Patient Care Endocrinology & Cardiology - October 2007 - (Page 23)

Troponins I Non-ACS elevations of cardiac troponin Not all elevations of troponin are caused by an ACS. Among patients in the intensive care unit, several conditions have been associated with significant elevations (see Table 1). The presence of tumor necrosis factor alpha (TNF-alpha) has been postulated as a cause of this phenomenon. In an experimental setting, TNF-alpha has been shown to increase the permeability of endothelial monolayers to macromolecules. In a rat model, mild ischemia has been shown to produce detectable levels of troponin as soon as 15 minutes after onset—too soon for cell death to have occurred. It has also been postulated that the capillary sludging that occurs in sepsis can trigger cTn release when it occurs in the myocardium. In several studies, the degree of cTn elevation corresponds to the levels of inflammatory mediators and cytokines, including various interleukins. The differentiation of cTn elevations caused by coronary events from those not related to an ACS continues to be a vexing clinical problem. The literature gives limited absolute guidance. The ECG may be of some value in that substantial ST-segment deviations suggest obstructive coronary disease in the absence of the usual confounders such as LV hypertrophy (LVH), left bundle branch block, and preexisting ST-T changes. Nonspecific ST changes are common but less helpful. In sepsis, for example, when patients often have hypotension and marked tachycardia, nondiagnostic STsegment deviations are common. In addition, ischemia in the setting of a fixed, noncritical coronary stenosis during a period of profound hypotension does not necessarily indicate the need for revascularization. In the experience of the author, the degree of cTn elevation can help differentiate cardiac from non-ACS causes. Elevations of cTn greater than approximately 4 to 6 mcg/L indicate a higher likelihood of ACS. The sensitivity and specificity are less than ideal, however. Consider this personal observation of an increase in cTnI to more than 100 mcg/L in a patient with aortic TABLE 1 Conditions associated with cardiac troponin elevations Cardiac Acute coronary syndrome Acutely decompensated congestive heart failure Severe tachyarrhythmias or bradyarrhythmias Pericarditis or myocarditis Cardiac surgery Cardiac contusion Post-PTCI or ablation Internal or external defibrillation Noncardiac Renal failure Sepsis Pulmonary embolus Stroke or subarachnoid hemorrhage Hypotension Critical illness Extremely high levels of exertion Key: PTCI, percutaneous transluminal coronary intervention. stenosis and rapid atrial fibrillation; subsequent coronary angiography showed no significant coronary artery disease (CAD). Troponin elevation in the absence of an ACS is not a rare phenomenon. In one series of 1000 consecutive patients presenting to an urban ED, 112 had elevations of cTnI, and 45% had a final diagnosis other than ACS. The most important fact regarding cTn elevation is that it appears to be a reliable predictor of morbidity and mortality even in individuals without significant CAD. In one recent study involving 2 distinct populations totaling more than 34,000 patients (half in the training set, the remainder in the validation set), cTn levels were a powerful predictor of death even after controlling for age, ECG changes, renal function, vital signs, and admitting complaint. The odds of death doubled for every 10-fold increase of cTn.2 In this study, detectable but low levels of cTn proved to be significant. Continued from page 24 OCTOBER 2007 PATIENT CARE ENDOCRINOLOGY & CARDIOLOGY 23

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Patient Care - Endocrinology & Cardiology - October 2007 Research Digest Contents Medicine in the News Recognizing and Managing Patients with the Metabolic Syndrome and Prediabetes Using Troponins to Evaluate Cardiac Injury The 15-Minute Visit Classified Advertising Clinical Clips

Patient Care Endocrinology & Cardiology - October 2007

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