Search

Melatonin, an endogenously produced hormone, might potentially limit the ischemia reperfusion injury and improve the efficacy of mechanical reperfusion with primary percutaneous coronary intervention (pPCI) in ST-segment elevation myocardial infarction (STEMI). This study was aimed to evaluate whether the treatment effect of melatonin therapy in patients with STEMI is influenced by the time to administration. We performed a post hoc analysis of the Melatonin Adjunct in the Acute Myocardial Infarction Treated With Angioplasty trial (NCT00640094), which randomized STEMI patients to melatonin (intravenous and intracoronary bolus) or placebo during pPCI. Randomized patients were divided into tertiles according to symptoms onset to balloon time: first tertile (136 ± 23 minutes), second tertile (196 ± 19 minutes), and third tertile (249 ± 41 minutes). Magnetic resonance imaging was performed within 1 week after pPCI. A total of 146 patients presenting with STEMI within 360 minutes of chest pain onset were randomly allocated to intravenous and intracoronary melatonin or placebo during pPCI. In the first tertile, the infarct size was significantly smaller in the melatonin-treated subjects compared with placebo (14.6 ± 14.2 vs 24.9 ± 9.0%; p = 0.003). Contrariwise, treatment with melatonin was associated with a larger infarct size in the group of patients included in the third tertile (20.5 ± 8.7% vs 11.2 ± 5.2%; p = 0.001), resulting in a significant interaction (p = 0.001). In conclusion, the administration of melatonin in patients with STEMI who presented early after symptom onset was associated with a significant reduction in the infarct size after pPCI., (Copyright © 2017 Elsevier Inc. All rights reserved.)

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., (Copyright © 2010 Elsevier Inc. All rights reserved.)

We evaluated the possible relation between circulating levels of nocturnal melatonin, C-reactive protein, and the development of adverse cardiovascular events in patients with ST-segment elevation myocardial infarction. Patients who had developed adverse events during follow-up had significantly lower nocturnal melatonin levels than patients without events.

C-reactive protein, a marker of inflammation, is increasingly measured to stratify risk for coronary artery disease and guide clinical management. Likewise, a relation has been suggested between decreased nocturnal melatonin levels and coronary artery disease. However, little is known about the association between melatonin and C-reactive protein in patients with ischemic heart disease.