Elevated Troponin I without ACS
August 1, 2008 4 minutes read
Elevated Troponin I without ACS
Abstract & Commentary
By Michael H. Crawford, MD, Professor of Medicine, Chief of Clinical Cardiology, University of California, San Francisco. Dr. Crawford is on the speaker's bureau for Pfizer. This article originally appeared in the July 2008 issue of Clinical Cardiology Alert. It was peer reviewed by Rakesh Mishra. Dr. Mishra is Assistant Professor of Medicine, Weill Medical College, Cornell University; Assistant Attending Physician, NewYork-Presbyterian Hospital. Dr. Mishra reports no financial relationship relevant to this field of study.
Source: Blich M, et al. Cardiac troponin I elevation in hospitalized patients without acute coronary syndromes. Am J Cardiol. 2008;101:1384-1388.
Elevated troponin i is a nonspecific finding, but suggests a poor prognosis regardless of its cause. These investigators from Israel sought to clarify these observations. They reviewed all patients admitted their hospital over a year with elevated troponin I. Those under 18 or with missing data were the only exclusions. The Abbot assay where values > 2 ng/mL were considered abnormal, was used. Acute coronary syndromes (ACS) were diagnosed in the usual fashion and divided into ST-elevation and non-ST-elevation myocardial infarction (MI). ACS did not include unstable angina without troponin release. Among 7473 patients in whom troponin I was measured, 901 were elevated (12%); after exclusions, 883 remained in the study group. Of the 883, 572 (65%) had ACS. In the 311 non-ACS patients with elevated troponin, 28% had sepsis, 16% had heart failure, 13% were post coronary bypass surgery, 10% had arrhythmias, 7% were post cardiopulmonary resuscitation, 7% had a CVA, 4% myocarditis, 4% acute bleeding, 3% chest contusion, 2% had pulmonary embolism, and 6% had other diagnoses. Almost all these conditions have been associated with troponin release, but their troponin levels were significantly lower compared to ACS patients, (15ng/mL vs 33 STEMI and 20 NSTEMI, p < .001). However, receiver operating curves showed that troponin was poor at discriminating ACS (63% accuracy) and worse if STEMI patients were excluded (58%). Of those without ACS who underwent coronary angiography, many had significant disease, the severity of which was not related to troponin levels. Mortality was higher in the non-ACS group vs ACS (37% vs 17% STEMI and 12% NSTEMI p < .01), and this difference persisted during the 30-month mean follow-up. Blich and colleagues concluded that troponin I release is frequent in hospitalized patients without ACS, and is associated with increased short- and long-term mortality. Most cases have an alternate explanation for the increase, and coronary angiography is of little additional value.
Commentary
An elevated troponin level almost always occasions hospital admission or, in hospitalized patients, a cardiology consultation. Without clinical evidence of ACS, we often refer to this phenomenon as "demand" related, meaning that oxygen supply has not met increased demand for a variety of reasons. This "diagnosis" is unsettling because we know many of these older, very sick patients are likely to have underlying coronary artery disease (CAD), but aggressively pursuing CAD diagnosis and treatment often seems inappropriate. Thus, we are left with an uncomfortable feeling that perhaps we should be doing more for the patient, especially given the poor prognosis of having a troponin elevation without ACS.
This paper does not provide any profound answers to this dilemma, but by detailing their experience, they provide reassurance for the rest of us. Fully one-third of hospitalized patients with an elevated troponin I do not have clinical evidence of ACS, but if studied, over half of them have significant CAD. Thus, the presence of CAD probably makes demand ischemia more likely to occur. Although troponin levels were generally lower in the non-ACS patients, the discriminatory value of the level was not high. However, almost all the non-ACS patients had other clinical conditions known to be associated with elevated troponin levels, and these conditions, plus an elevated troponin, represent a high-risk group. Perhaps the main message of the study is that an aggressive approach to CAD diagnosis and treatment is usually inappropriate because of the increased risk to such patients of an invasive procedure and antithrombic medications.
Let me give you an example from my experience. A man was seen in the emergency department for symptoms that could have been cardiac in origin, as well as hyperacute T-wave elevations on ECG. A troponin was sent and was elevated. Due to door-to-balloon time considerations, troponin results are obtained more quickly than other standard laboratory tests, so the patient was taken to the catheterization laboratory. Only after arterial access was obtained, was it learned that his other laboratory tests were consistent with diabetic ketoacidosis, a known cause of elevated troponin levels and an abnormal ECG. The outcome in this case was not ideal, and points to the value of taking a little time to consider other causes of an elevated troponin.
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