Context: The role of melatonin receptor in cardiomyocyte oxidative stress has not been investigated. Aim: The aim of our study is to verify the beneficial effects of melatonin receptors on cardiomyocyte viability under oxidative stress. Methods: Cardiomyocytes were treated with hydrogen peroxide. Cell viability was measured via MTT assay and TUNEL staining. Then, anti-oxidative factors measurement and signaling pathway analysis were performed via qPCR and ELISA. Results: Melatonin receptor activation could attenuate hydrogen peroxide-mediated cardiomyocyte death via reducing apoptosis. At the molecular levels, melatonin receptor activation reduced inflammation response and maintained mitochondrial membrane potential. In addition, melatonin receptor activation is associated with decreased oxidative stress and increased anti-oxidative factors. Finally, we found that melatonin receptor activation triggered an elevation in the activity and expression of ERK pathway and blockade of ERK pathway would abolish the beneficial effects exerted by melatonin receptors activation on cardiomyocyte survival under oxidative stress. Conclusions: Our data suggest that melatonin receptor could attenuate oxidative stress injury in cardiomyocyte through regulation of the ERK signaling pathway.

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Background: The de Winter electrocardiogram (ECG) pattern is a rare presentation of ST‐segment elevation myocardial infarction (STEMI) equivalent. The clinical profile of de Winter syndrome remains to be clarified.Methods: Medical records of 1865 consecutive patients with acute myocardial infarction admitted from November 2018 to July 2023 were screened. Twelve patients (0.6%) with de Winter syndrome were included. STEMI patients whose culprit vessel was the left anterior descending artery (LAD) but without de Winter ECG pattern were selected as controls after 1:2 matching for age and sex.Results: The de Winter syndrome patients were all male, aged 49.0 (46.3–52.5) years. The culprit lesion was the proximal LAD in seven patients (58.3%), the middle LAD in three (25%), the left main coronary artery in one (8.3%), and the ramus intermedius artery in the other. All of their culprit lesions had TIMI Thrombus Grade < 4, Cohen‐Rentrop Score ≤ 2, and residual stenosis ≥ 80% after pretreatment with thrombus aspiration or balloon predilatation. Intracoronary imaging data were available in four patients, showing severe atherosclerotic stenosis. Compared with STEMI, de Winter syndrome had a higher prevalence of prior recurrent angina (75.0% vs. 37.5%, p = 0.034), better coronary collateralization (Cohen‐Rentrop Score: 1 vs. 0, p = 0.001), lower thrombus burden (TIMI grade: 1 vs. 2, p = 0.005) but more severe atherosclerotic stenosis in the culprit lesions (90% vs. 60%, p < 0.001).Conclusions: The culprit lesions of de Winter syndrome have a low thrombus burden, severe atherosclerotic stenosis, and poor collateral circulation protection.