To assess whether habitual sleep duration or insomnia increase the incidence of hypertension. PubMed, EMBASE and Cochrane were searched without language restriction. Prospective cohort studies of ...adults with at least a 1-year follow-up duration were included. Habitual sleep duration or symptoms of insomnia were assessed as baseline exposure, and the outcome was incidence of hypertension. Subgroup, meta-regression and sensitivity analyses were conducted to assess heterogeneity, and Egger's test was used to assess publication bias. Eleven studies (17 cohorts) were included. Short sleep duration, sleep continuity disturbance (SCD), early-morning awakening (EMA) and combined symptoms of insomnia increased the risk of hypertension incidence (the relative risks (95% confidence intervals) were 1.21 (1.05-1.40) for short sleep duration, 1.20 (1.06-1.36) for SCD, 1.14 (1.07-1.20) for EMA and 1.05 (1.01-1.08) for combined insomnia symptoms). Less evidence exists to support conclusions about the association between long sleep duration or difficulty falling asleep (DFA) and hypertension incidence. No obvious heterogeneity or publication biases were found. Our meta-analysis demonstrates that short sleep duration and single/combined symptoms of insomnia (except DFA) are associated with an increased risk of hypertension incidence. It is important to consider sleep duration and insomnia during hypertension prevention and treatment. More laboratory studies on potential mechanisms and prospective observational studies with objective measures of sleep are needed.
Abstract Background Cardiovascular risk is inconsistent in the normal-weight, overweight, and obese individuals due to metabolic abnormality. We aimed to investigate combined effects of obesity and ...metabolic abnormality on the risk of cardiovascular disease and mortality. Methods The MEDLINE, EMBASE, Cochrane library, and references of relevant original articles prior to May 2013 were searched for prospective studies investigating cardiovascular risk and death associated with combined effects of obesity and metabolic syndrome or insulin resistance. Pooled relative risks (RR) and 95% confidence intervals (CI) were calculated using random-effects or fixed-effect models when appropriate. Results Fourteen perspective studies with a total of 299,059 participants and 12,125 cases of incident CVD, 2130 cases of CVD death, and 7071 cases of all-cause death were included in the meta-analysis. Compared with healthy normal-weight individuals, metabolically healthy overweight (MHOW) and obese (MHOB) individuals showed increased risk for CVD events, which appeared much stronger during the long-term follow-up period of > 15 years, with pooled RR of 1.47 (95% CI 1.37–1.58) in MHOW and 2.00 (95% CI 1.79–2.24) in MHOB. Normal-weight but metabolically abnormal individuals were at increased risk for CVD (pooled RR 1.81, 95% CI 1.56–2.10), CVD-related death (pooled RR 1.55, 95% CI 1.16–2.08), and all-cause death (pooled RR 1.27, 95% CI 1.10–1.47). Metabolically abnormal obese individuals were at the highest risk for CVD and mortality. Conclusion Individuals with metabolic abnormality, although at normal-weight, had an increased risk of CVD and mortality. Healthy overweight and obese persons had higher risk, which refuted the notion that metabolically healthy obese phenotype is a benign condition.
Unruptured intracranial aneurysm (UIA) is a life-threatening cerebrovascular condition. Whether changes in gut microbial composition participate in the development of UIAs remains largely unknown. We ...perform a case-control metagenome-wide association study in two cohorts of Chinese UIA patients and control individuals and mice that receive fecal transplants from human donors. After fecal transplantation, the UIA microbiota is sufficient to induce UIAs in mice. We identify UIA-associated gut microbial species link to changes in circulating taurine. Specifically, the abundance of Hungatella hathewayi is markedly decreased and positively correlated with the circulating taurine concentration in both humans and mice. Consistently, gavage with H. hathewayi normalizes the taurine levels in serum and protects mice against the formation and rupture of intracranial aneurysms. Taurine supplementation also reverses the progression of intracranial aneurysms. Our findings provide insights into a potential role of H. hathewayi-associated taurine depletion as a key factor in the pathogenesis of UIAs.
The relationship between dietary glycemic index, glycemic load and risk of coronary heart disease (CHD), stroke, and stroke-related mortality is inconsistent.
We systematically searched the MEDLINE, ...EMBASE, and Science Citation Index Expanded databases using glycemic index, glycemic load, and cardiovascular disease and reference lists of retrieved articles up to April 30, 2012. We included prospective studies with glycemic index and glycemic load as the exposure and incidence of fatal and nonfatal CHD, stroke, and stroke-related mortality as the outcome variable. Pooled relative risks (RR) and 95% confidence intervals (CI) were calculated using random-effects models.
Fifteen prospective studies with a total of 438,073 participants and 9,424 CHD cases, 2,123 stroke cases, and 342 deaths from stroke were included in the meta-analysis. Gender significantly modified the effects of glycemic index and glycemic load on CHD risk, and high glycemic load level was associated with higher risk of CHD in women (RR=1.49, 95%CI 1.27-1.73), but not in men (RR=1.08, 95%CI 0.91-1.27). Stratified meta-analysis by body mass index indicated that among overweight and obese subjects, dietary glycemic load level were associated with increased risk of CHD (RR=1.49, 95%CI 1.27-1.76; P for interaction=0.003). Higher dietary glycemic load, but not glycemic index, was positively associated with stroke (RR=1.19, 95% CI 1.00-1.43). There is a linear dose-response relationship between dietary glycemic load and increased risk of CHD, with pooled RR of 1.05 (95%CI 1.02-1.08) per 50-unit increment in glycemic load level.
High dietary glycemic load is associated with a higher risk of CHD and stroke, and there is a linear dose-response relationship between glycemic load and CHD risk. Dietary glycemic index is slightly associated with risk of CHD, but not with stroke and stroke-related death. Further studies are needed to verify the effects of gender and body weight on cardiovascular diseases.
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Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Vascular endothelial senescence contributes to atherosclerosis and coronary artery disease (CAD), but the mechanisms are yet to be clarified. We identified that microRNA‐216a (miR‐216a) significantly ...increased in senescent endothelial cells. The replicative senescence model of human umbilical vein endothelial cells (HUVECs) was established to explore the role of miR‐216a in endothelial ageing and dysfunction. Luciferase assay indicated that Smad3 was a direct target of miR‐216a. Stable expression of miR‐216a induced a premature senescence‐like phenotype in HUVECs with an impairment in proliferation and migration and led to an increased adhesion to monocytes by inhibiting Smad3 expression and thereafter modulating the degradation of NF‐κB inhibitor alpha (IκBα) and activation of adhesion molecules. Conversely, inhibition of endogenous miR‐216a in senescent HUVECs rescued Smad3 and IκBα expression and inhibited monocytes attachment. Plasma miR‐216a was significantly higher in old CAD patients (>50 years) and associated with increased 31% risk for CAD (odds ratio 1.31, 95% confidence interval 1.03‐1.66; P = .03) compared with the matched healthy controls (>50 years). Taken together, our data suggested that miR‐216a promotes endothelial senescence and inflammation as an endogenous inhibitor of Smad3/IκBα pathway, which might serve as a novel target for ageing‐related atherosclerotic diseases.
Fulminant myocarditis (FM) has unacceptable high mortality. This study aimed to evaluate the therapeutic efficacy of a life support-based comprehensive treatment regimen (LSBCTR), a completely novel ...treatment regimen, for FM. A total of 169 FM patients recruited from January 2008 to December 2018 were divided into two groups: patients receiving LSBCTR (81 cases), which includes (i) mechanical life support (positive pressure respiration, intra-aortic balloon pump with or without extracorporeal membrane oxygenation), (ii) immunomodulation therapy using sufficient doses of glucocorticoids and immunoglobulins, and (iii) application of neuraminidase inhibitors, and those receiving conventional treatment (88 cases). The endpoints were in-hospital death and heart-transplantation. Of all the population, 44 patients (26.0%) died in hospitals. In-hospital mortality was 3.7% (3/81) for LSBCTR group and 46.6% (41/88) for traditional treatment (P<0.001). Early application of LSBCTR, mechanical life support, neuraminidase inhibitors, and immunomodulation therapy significantly contributed to reduction in in-hospital mortality. This study describes a novel treatment regimen for FM patients that dramatically reduces in-hospital mortality. Its generalization and clinical application will efficiently save lives although further optimization is needed. This study offers an insight that virus infection induced inflammatory waterfall results in cardiac injury and cardiogenic shock and is the therapeutic target.
Background: The effect of green tea catechins (GTCs) with or without caffeine on glycemic control is controversial.Objective: We aimed to identify and quantify the effects of GTCs or GTC-caffeine ...mixtures on glucose metabolism in adults.Design: A comprehensive literature search was conducted to identify relevant trials of GTCs with or without caffeine on markers of glycemic control fasting blood glucose (FBG), fasting blood insulin (FBI), glycated hemoglobin (Hb A1c), and homeostatic model assessment of insulin resistance (HOMA-IR). Weighted mean differences were calculated for net changes by using fixed-effects models. Prespecified subgroup analyses were performed to explore the influence of covariates on net changes in FBG and FBI concentrations.Results: Twenty-two eligible randomized controlled trials with 1584 subjects were identified. Pooled analyses showed that FBG (−1.48 mg/dL; 95% CI: −2.57, −0.40 mg/dL) decreased significantly with GTCs with or without caffeine, whereas FBI (0.04 μU/mL; 95% CI: −0.36, 0.45 μU/mL), Hb A1c (−0.04%; 95% CI: −0.15, 0.08%), and HOMA-IR (−0.05; 95% CI: −0.37, 0.26) did not. Subgroup analyses indicated that the glucose-lowering effect was apparent when the duration of follow-up was over a median of 12 wk. Overall, no significant heterogeneity was detected for FBG, FBI, Hb A1c, or HOMA-IR.Conclusions: The meta-analysis showed that the administration of GTCs with or without caffeine resulted in a significant reduction in FBG. The limited data available on GTCs did not support a positive effect on FBI, Hb A1c, or HOMA-IR. Thus, more large and well-designed trials are needed in the future. This trial was registered at http://www.crd.york.ac.uk/prospero as CRD42012002139.
The molecular mechanisms that drive the development of cardiac hypertrophy in hypertrophic cardiomyopathy (HCM) remain elusive. Accumulated evidence suggests that microRNAs are essential regulators ...of cardiac remodelling. We have been suggested that microRNAs could play a role in the process of HCM. To uncover which microRNAs were changed in their expression, microRNA microarrays were performed on heart tissue from HCM patients (n = 7) and from healthy donors (n = 5). Among the 13 microRNAs that were differentially expressed in HCM, miR‐451 was the most down‐regulated. Ectopic overexpression of miR‐451 in neonatal rat cardiomyocytes (NRCM) decreased the cell size, whereas knockdown of endogenous miR‐451 increased the cell surface area. Luciferase reporter assay analyses demonstrated that tuberous sclerosis complex 1 (TSC1) was a direct target of miR‐451. Overexpression of miR‐451 in both HeLa cells and NRCM suppressed the expression of TSC1. Furthermore, TSC1 was significantly up‐regulated in HCM myocardia, which correlated with the decreased levels of miR‐451. As TSC1 is a known positive regulator of autophagy, we examined the role of miR‐451 in the regulation of autophagy. Overexpression of miR‐451 in vitro inhibited the formation of the autophagosome. Conversely, miR‐451 knockdown accelerated autophagosome formation. Consistently, an increased number of autophagosomes was observed in HCM myocardia, accompanied by up‐regulated autophagy markers, and the lipidated form of LC3 and Beclin‐1. Taken together, our findings indicate that miR‐451 regulates cardiac hypertrophy and cardiac autophagy by targeting TSC1. The down‐regulation of miR‐451 may contribute to the development of HCM and may be a potential therapeutic target for this disease.
It has been shown in previous studies that Chinese patients with acute aortic dissection (AD) were approximately 10 years younger than patients from western countries. However, there is a lack of ...studies concerning the age-related differences in clinical characteristics and outcomes in Chinese patients with acute AD. A total of 1,061 patients with AD (570 type A and 491 type B AD) were enrolled between 2006 and 2008. The clinical characteristics were compared between the patients in our study and those in the International Registry of Acute Aortic Dissection (IRAD). Compared with patients in the IRAD, those in our study were relatively younger, comprised more males, and had a higher proportion of Marfan syndrome but received fewer surgical interventions. When stratified by 10-year age, younger patients were more likely to have type A AD, familial AD, and Marfan syndrome, whereas older patients tended to comprise more females and type B AD. As age increased, the proportion of surgical intervention gradually decreased regardless of the type of AD. During a median follow-up of 2.2 years, 147 patients died, of whom 94 (63.9%) had type A AD and 53 (36.1%) had type B AD. Long-term mortality increased with increasing age, especially in patients above 70 years old. Furthermore, the recurrence rate of AD was higher in both the young and the older patients. In conclusion, compared with western patients with AD, Chinese patients have distinct characteristics and more attention should be paid to the young and older patients because of their high long-term mortality and recurrence rate.
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