September 28th, 2011
Troponin Elevation in Skeletal Muscle Disease: Vindication for the Consulting Cardiologist?
Beth Waldron, MA
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?
7 Responses to “Troponin Elevation in Skeletal Muscle Disease: Vindication for the Consulting Cardiologist?”
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I recommend serial enzymes, and if there is not a typical rise and fall, and if the CK-MB is negative, I recommend no further testing. For those patients, I try to state clearly in the chart that the troponin test is a false positive test and not an indicator of MI. Unfortunately, troponins are ordered so freely in the emergency room now that I see 1-2 of these “troponin consults” daily. I think “high-sensitivity” troponin assays should be renamed “low-specificity” troponin assays.
John, I bet there isn’t a cardiology fellow around who doesn’t agree with you on that last line.
Everything isn’t so simple, expecially in the emergency room. Not always we see the tipically “raise and fall” of TnI because the values are only 0.2 and around, for 12 or 24 hours, and then we make diagnosis of ACS (confirmed by CGF). Ok for the advice to observe the LV by echo, but even more I think for a Consultant Cardiologist, as me, it could be more useful to weighten the meaning of the tipical or suspect manner of the symptoms and risk-factors of patients, in order to give the full meaning of these little movements of TnI values.
Dr. Brush has very nicely summarized my own thoughts on this increasingly common and difficult problem. Like him, I do not think any decision (diagnosis) can be made on a single value. Instead, the total picture must be embraced including a detailed and competent history, relevant PE (heart murmurs, gallops, etc.) and use of a more specific assay such as CK MB. My message in working with cardiology fellows on this issue is that hypertroponinemia is not equivalent to clinical myocardial infarction or ACS. The “rush to judgment” in applying the ACS label based upon a single value can lead to mis-diagnosis with associated expensive and perhaps unnecessary testing.
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I’ve seen several cases of CPK and Transaminases elevations well above uuper normal limits with no symptoms or signs of CV problems. Asking the patient for previous unusual or strong physical activity, or muscle hits may be nearly diagnostic, but if you miss an actual CV problem because of that kind of history based diagnosis, I don’t know what the oppinion of the court will be in case of a malpractice complaint. May be obtaining an informed consent in writing from the patient is good enough ?. Defensive medicine some times helps a patient, but usually it can be too expensive, it would be good gathering data about the cost of QALY for an extended or restricted diagnostic tests policy, or the NN to Test to avoid an event.
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CV stratification of the patient as a whole i think is more applicable in ER’s ptn before reaching a final diagnosis of ACS, cTn T , Plus EKG finding , clinical presentation, CV risk factors ,resting TTE or CTCA in some ED may help us other than depending on single value of false +ve C Tr T, plus advanced skeletal muscle dis i think it is chronic issue , no one of them will be presented to ED by chest pain without any clinical sign of his chronic ms dis ?..
Non-cardiac troponin elevations are extremely rare with the exception of severe renal failure, “unexplained” ones are common. It happens a lot in sick, and more so, critically ill patients who are tachycardic, hypoxic and hypotensive, especially in the setting of renal failure. Those are non-ACS acute MIs(or type 2 MIs). The approach usually depends on an underlying problem rather than cardiac issues.
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