Circulating HtrA2 as a novel biomarker for mitochondrial induced cardiomyocyte apoptosis and ischemia-reperfusion injury in ST-segment elevation myocardial infarction

Background Ischemia-reperfusion (I/R) injury in ST-segment elevation myocardial infarction (STEMI) significantly contributes to overall myocardial damage. As a consequence of I/R injury in the heart, the high-temperature requirement protein A2 (HtrA2) is released from the mitochondrial intermembrane space of cardiomyocytes to the cytoplasm, whereupon it induces apoptosis. Methods Serum was obtained from STEMI ( n =37), non–ST-segment elevation myocardial infarction (NSTEMI) ( n =20), stable coronary artery disease (CAD) ( n =17) and patients with CAD excluded ( n =9). In STEMI, I/R injury was assessed via measurement of ST-segment resolution. Results HtrA2 was significantly increased in STEMI compared to NSTEMI, stable CAD and patients with CAD excluded (981.3 (IQR: 543.5–1526.2)pg/mL vs. 494.5 (IQR: 413.8–607)pg/mL vs. 291 (IQR: 239–458.5)pg/mL vs. 692.2 (IQR: 276.6–964.7)pg/mL; p ≤0.0001). STEMI patients with HtrA2 level of at least the median or above had a higher peak creatine kinase (CK) ( p =0.0002) and cardiac troponin T levels (cTnT) ( p =0.0019). Significantly more STEMI patients with HtrA2 levels of at least the median or above were identified as I/R injury (87% vs. 42%; p Conclusion HtrA2 shows promise as a novel potential biomarker for mitochondrial-induced cardiomyocyte apoptosis and may help to identify I/R injury after STEMI.