IntroductionEpidemiological evidence suggests that overweight and obesity have been associated with acute myocardial infarction (AMI). However, data on this issue are controversial. This study aims to use meta-analysis to determine whether overweight and obesity are related to AMI.Material and methodsWe searched PubMed and Embase databases up to October 23rd, 2013 for related literature. The association of overweight and obesity with AMI was assessed by odd ratio (OR) with 95% confidence interval (CI) as the effect size. Then subgroup analysis was performed according to gender, area and study type.ResultsFive primary studies (one cohort study and four case-control studies) were included in this meta-analysis involving 36 803 participants, 14 883 of whom had an AMI. There was a significant association between overweight and AMI (OR = 1.27, 95% CI: 1.21–1.33, p < 0.001). Similar results revealed a relation between obesity and AMI (OR = 1.22, 95% CI: 1.07–1.40, p = 0.003). Subgroup analysis showed that overweight and obesity were positively associated with AMI risk except for obese subjects in Europe. There was no publication bias (Begg's test p = 0.972, Egger's test p = 0.858).ConclusionsBoth overweight and obesity increased the incidence of AMI, and it is necessary to control weight to prevent AMI. A large number of studies is needed to explore the mechanisms that link overweight and obesity with AMI.

Ellagic acid ameliorates monocrotaline-induced pulmonary artery hypertension via exerting its anti-oxidative property inhibiting NLRP3 inflammasome signal pathway in rats.

conclusionsOur results suggest that dietary capsaicin protects against cardiac hypertrophy and fibrosis in pressure overload mice through TRPV1.

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Abstract. The angiotensin (Ang) II/Ang II receptor (ATR)-associated calcium signaling pathway is the major cause of ventricular remodelling in patients with congestive heart failure (CHF). However, the calcium-regulated proteinases responsible for Ang II-induced remodelling are not well understood. We investigated the profiles of the Ang II/ ATR/calpain/calcineurin (CaN) pathway in human failing heart. We measured both the plasma and cardiac levels of Ang II and cardiac mRNA expression of ATR in 39 patients with CHF and 38 healthy controls. Importantly, protein expression of calpains, cleavage of cain/cabin1 and activity of CaN were tested. Both plasma and cardiac levels of Ang II were significantly increased in patients with CHF (both p<0.01), and the plasma Ang II concentration was closely correlated with the parameters of ventricular remodelling (r=±0.29-0.65, p<0.05 or <0.01). In addition, the cardiac level of AT1R but not AT2R was significantly upregulated in mild failing hearts (p<0.05) but dramatically downregulated in severe failing ones (p<0.01). CHF was associated with a marked upregulation of calpains, an increased cleavage of cain/cabin1, and the activation of CaN in the failing ventricular tissue. In patients with CHF, calpain upregulation was associated with an increase in cleavage of cain/cabin1 and the activation of CaN, indicating that these changes in calciumregulated proteinases contribute to Ang II-induced cardiac remodelling.