Elevated Troponin Levels Are Associated with Sympathoadrenal Activation in Acute Ischaemic Stroke

Abstract

Background: It has been hypothesised that elevated serum troponin levels in acute stroke are due to myocardial damage caused by sympathoadrenal activation, which, in turn, may be due particularly to insular damage. We aimed to determine the factors associated with troponin elevation in ischaemic stroke and the prognostic value of this finding. Methods: We studied 222 consecutive acute ischaemic stroke admissions. Serum troponin I and catecholamines were measured. Ischaemic damage on brain computed tomography (CT) scan was graded using the Alberta Stroke Program Early CT Score (ASPECTS). Electrocardiograms were classified using the Minnesota Code and the European Society of Cardiology/American College of Cardiology criteria for acute myocardial infarction. The Rankin scale was recorded at 30 days. Results: Forty-five patients (20%) had troponin I >0.2 µg/l. These troponin-positive patients had higher epinephrine levels (median 0.27 vs. 0.17 nmol/l; p = 0.0002) and were more likely to have electrocardiograms coded as definite or possible acute myocardial infarction (odds ratio 3.35; 95% CI 1.26–8.93), compared with those with troponin ≤0.2 µg/l, in univariate analysis. There were no significant associations between troponin I score and ASPECTS or insular damage on brain CT. In logistic regression analyses, elevated troponin was significantly associated with age, elevated serum creatinine and epinephrine; however, increased troponin was not an independent predictor of death or dependency (Rankin >2) at 30 days. Conclusions: Raised troponin I is associated with elevation of circulating epinephrine in acute ischaemic stroke. Activation of the sympathoadrenal system may be an important contributor to myocardial damage in these patients. Increased troponin is not associated with insular damage and does not independently predict poor outcome.

Initial Troponin Level as a Predictor of Prognosis in Patients with Intracerebral Hemorrhage

“…Cardiac troponin elevations have been reported in numerous conditions such as sepsis, pulmonary embolism, pericarditis, chronic renal failure, major trauma, stroke and SAH 3,14,19) . The presumed cause for this elevation in acute neurologic disease is related to an increase in systemic cathecolamines 4) . This association has not been fully described in ICH.…”

“…In a study of a heterogeneous group of patients with strokes, head injuries, and seizures, elevated cTnI levels were observed in 19% of the patients and correlated with poor prognosis 10) . It has been suggested that elevated troponin may be a marker of increased mortality in patients with acute ischemic stroke 9,17) , although some investigators reported no relationship between cTnT and prognosis 4,12) . However, only a few studies have examined the relation between cTnT and prognosis of ICH, and results were largely inconclusive 15,22) .…”

Application and Interpretation of High-Sensitivity Cardiac Troponin Assays in Patients With Acute Ischemic Stroke

“…50 In addition, it has been demonstrated that stroke patients with cTn elevation have higher circulating catecholamine levels than those without. 51 In summary, autonomic imbalance with exaggerated sympathetic activity after stroke may lead to cardiac contraction band necrosis, and cardiac dysfunction with subsequent cTn release. Direct stroke-induced myocardial injury is thus likely to contribute to a relevant proportion of cTn elevation in patients with ischemic stroke.…”

Impact of troponin I on outcome of ischemic stroke patients

“…Stroke poses an increased risk for electrocardiographic changes, cardiac arrhythmias, and myocardial cell damage [6]. It has been shown that highly specific myocardial necrosis markers such as troponin can be increased in stroke victims, a phenomenon that has been explained by several pathophysiologic mechanisms: primary cardiac damage with secondary cardioembolic cerebral ischemia or primary cerebral ischemia with secondary cardiac damage caused by increased levels of catecholamines (caused by sympathetic system activation) [7][8][9][10]. Some studies associate increased troponin levels with a certain localization of stroke: insular or right hemisphere [11][12][13].…”