Methods

All consecutive patients with ischemic stroke admitted to the Comprehensive Stroke Center of University Hospital Olomouc <12 hours after stroke onset were enrolled in the prospective observational study in 2011 ( ClinicalTrials.gov identifier NCT01541163 ).

The following examinations were performed: (1) neurologic and physical examinations, including scoring of neurologic deficit using the National Institutes of Health Stroke Scale (NIHSS) at admission and on day 30, (2) brain computed tomography or magnetic resonance imaging at admission, (3) laboratory tests at admission, (4) electrocardiography at admission and 4 hours later, (5) transesophageal or transthoracic echocardiography and 24-hours electrocardiographic (ECG) Holter monitoring <15 days after stroke onset, and (6) neurosonologic examination <60 hours of stroke onset. Epidemiologic data (occurrence of arterial hypertension, diabetes mellitus, hyperlipidemia [previously detected disorders of lipid metabolism resulting in abnormally high levels of cholesterol, triglycerides, and lipoproteins in plasma], coronary heart disease [CHD], MI in the medical history, congestive heart failure, renal failure, stroke in the medical history, atrial fibrillation, renal insufficiency, alcohol abuse [positive carbohydrate-deficient transferrin test results], smoking [>5 cigarettes/day], thrombophilia, use of hormonal contraception, anticoagulation therapy, and antiplatelet therapy in the medical history) was acquired in all patients. The cause of ischemic stroke was classified according to the Trial of Org 10172 in Acute Stroke Treatment (TOAST) classification.

MI was assessed according to the third universal definition of MI. According to this definition, diagnosis of MI was made if the patient met the following criteria: detection of an increase and/or a decrease in cardiac cTnT with ≥1 value higher than the the 99th percentile upper reference limit and ≥1 of the following: (1) symptoms of ischemia, (2) development of pathologic Q waves on electrocardiography, (3) new or presumed new significant ST-T changes or new left bundle branch block, (4) identification of an intracoronary thrombus on angiography or autopsy, and (5) imaging evidence of new loss of viable myocardium or a new regional wall motion abnormality.

Electrocardiography was performed at admission and 4 hours later using a Philips HP M 1770A (Philips/Hewlett-Packard, Shanghai, China) apparatus. All electrocardiograms were evaluated by a single cardiologist (M.H.) blinded to patient diagnosis. The ECG findings were evaluated as follows : pattern 1 = possible ECG abnormalities of myocardial ischemia (ECG manifestations of acute myocardial ischemia in the absence of left ventricular hypertrophy and left bundle branch block); pattern 2 = suspected ECG abnormalities of myocardial ischemia (ECG manifestations of acute myocardial ischemia in the presence of left ventricular hypertrophy and left bundle branch block); pattern 3 = ECG changes associated with previous MI; and pattern 4 = normal ECT or other pathologic findings.

All laboratory analyses were performed in the certified laboratories of the Department of Hemato-Oncology and the Department of Clinical Biochemistry at University Hospital Olomouc. The following tests were done in patients meeting the inclusion criteria: (1) standard laboratory panel, (2) basic coagulation parameters, (3) serum markers <12 hours after stroke onset (N-terminal pro–brain natriuretic peptide [NT-proBNP], pro–atrial natriuretic peptide, creatine kinase-MB mass, cTnT, interleukin-6, procalcitonin, high-sensitivity C-reactive protein, and d -dimer), (4) repeated serum level of cTnT performed 4 hours after the first sample was done, and (5) serum markers <60 hours after stroke onset (glycosylated hemoglobin and serum lipids). The details and normal values of the specific methods were published previously.

Normality of distribution was checked using the Shapiro-Wilk test. All parameters with non-normal distributions are presented as means, medians, and interquartile ranges. Spearman’s rank correlation analysis was performed to assess the associations between cTnT and age, gender, and laboratory test results. Differences in the presence of elevated and normal values of cTnT in patients with impaired different brain vascular territory, medical histories, ECG findings, and severity of neurologic deficit measured using the NIHSS were statistically evaluated using Student’s t tests, Mann-Whitney U tests, and Fisher’s exact tests. Multiple logistic regression analysis was used to determine the factors associated with cTnT elevation in patients with AIS. A p value <0.05 was considered statistically significant. Data were analyzed using SPSS version 15 (SPSS, Inc., Chicago, Illinois).

The entire study was conducted in accordance with the Declaration of Helsinki of 1975 (as revised in 2004 and 2008). The study was approved by the ethics committee of University Hospital Olomouc. All patients provided written informed consent before enrollment.

Results

In total, 107 consecutive patients with AIS (65 men, median age 68 years, mean age 67.2 ± 14.2 years) were enrolled in the prospective study. Patients’ demographic and baseline characteristics are listed in Table 1 . Elevated serum levels of cTnT (>0.014 μg/L) were present in 39 patients with AIS (36%). Elevated blood levels of cTnT were significantly correlated with the occurrence of CHD: 56% patients (18 of 32) with known CHD and 47% patients (9 of 19) with new ischemic heart disease but only 21% patients (12 of 56) without CHD presented with elevated levels of cTnT (p = 0.01). Within 30 days of stroke onset, 3 of the 39 patients (8%) with elevated cTnT and 2 of the 67 patients (3%) with normal values of cTnT died (p = 0.35). One patient with elevation of cTnT underwent acute coronary artery bypass graft surgery 13 hours after symptom onset. This was complicated by cardiac arrest at the end of procedure and, after successful resuscitation, the patient’s 30-day clinical outcome was 5 points on the modified Rankin scale (permanent dependency).

Twenty-four patients (22%) presented with elevated cTnT together with new or presumed new significant ST-T changes or new left bundle branch block on electrocardiography (passing criteria of the third universal definition of MI; Table 2 ). Of these, only 1 patient presented with elevated cTnT, possible ECG abnormalities of myocardial ischemia (pattern 1), and typical chest pain. Possible ECG abnormalities of myocardial ischemia (pattern 1) without elevated cTnT were detected in 27 patients (25%), while suspected ECG abnormalities of myocardial ischemia (pattern 2) were seen in 11 patients (10%).

The cTnT level was positively correlated with age (r = 0.448) and the levels of NT-proBNP (r = 0.528), cystatin C (r = 0.457), creatine kinase-MB mass (r = 0.253), urea (r = 0.281), and creatinine (r = 0.161) and negatively correlated with albumin (r = −0.219). When comparing subgroups of patients with elevated and normal cTnT values, cystatin C >1.44 mg/L (11% vs 0%, p = 0.012), NT-proBNP >125 μg/L (85% vs 59%, p = 0.010), creatinine >90 μmol/L (44% vs 19%, p = 0.002), atrial fibrillation (28% vs 6%, p = 0.003), known CHD (41% vs 18%, p = 0.012), newly diagnosed CHD (8% vs 0%, p = 0.046), and ECG changes associated with previous MI (pattern 3; 36% vs 10%, p = 0.002) were found more frequently in the first subgroup (i.e., patients with elevated cTnT). The results of the binary logistic regression analysis are listed in Table 3 .

Table 3

Results of binary logistic regression with unadjusted odds ratio for qualitative and quantitative parameters and dependent variable cardiac troponin T >0.014 μg/L

Variable	Odds Ratio	95% Confidence Interval	p Value
Age	1.058	1.020–1.097	0.003 ∗
Gender	1.25	0.554–2.819	0.591
Arterial hypertension	1.308	0.565–3.030	0.531
Diabetes mellitus	2.333	0.937–5.809	0.069
Hyperlipidemia	1.146	0.484–2.714	0.756
Ischemic heart disease	3.246	1.330–7.922	0.010 ∗
MI in medical history	3.500	0.954–12.839	0.059
Stroke in medical history	2.279	0.866–5.998	0.095
Atrial fibrillation	6.286	1.842–21.452	0.003 ∗
Alcohol abuse	1.171	0.187–7.331	0.866
Daily smoking	0.848	0.291–2.474	0.763
Antiplatelet therapy	2.057	0.908–4.659	0.084
Anticoagulation therapy	2.750	0.439–17.224	0.280
ECG changes associates with previous MI	4.880	1.760–13.529	0.002 ∗
NT-proBNP (>2,000 ng/L)	8.449	2.153–33.158	0.002 ∗
Glomerular filtration rate (Modification of Diet in Renal Disease equation) <1.5 ml/min/1.73 m 2	1.083	0.472–2.484	0.850
Cystatin C	17.963	2.965–108.8	0.002 ∗
Creatine kinase-MB mass	1.334	1.083–1.644	0.007 ∗
Total serum protein	0.998	0.921–1.081	0.958
Albumin	0.907	0.809–1.017	0.094
C-reactive protein	1.007	0.985–1.030	0.531
Fibrinogen	0.961	0.852–1.085	0.521
Urea	1.221	1.034–1.443	0.019 ∗
Creatinine	1.017	1.000–1.035	0.046 ∗

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