September 28th, 2011
Troponin Elevation in Skeletal Muscle Disease: Vindication for the Consulting Cardiologist?
In an elegant study that will resonate with the anecdotal experience of many consulting cardiologists, Jaffe and colleagues provide strongly suggestive evidence that elevations in “cardiac” troponin T may not be quite as specific for cardiac muscle injury as has been claimed (see CardioExchange News blog). Among patients with skeletal myopathies who had elevations in cTnT but not cTnI, the investigators first excluded (within the limits of clinically available testing) a likely cardiac source of cTnT elevation. Then, from skeletal muscle biopsy specimens, they identified cTnT immunoreactivity within skeletal muscle.
I think it is clear that, in an era of increasingly sensitive troponin assays, we have a specificity problem when >50% of troponin elevations among hospitalized patients result from processes other than an acute coronary syndrome. Usually, such elevations arise from nonischemic causes of cardiac injury. These new findings, however, suggest that at least in some individuals with advanced skeletal muscle injury or chronic disease, cTnT elevation may not indicate cardiac injury at all. Whether this phenomenon is restricted to rare patients with advanced skeletal muscle disease or explains an important proportion of the “unexplained” cTnT elevations we see in the hospital is not clear. Moreover, although the limited data available suggest that skeletal muscle expression is more common with cTnT than with cTnI, we do not yet know whether similar or related issues contribute to specificity problems with cTnI as well.
We need to be careful not to over-interpret these findings, since the large majority of “non-ACS” troponin elevations do reflect cardiac injury. Because we have no good data to guide our care of patients with troponin elevations that do not appear to arise from ACS, our job as consultants is to arrive at a prudent, common-sense strategy that recognizes that these individuals are at high risk but that does not expose them to misguided over-testing. Recent work suggests that structural heart disease (LVH, LV dysfunction), rather than coronary disease, is frequently the culprit source of injury. In such cases, the troponin elevation is typically low-level and chronic, and there is really no indication for inpatient evaluation. In other cases, transient hemodynamic stressors may “unmask” structural heart disease and lead to transient troponin elevations. In the hospital, when I get the standard “troponin consult,” and no evidence supports acute ischemia or pulmonary embolism (which must be considered in the differential diagnosis), my strategy is to perform an echocardiogram to evaluate for structural heart disease, treat with low-dose aspirin with or without a beta-blocker, and “let the dust settle” before determining if any additional testing is needed.
What is your approach to the “unexplained” troponin elevation?