Background: Hypertension is a major worldwide public health problem. Previous studies have indicated that ambient temperature is associated with blood pressure (BP), but the nature of this association remains unclear. Objective: The objective of this meta-analysis was to investigate the relationship between ambient temperature and BP. Methods: We performed a systematic search of the literature indexed in PubMed, Web of Science, and ScienceDirect between 1980 and 2016. The pooled effect sizes for exposure to low/moderate temperatures, as well as high-temperature exposure, were calculated using a random-effects model. Results: Fifteen studies were included in this meta-analysis. Twelve of these reported the effects of low/moderate-temperature exposure, two reported the effects of high-temperature exposure, and one reported the effects of both low/moderate- and high-temperature exposure. For low/moderate-temperature exposure, 1°C decrease in temperature was associated with 0.40 mmHg (95% confidence interval [CI]: 0.34–0.46) increase in systolic BP and 0.13 mmHg (95% CI: 0.08–0.18) increase in diastolic BP. For high-temperature exposure, the relationship between BP and temperature was not statistically significant. Conclusion: For low/moderate-temperature exposure, a decrease in temperature was associated with an increase in BP. In contrast, the relationship between high-temperature exposure and BP was not statistically significant.

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Pneumothorax is a relatively common early complication after pacemaker implantation due to subclavian vein puncture, while pneumothorax associated pneumomediastinum and subcutaneous emphysema are rather unusual. Herein, we reported a case of bilateral pneumothorax associated with pneumomediastinum and widespread bilateral subcutaneous emphysema after pacemaker implantation due to percutaneous subclavian vein approach after multiple attempts and was successfully relieved by continuous low-volume oxygen inhalation, subcutaneous needles, and incision drainage.

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Inflammatory processes play an important role in the development of atherosclerotic disease. However, the relationship between white blood cell (WBC) count and the risk of peripheral arterial disease (PAD) is not well established, especially in the Chinese population. A total of 9113 Chinese participants without acute inflammation from an atherosclerosis cohort were included in our analysis. Ankle-brachial index (ABI) was measured using Omron BP-203RPEIII machine. PAD was defined as ABI <0.9. Multivariate regression model was used to evaluate the association of WBC count and PAD status. Mean (standard deviation [SD]) WBC was 6.07 ± 1.59 × 10⁹/L. Mean (SD) ABI was 1.10 ± 0.09 and the prevalence of PAD was 2.4%. WBC count was significantly associated with PAD (odds ratio [OR] = 1.25, 95% confidence interval [CI]: 1.16–1.34, P < 0.001) with every 1 × 10⁹/L increase of WBC count. This relationship remained statistically significant (OR = 1.19, 95% CI: 1.10–1.28, P < 0.001) after adjustment for sex, age, body mass index, current smoking and drinking status, hypertension, diabetes mellitus, dyslipidemia, history of stroke and coronary heart disease, antihypertensive agents, lipid-lowering agents, and hypoglycemic agents. Consistently, PAD ratio was also dose-dependent related to the quartiles of WBC count in multivariate regression model (OR = 1.66, 95% CI: 1.05–2.64, P = 0.032; OR = 2.51, 95% CI: 1.61–3.92, P < 0.001, for Q3 or Q4 vs. Q1 group, respectively). Elevated WBC count independently associates with high PAD prevalence in a Chinese community-based population, which supports the hypothesis that systemic inflammation acts as a pivotal part in the etiology of the atherosclerotic cardiovascular disease.

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Objective: The objective of this study is to evaluate novel variations in a Chinese family of Han ethnicity, with arrhythmogenic right ventricular cardiomyopathy (ARVC) by the powerful technology of whole-exome sequencing (WES). Methods: Genomic DNA from representative family members was extracted and processed for WES via standardized methods. The exome sequence data were analyzed by Genome Analysis Toolkit software. Sanger sequencing was performed on DNA from the proband for genotype confirmation and from the other family members for familial co-segregation analysis. Results: A rare single nucleotide variant c.1592T>G (p.Phe531Cys) in exon 10 of desmoglein-2 (DSG2) was identified by WES in the affected individuals but not in the healthy control, which was confirmed by Sanger sequencing, suggesting that the mutation probably was a causal mutation for the familial disorder of ARVC. Conclusion: We identified a rare disease-causing mutation of the DSG2 gene associated with familial ARVC. The results might contribute to the early genetic analysis in inherited cardiomyopathies.

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Enhanced fibrosis and reactive oxygen species (ROS) generation are two major features of aged heart. Since a loss-of-function mutation of ALDH2 was found in nearly half of East Asian population, we explored the impact of ALDH2 deficiency on the process of aging in the heart. We found that the body weight increased profoundly in aged wild-type (WT) mice but not in ALDH2 knockout (KO) mice. However, the ratio of heart weight to body weight increased significantly only in KO mice. Echocardiographic assessment showed that left ventricular ejection fraction of aged WT mice was significantly decreased, which was further aggravated by ALDH2 deficiency. Further study revealed that the compromised cardiac function of aged KO mice might be resulted from PI3K/Akt pathway-mediated fibrosis formation, as shown by remarkable upregulation of collagen I, transforming growth factor-β, and α-smooth muscle actin expression. Aging-induced ROS generation was quantified by the expression of 4-hydroxy-2-nonenal-adducted proteins, which was notably increased in the myocardium of aged KO mice. Besides, the expression of cleaved caspase-3 and 8-oxoguanine DNA glycosylase also increased significantly in the myocardium of aged KO mice. Further study demonstrated that increased ROS generation stimulated a prominent upregulation of ROS scavenger SOD2 expression in the myocardium of aged WT mice but not in KO mice. Our findings suggest that mitochondrial ALDH2 deficiency accelerates aging in the heart by increasing fibrosis formation and oxidative stress.

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