Elevated troponin levels are associated with sympathoadrenal activation in acute ischaemic stroke.
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 microg/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 < or = 0.2 microg/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.
Barber
M
M
University Division of Cardiovascular and Medical Sciences, Royal Infirmary, Glasgow, UK. M.Barber@clinmed.gla.ac.uk
Morton
J J
JJ
Macfarlane
P W
PW
Barlow
N
N
Roditi
G
G
Stott
D J
DJ
D000208:Acute Disease; D000311:Adrenal Glands / Q000294:innervation*; D000368:Aged; D000369:Aged, 80 and over; D002545:Brain Ischemia / Q000097:blood / Q000150:complications* / Q000401:mortality / Q000473:pathology / Q000503:physiopathology; D002395:Catecholamines / Q000097:blood; D015331:Cohort Studies; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000209:etiology / Q000401:mortality / Q000473:pathology / Q000503:physiopathology; D016017:Odds Ratio; D011159:Population Surveillance; D011237:Predictive Value of Tests; D011379:Prognosis; D018570:Risk Assessment; D012606:Scotland / Q000453:epidemiology; D012720:Severity of Illness Index; D020521:Stroke / Q000097:blood* / Q000209:etiology / Q000401:mortality / Q000473:pathology / Q000503:physiopathology; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D013997:Time Factors; D014057:Tomography, X-Ray Computed; D019210:Troponin I / Q000097:blood*
D002395:Catecholamines; D019210:Troponin I