1 Department of Epidemiology, School of Public Health, University of North Carolina, Chapel Hill, NC.
2 Collaborative Studies Coordinating Center, Department of Biostatistics, School of Public Health, University of North Carolina, Chapel Hill, NC.
3 Division of Epidemiology and Clinical Applications, National Heart, Lung, and Blood Institute, Bethesda, MD.
4 Department of Epidemiology, School of Public Health, State University of New York, Albany, NY.
5 Department of Epidemiology and Health Services Evaluation, Faculty of Health Sciences, Ben Gurion University of the Negev, Beersheva, Israel.
6 Department of Pediatrics, School of Medicine, University of Mississippi, Jackson, MS.
7 Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis, MN.
Received for publication September 16, 2004; accepted for publication September 22, 2004.
We thank Dr. Roger for her discerning and perceptive remarks (1) on our article (2). We would like to follow up on two of the important points she raised.
The first point relates to the adoption of troponin in community practice and its impact on evaluating trends in hospitalized myocardial infarction. Dr. Roger astutely raises the issue of site-specific differences in the adoption of troponin. In the Atherosclerosis Risk in Communities (ARIC) Study communities, the use of troponin among cases discharged with ARIC target codes changed rapidly during the study period, increasing from less than 10 percent in 1996 to over 90 percent in 2001. If the change had occurred in a random manner across study centers, this would not have posed a particular problem in developing methods for adjustment. However, in multicommunity surveillance studies such as the ARIC Study, the adoption of troponin between and within communities is varied. For example, in some communities, more than two thirds of eligible cases had troponin measurements without a creatine kinase MB fraction measurement, indicating the replacement of older biomarkers. In other communities, the addition of troponin to existing biomarkers was the predominate practice. In these communities, only a small percentage of cases (<5 percent) had a stand-alone troponin measurement. Further complicating this was the within-community variation. Within a single community, some hospitals supplemented their biomarker armamentarium while others were full adopters of troponin.
One focus of our future work will be finding ways to adjust event rates, not only for greater sensitivity to troponin use but also to account for the fact that in some hospitals old biomarkers have been dropped. This applies to shifts in biomarkers that predate the troponin era as well (e.g., lactate dehydrogenase, lactate dehydrogenase isoenzymes, creatine kinase, creatine kinase MB, and creatine kinase MB mass). Such adjustments will allow us to evaluate long-term trends in a multicommunity environment where mandating study centers to retain a certain set of biomarkers may not be practical.
The second point relates to our use of two times the upper limit of normal to define an abnormal biomarker and Dr. Rogers correct assertion that this is "at variance with the current guideline-based definition" (1, p. 1149). As Dr. Roger noted, the recent American Heart Association Scientific Statement on Case Definitions for Acute Coronary Heart Disease in Epidemiology and Clinical Research Studies outlines definitions for biomarker evidence based primarily on rising or falling patterns in the setting of clinical cardiac ischemia (3). However, 5 years before the American Heart Association Scientific Statement was published, we were faced with the transition toward use of troponin in the ARIC communities and how to deal with its impact on our diagnostic algorithm. In the absence of a clear consensus at the time, we chose to apply the same thresholds as were used for creatine kinase (i.e., two times the upper limit of normal). This approach favors consistency, greater specificity, and transparency of application. This was a reasonable approach to take during the transition phase that characterized most hospitals in recent years. As Dr. Roger suggested, the impact on trends of adopting new case definitions will be examined, but this may be best applied when the use of troponin in the community has stabilized somewhat. Of course, considering dynamic changes in any diagnostic element and interpreting their impact requires greater reliance on information that speaks to the timing of symptom onset and laboratory measurements, as well as the specifics of type and severity of trauma.
We fully agree with Dr. Rogers conclusions that these and future changes in diagnostic criteria underscore the importance of continued long-term, detailed monitoring of myocardial infarction in communities.
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