Info

hosp 1994

3 wks 1995

34 mos 1995

Favors low risk

Favors high nsK

hosp 1994

hosp 1994

3 wks 1995

34 mos 1995

Favors low risk

Favors high nsK

Fig. 6. Cumulative odds ratios for use of cTnT in patients without infarction for an outcome of infarction or cardiac death (top) or for an outcome of coronary artery revascularization (bottom). Squares indicate the actual values; lines indicate the 95% confidence intervals. Reproduced with permission from ref. 107.

group (49 and 29%, respectively). Furthermore, serial testing of TnT over an 8-h period (compared to CK-MB analysis over 12 h) detected the only patients who were CK-MB-positive. No patient who was cTnT-negative at 8 h later had positive CK-MB. In short-term follow-up (mean 21 d), there were no deaths in either group, but at 2 yr mortality was 27% in the cTnT-positive group compared with 7% in the cTnT-negative patients.

Hamm and colleagues recently reported the use of serial bedside testing for cTnT and cTnI at baseline and at 4 h after presentation in the ED with acute chest pain (45). In their outcome study of 773 consecutive patients presenting within 12 h of onset of symptoms and without ST-segment elevation on initial ECG, the use of qualitative monoclonal antibody-based bedside assays for cTnT and cTnI identified by 4 h after presentation 94 and 100%, respectively, of patients later determined to have MI by follow-up CK and CK-MB testing. Among unstable angina patients, 22% were positive by TnT and 36% by TnI bedside testing. Importantly, the 30-d risks of death or nonfatal MI in patients negative for TnT or TnI were only 1.1 and 0.3%, respectively. These results may be further enhanced by development of a cTnT device having a lower cutoff (0.08 vs 0.2 ng/mL) and greater cardiac specificity.

In a recent study of 1005 patients from six chest pain units in U.S. hospitals, the Chest Pain Evaluation by Creatine Kinase-MB, Myoglobin, and Troponin I (CHECKMATE) Investigators demonstrated the utility of multimarker strategies (MMS) of cardiac marker testing at the point-of-care compared with single marker testing in the local lab

Fig. 7. Overlap of myoglobin, CK-MB, and Tnl positivity during sampling. Reprinted with permission from ref. 111.

Fig. 7. Overlap of myoglobin, CK-MB, and Tnl positivity during sampling. Reprinted with permission from ref. 111.

oratory (111). In that study, MMS-1, which combined myoglobin, an early marker, with cTnl and CK-MB, later but specific markers, identified more positive patients at baseline (18.9%) or on serial testing (23.9%) than either a two-marker strategy (MMS-2), with CK-MB and cTnl (14.3 and 18.8%, respectively), or the single marker local laboratory strategy of CK-MB testing (5.2 and 8.8%, respectively), p = 0.001 for all comparisons. As shown in Fig. 7, among chest pain unit patients, no single marker, even with serial testing, was able to detect all patients at risk for subsequent cardiac events. Only 40% of patients were positive by more than one marker, and 21% of patients were positive only by myoglobin. The median time to detection of positive patients by MMS-1 was also shorter (2.5 h) compared with single marker local laboratory testing (3.4 h, p = 0.0001). Importantly, MMS-1 was also the best strategy for discriminating patients at risk for mortality and death or MI at 30 d.

As these studies suggest, the use of very specific cardiac markers or panels of markers and new testing strategies can identify early a subset of patients (of those who present without high risk features) who might benefit from earlier intervention. The challenge for future research in this area will be to identify which medical or interventional strategies can modify the future risk these patients face. Further, because these markers also identify a low risk population earlier than conventional testing might allow, the potential exists for further reductions in length of stay and expensive diagnostic testing, thus amplifying the cost savings possible through the use of Chest Pain Units.

For evaluation of the thousands of patients with acute nontraumatic chest pain who present to ED each year, serum markers of myocardial injury (alone or in combination) will continue to play an increasingly important role, not only in diagnosis and triage decisions, but also in identifying patients who are at increased risk for adverse outcomes in both the short and long term. In both regards, their utility extends across the spectrum

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