Patient Care Endocrinology & Cardiology - October 2007 - (Page 25)

Troponins I inhibitors, angiography, and possibly revascularization. In studies of patients with non-ACS-related increases in cTn, it has been found that cTn elevation is a marker of increased cardiac and all-cause morbidity and mortality. The causes of these elevations may involve serious medical conditions that require a meticulous evaluation and aggressive therapy. In the setting of renal failure, elevations of troponin usually trigger an evaluation for the presence of obstructive CAD. Even when they are not found by noninvasive testing, we would recommend aggressive risk-factor modification such as tighter control of BP (both during dialysis and at other times), glucose, and lipids. If not contraindicated, a daily aspirin should be prescribed. In those patients with conditions such as stroke and sepsis, little evidence suggests that specific measures directed at the heart improve the adverse prognosis signaled by the cTn elevation. A workup to exclude an ACS is necessary, and the intensity of the workup is guided by the pretest likelihood of CAD. When not contraindicated because of bleeding or hypotension, an aspirin and/or beta-blocker is recommended. There is evidence that stress and catecholamines are involved in the genesis of critical illness cardiomyopathy; hence the suggestion for beta-blockade. No prospective studies support this, however. In various critical care units, a consultation with the cardiology service is usually obtained to help differentiate those individuals who may have a primary cardiac abnormality as a cause of the biomarker increase. As a rule, serial measurements of the biomarker are obtained, as are serial ECGs. In addition, an echocardiogram is usually done to assess for any structural heart disease. In light of the association between cTn elevations and serious medical conditions and excess mortality, it is the policy at our institution to evaluate all patients with detectable levels of cTn. If the cTn is detectable but low (cTnI 0.5 ng/mL), a general medical evaluation, often with admission and observation, is mandatory. If the elevation is higher than 0.5 ng/mL, the patient is automatically evaluated by the cardiology service. Express Stop Stroke has also been noted to cause an increase in cardiac troponin, and, as in other conditions, these elevations portend an increased mortality. In a patient with an unexpected elevation, other cardiac markers such as myoglobin and CPK are also determined. A baseline echocardiogram is obtained. If the remainder of the evaluation is negative and cardiac causes, pulmonary emboli, and sepsis are excluded, the patient is discharged. It is our policy in this setting to determine the troponin level again weeks to months later. The echocardiogram is also repeated after an appropriate delay, because this may unmask a subtle cardiac inflammatory condition that might be expected to produce LV dysfunction over time. If all of these tests and examinations are negative and the levels are stable, this patient probably belongs in the 1% tail of the bell curve. I REFERENCES 1. Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction. J Am Coll Cardiol. 2004;44(3):671-719. 2. Waxman DA, Hecht S, Schappert J, et al. A model for troponin I as a quantitative predictor of in-hospital mortality. J Am Coll Cardiol. 2006; 48(9):1755–1762. 3. James P, Ellis CJ, Whitlock RM, et al. Relation between troponin T concentration and mortality in patients presenting with an acute stroke: observational study. BMJ. 2000;320(7248):1502-1504. 4. Apple FS, Murakami MM, Pearce LA, et al. Predictive value of cardiac troponin I and T for subsequent death in end-stage renal disease. Circulation. 2002;106(23):2941-2945. 5. Freda BJ, Tang WH, Van Lente F, et al. Cardiac troponins in renal insufficiency: review and clinical implications. J Am Coll Cardiol. 2002; 40(12):2065-2071. 6. Ooi DS, Isotalo PA, Veinot JP. Correlation of antemortem serum creatine kinase, creatine kinase-MB, troponin I, and troponin T with cardiac pathology. Clin Chem. 2000;46(3):338-344. 7. Antman EM. Decision making with cardiac troponin tests. N Engl J Med. 2002;346(26):2079-2082. OCTOBER 2007 PATIENT CARE ENDOCRINOLOGY & CARDIOLOGY 25

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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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