Type 1 cardiorenal syndrome (CRS1) is characterized by acute cardiac disease (e.g., acute heart failure [AHF]), leading to acute kidney injury. Sirtuin 1 (SIRT1), an NAD+‐dependent deacylase, has been found to be associated with CRS1. To confirm whether a correlation exists between SIRT1 variants and the risk of CRS1, the association between the prevalence of CRS1 and single‐nucleotide polymorphisms (SNPs) within the SIRT1 gene was investigated in AHF patients. A total of 316 Chinese AHF participants (158 patients with CRS1 and 158 age‐ and sex‐matched controls) were recruited for the present observational study to investigate the association between nine common SIRT1 SNPs (i.e., rs7895833 G > A, rs10509291 T > A, rs3740051 A > G, rs932658 A > C, rs33957861 C > T, rs7069102 C > G, rs2273773 T > C, rs3818292 A > G, and rs1467568 A > G) and the susceptibility to CRS1. Significant differences in genotype distribution between the control and CRS1 groups were found for rs7895833 and rs1467568. After applying a Bonferroni adjustment, the A allele of rs7895833 was still found to be protective (p = 0.001; odds ratio [OR] = 0.77) against CRS1 in this study population. The AA genotype of rs7895833 and the GA genotype of rs1467568 were associated with a significantly reduced risk of CRS1 (OR = 0.23 and 0.49, respectively). rs7895833 and rs1467568 were further analyzed as a haplotype, and the GA haplotype (rs7895833‐rs1467568) exhibited a significant association with CRS1 (p = 0.008), while the AA haplotype showed a significant protective effect (p = 0.022). Our study showed that SIRT1 rs7895833 and rs1467568 polymorphisms had a significant effect on the risk of developing CRS1 in a population in China.

Background. Myocardial ischemia/reperfusion injury (MIRI) usually induces serious health problems.Objectives. This study attempted to explore protective effects of (−)-epigallocatechin-3-gallate (EGCG) on MIRI and the associated mechanism. Materials and methods.Ischemia/reperfusion of an isolated rat heart (I/R model) and the MIRI model were used in this study. Myocardial infarction was measured with staining with 2,3,5-triphenyltetrazolium chloride (TTC). Ca 2+ and troponin T (TnT) concentrations in coronary perfusion fluid were evaluated using the chromatometry method. Ca 2+ concentration in cardiomyocytes was determined with detecting Ca 2+ fluorescence intensity. The ultrastructure of cardiomyocytes was observed using transmission electron microscopy (TEM). β-nicotinamide adenine dinucleotide (NAD + ) of cardiomyocytes was also determined. Results.The EGCG (I/R+EGCG) significantly reduced myocardial infarction size of isolated rat heart compared to I/R rats (p < 0.05), remarkably increased Ca 2+ and decreased TnT concentrations in coronary perfusion fluid of I/R rats compared to the I/R model (p < 0.05), as well as markedly decreased intracellular Ca 2+ concentration and promoted NAD + concentration in cardiomyocytes compared to I/R rats (p < 0.05). It also obviously maintained the mitochondrial structure in cardiomyocytes of I/R rats and improved the ultrastructure of cardiomyocytes of MIRI rats. Lonidamine (LND) treatment (I/R+EGCG+LND group) significantly blocked the effects of EGCG on I/R injury compared to the I/R+EGCG group (p < 0.05). The EGCG (MIRI+EGCG) significantly decreased myocardial infarction size compared to MIRI rats (p < 0.05) and remarkably enhanced Ca 2+ and reduced TnT concentrations in the pulmonary artery compared to that of MIRI rats (p < 0.05). Conclusions.The EGCG decreased myocardial infarction size in both I/R models and MIRI models by reducing intracellular Ca 2+ concentration, increasing TnT concentration, promoting NAD + concentration, and improving the ultrastructure of cardiomyocytes.

A 57-year-old man suffered chest pain during the COVID-19 pandemic, but he delayed medical treatment due to fear of infection. Four months later, symptoms chest tightness and shortness of breath appeared. Electrocardiogram (ECG) revealed old myocardial infarction; color sonography and myocardial CT revealed apical myocardial defect. He refused surgery and percutaneous transcatheter closure, and follow-up observation. After 22 months, the symptoms of chest tightness and shortness of breath aggravated. He recovered after percutaneous transcatheter closure, and was discharged. This case shows delayed closure is one of the possible options for the patients without severe organ dysfunction or hemodynamic disturbance.

A 57-year-old man suffered chest pain during the COVID-19 pandemic, but he delayed medical treatment due to fear of infection. After 4 months, symptoms of chest tightness and shortness of breath appeared. Electrocardiogram (ECG) revealed old myocardial infarction; color sonography and myocardial computed tomography revealed apical myocardial defect. He refused surgery and percutaneous transcatheter closure, and follow-up observation. After 22 months, the symptoms of chest tightness and shortness of breath aggravated. He recovered after percutaneous transcatheter closure, and was discharged. This case shows delayed closure is one of the possible options for patients without severe organ dysfunction or hemodynamic disturbance.