A Comparison of Biomarker Rise in Type 1 and Type 2 Myocardial Infarction.

Abstract Background: Despite differing underlying pathophysiology, type 1 and type 2 myocardial infarction share many of the same diagnostic criteria and can be challenging to differentiate in clinical practice. Correctly differentiating type 1 from type 2 myocardial infarction is important because the two are managed differently. The aim of this study was to compare the patterns of rise of cardiac troponin (cTn) and creatine kinase MB (CK-MB) in type 1 versus type 2 myocardial infarction. Methods: We analyzed retrospective data on 200 patients with myocardial infarction (97 with type 1, 103 with type 2), excluding patients with ST-segment elevation myocardial infarction. The percent rise from trough to peak values and the ratio of the peak to the upper limit of normal (RULN) were calculated for both cTnT and CK-MB. The ratio of peak cTnT to peak CK-MB was also calculated before and after adjusting for sex, glomerular filtration rate (GFR), and infarct size. Results: Type 1 myocardial infarction tended to be larger than type 2 myocardial infarction, with a significantly higher mean % rise for both cTnT and CK-MB as well as higher mean RULN (207 vs. 86 for cTnT, p=0.02; 9 vs. 4 for CK-MB, p=0.002). There was a trend toward a higher rise of cTnT than CK-MB in type 2 compared to type 1 myocardial infarction, as demonstrated by the ratio of peak cTnT to peak CK-MB (0.09 in type 2 myocardial infarction vs. 0.06 in type 1 myocardial infarction, p=0.06). This difference persisted after adjusting for sex, GFR, and infarct size (p=0.05). Conclusion: Both cTnT and CK-MB rise higher in type 1 than in type 2 myocardial infarction. Meanwhile, cTnT tends to rise out of proportion to CK-MB in type 2 myocardial infarction. These patterns may have considerable implications for the differentiation and subsequent treatment of patients with type1 versus type 2 myocardial infarction.