Elevated Cardiac Troponin Levels in Critically Ill Patients: Prevalence, Incidence, and Outcomes

Wendy Lim, MD; Deborah J. Cook, MSc(Epid), MD; Lauren E. Griffith, MSc(Math); Mark A. Crowther, MSc, MD; P. J. Devereaux, MSc, MD

Disclosures

Am J Crit Care. 2006;15(3):280-288. 

In This Article

Abstract and Introduction

Abstract

Background: Levels of cardiac troponin, a sensitive and specific marker of myocardial injury, are often elevated in critically ill patients.
Objectives: To document elevated levels of cardiac troponin I in patients in a medical-surgical intensive care unit and the relationship between elevated levels and electrocardiographic findings and mortality.
Methods: A total of 198 patients expected to remain in the intensive care unit for at least 72 hours were classified as having myocardial infarction (cardiac troponin I level ≥1.2 µg/L and ischemic electrocardiographic changes), elevated troponin level only (≥1.2 µg/L and no ischemic electrocardiographic changes), or normal troponin levels. Events were classified as prevalent if they occurred within 48 hours after admission and as incident if they occurred 48 hours or later after admission. Factors associated with mortality were examined by using regression analysis.
Results: A total of 171 patients had at least one troponin level measured in the first 48 hours. The prevalence of elevated troponin level was 42.1% (72 patients); 38 patients (22.2%) had myocardial infarction, and 34 (19.9%) had elevated troponin level only. After the first 48 hours, 136 patients had at least 1 troponin measurement. The incidence of elevated troponin level was 11.8% (16 patients); 7 patients (5.1%) met criteria for myocardial infarction, and 2 (1.5%) had elevated troponin level only. Elevated levels of troponin I at any time during admission were associated with mortality in the univariate but not the multivariate analysis.
Conclusions: Elevated levels of cardiac troponin I in critically ill patients do not always indicate myocardial infarction or an adverse prognosis.

Introduction

The introduction of assays for cardiac troponins I and T, which are highly sensitive and specific biomarkers for myocardial cell damage, has resulted in increasing detection and diagnosis of acute coronary syndromes. Elevated serum levels of cardiac troponin indicate myocardial damage but not the underlying mechanism, suggesting that clinical evidence of coronary thrombosis is needed to establish a diagnosis of myocardial infarction.[1]

Elevated levels of cardiac troponin not due to acute coronary syndromes have been reported in various populations of patients in the intensive care unit (ICU): heterogeneous medical and surgical patients and critically ill patients with systemic hypotension and with conditions such as trauma, sepsis, pulmonary embolism, stroke, renal failure, and chronic obstructive pulmonary disease.[2,3,4,5,6,7,8,9] The prevalence of increased levels ranges from 15% to 70%[10,11,12] in the general ICU population, and estimates for the prevalence in critically ill patients with sepsis or septic shock are 31% to 80%.[2,3,4,5,10,13] Abnormal serum levels of cardiac troponin have been detected in critically ill patients with noncardiac diagnoses[14,15]; in the study by Ammann et al,[14] more than 70% of ICU patients with elevated cardiac troponin levels did not have flow-limiting coronary artery disease as indicated by stress echocardiography or by findings at autopsy.

Elevated troponin levels are clinically important because they may act as an adverse prognostic marker.[16] The prognostic value of elevated serum levels of cardiac troponin is well recognized outside the ICU setting.[17,18] However, in critically ill patients, the prognostic value and the relationship between elevated cardiac troponin levels and a diagnosis of myocardial infarction remain uncertain. In the consensus document[1] of the Joint European Society of Cardiology/American College of Cardiology (ESC/ACC) Committee, myocardial infarction is defined on the basis of pathological findings or on the basis of a typical rise and fall in biochemical markers of myocardial necrosis and the presence of at least one of the following: ischemic signs and symptoms, electrocardiographic (ECG) signs of ischemia or necrosis, or a coronary artery intervention.[1] In the ICU, endotracheal intubation, coma due to underlying illness, and use of sedatives and narcotics all limit the ability of patients to report symptoms associated with ischemia. Therefore, in practice, a combination of elevated levels of cardiac troponin and ECG changes indicating ischemia are frequently used to establish a diagnosis of myocardial infarction in the ICU. Use of coronary angiography, routine echocardiography, and continuous ECG recordings is either not feasible on a routine basis or has not been well studied in critically ill patients. Nevertheless, recognition of myocardial infarction in critically ill patients most likely is important because the development of myocardial infarction may contribute to increased morbidity and mortality.[19]

Outside the ICU setting, patients with a diagnosis of myocardial infarction benefit from thrombolytic therapy, coronary revascularization, and use of anticoagulants, antiplatelet agents, β-blockers, statins, and angiotensin-converting enzyme inhibitors. However, myocardial infarction due to nonthrombotic mechanisms may not respond favorably to antithrombotic agents, and the impact of these therapies on outcomes in ICU patients with myocardial infarction is unknown. Furthermore, the risk-benefit ratio of these agents in the ICU may differ considerably from when they are used in patients with myocardial infarction outside the ICU. A fundamental understanding of the prognostic significance of elevated levels of cardiac troponin and their relationship to myocardial infarction in critically ill patients is therefore an important first step toward devising and testing appropriate management strategies.

We designed this study to document the prevalence and incidence of elevated serum levels of cardiac troponin I and myocardial infarction among critically ill patients; compare the morbidity and mortality of patients with myocardial infarction, patients with elevated levels of cardiac troponin I alone, and patients with normal cardiac troponin I levels; and assess whether elevated levels of cardiac troponin I are a predictor of ICU and hospital length of stay and mortality. We did not systematically screen patients by measuring levels of cardiac troponin and obtaining ECGs. Rather, we documented all the available results of tests ordered by the ICU team; hence, we determined the clinically recognized incidence and prevalence rates of elevated levels of cardiac troponin I and myocardial infarction.

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