Endogenous serum erythropoietin and no-reflow in patients with ST-elevation myocardial infarction

Background In models of acute ischaemia, erythropoietin (EPO) administration has been found to attenuate vascular injury largely through reduced apoptosis, suppressed inflammation and increased nitric oxide availability. We studied the association between circulating endogenous EPO and no-reflow in patients with first ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI). Methods Blood sampling was performed before PPCI. Consecutive patients with (n=24) or without (n=24) evidence of angiographic no-reflow after PPCI were enrolled. Angiographic no-reflow was defined as Thrombolysis in Myocardial Infarction (TIMI) flow ≤2 or as TIMI flow=3 but with myocardial blush grade -1, P=0·001, and 4·0 (0·6-7·1) vs. 9·3 (1·0-12·6) mIUmL ^-1, P=0·01, respectively]. At multivariable analysis, decreasing EPO tertiles and left anterior descending as the infarct-related artery were the only factors that predicted both angiographic and ECG no-reflow (P=0·017 and P=0·02 for EPO; P0·05 for left anterior descending artery, respectively). Conclusions We found an independent, graded, inverse relation between endogenous EPO levels and angiographic and ECG no-reflow following PPCI. In animal models of ischaemia, EPO has been found to be protective. In humans, endogenous EPO may contribute to offset the mechanisms responsible for no-reflow.