Patient Care Endocrinology & Cardiology - October 2007 - (Page 24)

I Troponins In patients with acute coronary syndrome, the mere detection of cardiac troponin—even at a level below what is regarded as an MI threshold—identifies a high-risk subgroup and triggers more aggressive therapy. Specific causes of cardiac troponin elevation Two common situations associated with elevations of cTn in clinical practice are critical illness and renal failure. Several studies of varying design have looked at the role of cTn in critically ill patients. In this population, common diagnoses include sepsis, systemic immune response syndrome (SIRS), and hypotension. Each of these has been associated with increased mortality. The percentage of patients with detectable cTn levels is as high as 85%. In these studies, the Acute Physiology and Chronic Health Evaluation II (APACHE II) score is a predictor of cTn positivity, as is the presence of multiorgan dysfunction. In many, but not all, studies, cTn status proved to be an independent predictor of mortality. In this setting, overt cardiac dysfunction, usually identified by a depressed ejection fraction on echocardiography and susceptibility to ischemia secondary to known CAD, is common. The LV dysfunction, which can be severe, is often transitory. In one report, cTn levels as high as 15 /L were seen. In one of the larger studies documenting the poorer prognosis in the patients with cTn elevations, significant CAD was excluded in 72% of the troponinpositive patients. Stroke has also been noted to cause an increase in cTn, and, as in other conditions, these elevations portend an increased mortality. In one study, cTn was measured in 181 consecutive patients with acute stroke over a 9-month period. The in-hospital mortality for the 17% of patients who were cTn pos- itive was 40%, compared to 13% among patients with negative tests.3 CAD is quite prevalent in patients with chronic kidney disease (CKD). In some studies, the prevalence of CAD in these patients is as high as 73%.4 Up to half of deaths in patients with CKD are attributable to CAD. Elevations in cTn are common in these patients. Elevations of cTnI were seen in up to 7% of patients with renal failure. The proportion of cTnT elevations is much greater, as high as 53% in one study.5 The discrepancy is due in part to the fact that cTnT (but not cTnI) is broken down into smaller proteins whose excretion is renally mediated. This may explain the persistence of the troponin, but not its initial release. Mechanisms that have been proposed to explain this elevation include endothelial dysfunction, acute cardiac stretch, intradialysis hypotension and hypertension, use of iron sucrose, and LVH. The prevalence of pathologic processes found at autopsy in these patients is high, although the findings may be nonspecific and include patchy fibrosis or degenerative myocyte changes—in addition to findings compatible with MI.6 These patients often do not have clinical or ECG features of an ACS, and the cTn elevations are chronic. In several studies, angiography has been performed confirming the absence of significant obstructive CAD. All of the studies, however, confirm the significantly elevated all-cause and cardiac mortality in this group of patients. Those with increases in the level of cTn over time may belong to a higher-risk subgroup. Clinical management Measurement of troponin in a variety of settings allows physicians to refine their prognostications.7 In patients with ACS, the mere detection of cTn— even at a level below what is regarded as an MI threshold—identifies a high-risk subgroup and triggers more aggressive therapy. This might include antiplatelet therapy with GP IIb/IIIa 24 PATIENT CARE ENDOCRINOLOGY & CARDIOLOGY www.patientcareonline.com http://www.patientcareonline.com

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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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