CLINICAL RESEARCH: ACUTE CORONARY SYNDROMES
Implication of different cardiac troponin I levels for clinical outcomes and prognosis of acute chest pain patients
Michael C. Kontos, MD*  ,*,
Rakesh Shah, MD*,
Lucie M. Fritz, PhD ,
F. Philip Anderson, PhD,
James L. Tatum, MD,
Joseph P. Ornato, MD and
Robert L. Jesse, MD, PhD*
* Department of Internal Medicine, Cardiology Division, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia, USA
Department of Emergency Medicine, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia, USA
Department of Pathology, Clinical Chemistry Division, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia, USA
Department of Radiology, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia, USA
Manuscript received May 20, 2003;
revised manuscript received September 30, 2003,
accepted October 6, 2003.
* Reprint requests and correspondence: Dr. Michael C. Kontos, Room 7-074, Heart Station, North Hospital, P.O. Box 980051, Medical College of Virginia, 12th and Marshall Streets, Richmond, Virginia 23298-0051, USA.
mkontos{at}hsc.vcu.edu
OBJECTIVES: We compared outcomes in patients with non–ST-segment elevation acute coronary syndromes (ACS) according to the degree of cardiac troponin I (cTnI) elevation.
BACKGROUND: Controlled trials of high-risk patients have found that troponin elevations identify an even higher risk subset. It is unclear whether outcomes are similar among a lower risk, heterogeneous patient group. Also, few studies have reported outcomes other than myocardial infarction (MI) or death, based on the peak troponin value.
METHODS: Consecutively, admitted patients without ST-segment elevation on the initial electrocardiogram underwent serial marker sampling using creatine kinase (CK), CK-MB fraction, and cTnI. Patients were grouped according to peak cTnI: negative = no detectable cTnI; low = peak greater than the lower limit of detectability but less than the optimal diagnostic value; intermediate = peak greater than or equal to the optimal diagnostic value but less than the manufacturer's suggested upper reference limit (URL); and high = peak greater than or equal to the URL. Thirty-day outcomes included cardiac death, MI based on CK-MB, revascularization, significant disease, and a reversible defect on stress testing. Six-month mortality was also determined. Negative evaluations for ischemia included nonsignificant disease, no reversible stress defect, and negative rest perfusion imaging.
RESULTS: Of the 4,123 patients admitted, 893 (22%) had detectable cTnI values. Cardiac events and positive test results at 30 days and 6-month mortality increased significantly with increasing cTnI values. Negative evaluations for ischemia were significantly and inversely related to peak cTnI values. Although adverse events were significantly more common in patients with a low cTnI value than in those with negative cTnI, negative evaluations for ischemia were frequent.
CONCLUSIONS: Increased cTnI values are associated with worse outcomes. Although low cTnI values are associated with adverse events, they do not have the same implication as higher cTnI values, and nonischemic evaluations are frequent.
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Abbreviations and Acronyms
| | ACS | = acute coronary syndromes | | CCU | = coronary care unit | | CI | = confidence interval | | CK | = creatine kinase | | cTnI | = cardiac troponin I | | cTnT | = cardiac troponin T | | CV | = coefficient of variation | | ED | = emergency department | | ESC/ACC | = European Society of Cardiology/American College of Cardiology | | LLD | = lower limit of detectability | | MI | = myocardial infarction | | MPI | = myocardial perfusion imaging | | URL | = upper reference limit |
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