December 27th, 2011
Possible Role for New Troponin Test to Diagnose MI
Larry Husten, PHD
A new study from Germany provides evidence that a new high-sensitive troponin I (hsTnI) assay may improve and speed the early diagnosis of acute MI. In an article published in JAMA, Till Keller and colleagues report on 1818 patients with acute chest pain in whom numerous biomarker tests were conducted at admission and at 3 and 6 hours after admission. They compared the diagnostic performance of hsTnI with that of contemporary troponin I and other biomarkers.
The hsTnI assay provided more diagnostic information than contemporary TnI, as measured by the area under the receiver operating characteristic (ROC) curve on admission:
- 0.96 (95% CI, 0.95-0.97) for hsTnI, versus 0.92 for contemporary TnI (95% CI, 0.90-0.94); P<.001
As anticipated, the hsTnI was better than contemporary TnI in detecting lower concentrations of troponin I and in the first hours after the onset of chest pain. Both troponin tests were superior to the other biomarkers that were included in the study.
The authors examined various time points and cutoffs for “rule-out MI.” The highest negative predictive value, 99.6%, was provided by hsTnI at 3 hours after admission using the 99th-percentile cutoff. The authors commented that their results suggest that “ruling out MI appears feasible as early as 3 hours after admission in a large proportion of patients with chest pain.”
For “rule-in MI,” the relative change in hsTnI within 3 hours after admission, in addition to the 99th-percentile cutoff, provided the highest positive predictive value: 96.5%.
THE negative predictive value of the 3 hour “conventional” trop I is really the same as the higher sensitivity assay. Also, the positive predictive value using the admission assay and the relative increase at 3 hours is better with the conventional one. So for me the study helps me interpret our current assay.
The era of “high sensitivity” troponin is here to stay. This will improve early detection both in the acute diagnostic area for patients presenting with ACS, as well as in the long term prevention arena (Apple F, AHA, 2010). However, with new technologies, new problems arise. For instance, in the Minnesota Heart Study, a troponin I greater than 10 PICOGRAMS/mL predicted an odds ratio of 6.5 for the 15 year prediction of coronary events in an unselected adult primary prevention population. We are left with the question, however, of what to do with a borderline elevated troponin in this population. Also, in the acute care setting, what do we do with a borderline elevated high sensitivity troponin in a patient presenting with chest pain? Clearly the era of high sensitivity troponin is arriving, but only more research will elucidate the myriad of questions about clinical management that arise with this new technology.