concentrations within the reference range for the healthy population (99th percentile) (earlier test version 0 – 0.3 ng/ml, modern version 0 – 0.04 ng/ml), 1 = cTnI concentrations above reference values (earlier test version > 0.3 ng/ml, modern version > 0.04 ng/ml).

A parametric Students t-test for independent groups and its nonparametric counterpart, the U-test, were used to determine the significance of the differences between variables in the groups analyzed. A chi-square test with Yates’ correction and Fisher’s exact test for counts less than five were employed to demonstrate a relationship between studied variables. A chi-square Mantel-Haenszel test was applied to analyze the mutual influence of given variables in separate subgroups for several independent two-way tables (2 x 2). A Kaplan-Meier method and log-rank test were employed to analyze the survival time. Multivariate logistic regression analysis using Enter and Forward stepwise Wald modeling was applied to determine the influence of selected independent factors on the prevalence of elevated cTnI concentration. A nonparametric Cox proportional hazard model using the Forward stepwise Wald method was employed to determine the influence of analyzed factors on increased prediction of mortality during the first 30 and 180 days after onset of IS symptoms. The results were assumed to be reliable at a significance level α < 0.05. Statistical analyses were performed using the SPSS version 11.5 (SPSS Inc.).

Sixty-seven patients (25.7%) died during the six-month observation period. Early mortality (< 30 days) occurred in 42 cases (16.1%). Elevated cTnI concentration on admission was observed in 16.5% (43/261) of the patients included in the study and in 28.4% (19/67) of the patients who died during the observation period (p < 0.002) (U-test). An elevated cTnI on admission was observed regardless of the length of the survival period i.e. either < 30 days (p < 0.021) or > 30 days after IS (p < 0.002) (U-test). The most common locations for the ischemic lesion were the right (42%, 73/174) and left (33.3%, 58/174) middle cerebral artery (MCA) territories. There was a significant difference between groups with respect to frequency of lesion location in the right MCA territory. This lesion location was observed in 35.1% (46) of patients who survived throughout and 62.8% (26) of patients who died during the study period (p < 0.001) (U-test). The features of cerebral edema in the CT scan taken on admission to hospital in 19.4% (50) patients with IS but in 28.8% (19) of those who died and in 16.1% (31) patients who survived were present (p < 0.025) (U-test). No abnormalities on 12-lead ECG were observed in 27.2% (72) of patients with IS. On ECG, the frequency of abnormalities was significantly different between groups (heart rate [HR] > 100/min and features of previous MI). The prevalence of features of acute MI, HR < 50/min and repolarization abnormalities trended towards significance (U-test) (tab. 1).