Objective Up to 62% of perimenopausal women have depression symptoms. However, there is no efficacy treatment. The aim of this study is to compare the clinical efficacy and safety of EA therapy and escitalopram on perimenopause women with mild-moderate depressive symptom. Method A multicenter, randomized, positive-controlled clinical trial was conducted at 6 hospitals in China. 242 perimenopause women with mild-moderate depressive symptom were recruited and randomly assigned to receive 36 sessions of EA treatment or escitalopram treatment. The primary outcome measure was the 17-item Hamilton Depression Rating Scale (HAMD-17). The secondary outcome measures include menopause-specific quality of life (MENQOL) and serum sexual hormones which include estrogen, follicle-stimulating hormone, and luteinizing hormone. Results 221 (91.3%) completed the study, including 116 in the EA group and 105 in the escitalopram group. The baseline levels of demographic and outcome measurements were similar in the two groups. In the intervention period, there was no difference between two groups. However, in the follow-up, both HAMD-17 and MENQOL were significantly decreased, and at week 24 the mean differences were −2.23 and −8.97, respectively. There were no significant differences in the change of serum sexual hormones between the two groups. No serious adverse events occurred. Conclusion EA treatment is effective and safe in relieving depression symptom and improving the quality of life in the perimenopausal depression. Further research is needed to understand long-term efficacy and explore the mechanism of this intervention. This study is registered with ClinicalTrials.gov NCT02423694.

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The aim of this paper is to observe the change of mitochondrial aldehyde dehydrogenase 2 (ALDH2) when diabetes mellitus (DM) rat heart was subjected to ischemia/reperfusion (I/R) intervention and analyze its underlying mechanisms. DM rat hearts were subjected to 30 min regional ischemia and 120 min reperfusion in vitro and pretreated with ALDH2 activator ethanol (EtOH); cardiomyocyte in high glucose (HG) condition was pretreated with ALDH2 activator Alda-1. In control I/R group, myocardial tissue structure collapse appeared. Compared with control I/R group, left ventricular parameters, SOD activity, the level of Bcl-2/Bax mRNA, ALDH2 mRNA, and protein expressions were decreased and LDH and MDA contents were increased, meanwhile the aggravation of myocardial structure injury in DM I/R group. When DM I/R rats were pretreated with EtOH, left ventricular parameters, SOD, Bcl-2/Bax, and ALDH2 expression were increased; LDH, MDA, and myocardial structure injury were attenuated. Compared with DM + EtOH I/R group, cyanamide (ALDH2 nonspecific blocker), atractyloside (mitoPTP opener), and wortmannin (PI3K inhibitor) groups all decreased left ventricular parameters, SOD, Bcl-2/Bax, and ALDH2 and increased LDH, MDA, and myocardial injury. When cardiomyocyte was under HG condition, CCK-8 activity and ALDH2 protein expression were decreased. Alda-1 increased CCK-8 and ALDH2. Our findings suggested enhanced ALDH2 expression in diabetic I/R rats played the cardioprotective role, maybe through activating PI3K and inhibiting mitoPTP opening.

Few studies have compared the clinical manifestations of patients with premature acute coronary syndrome (ACS) and late-onset ACS as well as the adverse cardiovascular events following percutaneous coronary intervention (PCI). To investigate the clinicopathological characteristics of patients with premature ACS and adverse cardiovascular events following PCI, a total of 726 patients with ACS undergoing PCI were divided into two groups: A premature ACS group and a late-onset ACS group. Following discharge, all patients were followed-up for an average of 23.5±5.3 months. Clinical characteristics, Gensini scores, vascular lesions and adverse cardiovascular events were compared between the two groups. There were no significant differences in smoking, diabetes, ACS composition ratio, baseline treatment of coronary heart disease, high-density lipoprotein level and C-reactive protein levels between the two groups. Sex and hypertriglyceridemia were determined to be independent risk factors of premature ACS, while age, hypertension and a high Gensini score were independent risk factors for adverse cardiovascular events in patients with ACS following PCI. Furthermore, the prevalence of premature ACS was significantly higher in females. Although serum levels of fasting blood glucose, total cholesterol, triglycerides and low-density lipoprotein were also significantly higher in patients with premature ACS compared with patients with late-onset ACS, patients with premature ACS exhibited fewer vascular lesions compared with patients with late-onset ACS. Furthermore, the incidence of adverse cardiovascular events in patients with ACS following PCI did not differ significantly between premature and late-onset ACS groups. Taken together, these results suggest that female patients should be closely observed for early risk factors of premature ACS to prevent and reduce the occurrence of adverse cardiovascular events in patients with ACS following PCI.

Clopidogrel resistance in patients with acute coronary syndrome (ACS) is one of the key causes of recurrent cardiovascular disease (CVD) events after percutaneous coronary intervention (PCI). Clopidogrel targets the platelet membrane receptor P2RY12 to inhibit platelet aggregation via adenosine diphosphate (ADP). This study aimed to investigate the relationships between P2RY12 polymorphisms and the risk of clopidogrel resistance and adverse CVD events after PCI. From January 2015 to December 2014, patients who had been diagnosed with ACS undergoing PCI and treated with clopidogrel were recruited for this prospective cohort study (N = 498). Data regarding demographics, medication intake, and ACS lesion were recorded, and whole blood samples were collected for biochemical tests, ADP-induced platelet aggregation ratio detection, and P2RY12 genotyping. P2RY12 genotyping was performed by polymerase chain reaction. The left ventricular ejection fraction was calculated by echocardiography. After 3 to 12 months of follow-up, data regarding any adverse CVD event or death were recorded. The allele frequencies for the T variation alleles in C34T and G52T of P2RY12 were 20.3% and 11.6%, respectively. Patients with T variations at C34T or G52T of P2RY12 had a significantly higher risk of clopidogrel resistance (C34T: P < 0.001; G52T: P = 0.003) and total cardiovascular events (C34T: P = 0.013; G52T: P = 0.018) compared to those with the wild-type genotype. Moreover, multivariable logistic regression showed that patients with the T variations in C34T (odds ratio [OR]: 2.89 (95% confidence interval [CI]: 1.48-5.64), P = 0.002) and G52T (OR: 3.68 [95% CI: 1.71-7.92], P = 0.001) also had a significantly higher risk of clopidogrel resistance. Also, the T variations in C34T (OR: 2.68 [95% CI: 1.07-6.73], P = 0.035) and G52T (OR: 5.64 [95% CI: 1.52-20.88], P = 0.010) significantly increased the risk of post-PCI CVD events after accounting for confounding factors. The P2RY12 gene polymorphisms C34T and G52T were significantly associated with a higher risk of clopidogrel resistance and sequential cardiovascular events in Chinese ACS patients after PCI.Abbreviations: ACS = acute coronary syndrome, ADP = adenosine diphosphate, CAD = coronary artery disease, CI = confidence interval, CVD = cardiovascular disease, CYP = cytochrome P450, LVEF = left ventricular ejection fraction, OR = odds ratio, PAR = platelet aggregation ratio, PCI = percutaneous coronary intervention, PCR = polymerase chain reaction, STEMI = ST segment elevated myocardial infarction.

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