Troponin rise in hospitalized patients with nonacute coronary syndrome: retrospective assessment of outcomes and predictors.
BACKGROUND
Cardiac troponin is elevated in several clinical settings apart from thrombotic acute coronary syndrome (ACS) and is associated with increased adverse events. It is not clear whether troponin elevation in type II myocardial infarction (MI) is associated with increased cardiovascular events. Our objectives were to identify the cause of mortality in type II MI and to attempt to establish the threshold range of cardiac troponin-I (cTnI) elevation as well as clinical factors associated with adverse outcomes in type II MI.


METHODS
This retrospective cohort study included 245 patients presenting with a noncardiac primary diagnosis associated with cTnI elevation at a single centre from January 2003 to December 2011. Primary outcome was a composite of cardiovascular and noncardiovascular mortality. Secondary outcomes included subsequent stroke, ACS, and heart failure (HF).


RESULTS
At 1 year, ACS occurred in 13 patients (5.3%), stroke was seen in 10 (4.1%) patients, and HF occurred in 19 (7.8%) patients. Overall 1-year mortality included 102 events (41.6%), with 10 cardiovascular deaths (9.8%), 65 noncardiovascular deaths (63.7%), and 27 (26.5%) deaths from unknown causes. In multivariable analysis, factors independently associated with increased overall 1-year mortality included cTnI elevation ≥ 4.63 μg/L (odds ratio [OR], 3.37; 95% confidence interval [CI], 1.55-7.34; P = 0.002), age ≥ 70 years (OR, 2.44; 95% CI, 1.40-4.29; P = 0.002), and estimated glomerular filtration rate < 30 mL/min/1.73m(2) (OR, 2.40; 95% CI 1.31-4.40; P = 0.005).


CONCLUSIONS
Unlike the published literature, our study includes a variety of both operative and nonoperative clinical settings associated with troponin elevation. We illustrate that although overall mortality is high after type II MI, the majority of mortality is caused by noncardiovascular events.
Division of Cardiology, Department of Medicine, Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, Canada.
Sumandeep
S
Dhesi
Division of Cardiology, Department of Medicine, Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, Canada.
Miriam
M
Shanks
Division of Cardiology, Department of Medicine, Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, Canada. Electronic address: wayne.tymchak@albertahealthservices.ca.
Wayne J
WJ
Tymchak
D054058:Acute Coronary Syndrome / Q000097:blood; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood; D005260:Female; D006333:Heart Failure / Q000097:blood* / Q000401:mortality; D006760:Hospitalization; D006801:Humans; D007297:Inpatients / Q000706:statistics & numerical data; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000175:diagnosis / Q000401:mortality; D011237:Predictive Value of Tests; D012189:Retrospective Studies; D018570:Risk Assessment; D012307:Risk Factors; D012680:Sensitivity and Specificity; D020521:Stroke / Q000097:blood* / Q000401:mortality; D014336:Troponin / Q000097:blood*; D019209:Troponin C / Q000097:blood; D019210:Troponin I / Q000097:blood; D020107:Troponin T / Q000097:blood
D015415:Biomarkers; D014336:Troponin; D019209:Troponin C; D019210:Troponin I; D020107:Troponin T