Usefulness of intraplatelet melatonin levels to predict angiographic no-reflow after primary percutaneous coronary intervention in patients with ST-segment elevation myocardial infarction.

Platelet aggregates appear to have a pathogenic role in the no-reflow phenomenon, which is associated with impaired clinical outcome in patients with ST-segment elevation myocardial infarction (STEMI). Melatonin, a hormone that plays a major role in biological circadian rhythms, is present in human platelets. Lowered circulating melatonin levels predict poor outcome in patients with STEMI undergoing primary percutaneous coronary intervention (PPCI). We investigated whether intraplatelet melatonin levels correlate with angiographic no-reflow after PPCI in patients with STEMI. We studied 180 consecutive patients with a first STEMI who underwent PPCI within 6 hours from onset of symptoms. Intraplatelet melatonin levels were measured in platelet-rich plasma using an enzymatic immunoassay method. After PPCI, angiographic no-reflow (defined as Thrombolysis In Myocardial Infarction grade < 2 flow) was observed in 63 patients (35%). Patients with angiographic no-reflow had lower intraplatelet melatonin levels compared to patients without no-reflow (12.32 ± 3.64 vs 18.62 ± 3.88 ng/100,000 platelets, p < 0.0001). After adjusting by potential confounders, binary logistic regression analysis showed that intraplatelet melatonin levels were the only significant predictor of angiographic no-reflow (odds ratio 1.58, 95% confidence interval 1.37 to 1.82, p < 0.0001). In conclusion, low intraplatelet melatonin concentration predicts angiographic no-reflow after PPCI in patients with STEMI.