Weiyi Mai

Association between prediabetes and risk of cardiovascular disease and all cause mortality: systematic review and meta-analysis

Objectives To evaluate associations between different definitions of prediabetes and the risk of cardiovascular disease and all cause mortality. Design Meta-analysis of prospective cohort studies. Data sources Electronic databases (PubMed, Embase, and Google Scholar). Selection criteria Prospective cohort studies from general populations were included for meta-analysis if they reported adjusted relative risks with 95% confidence intervals for associations between the risk of composite cardiovascular disease, coronary heart disease, stroke, all cause mortality, and prediabetes. Review methods Two authors independently reviewed and selected eligible studies, based on predetermined selection criteria. Prediabetes was defined as impaired fasting glucose according to the criteria of the American Diabetes Association (IFG-ADA; fasting glucose 5.6-6.9 mmol/L), the WHO expert group (IFG-WHO; fasting glucose 6.1-6.9 mmol/L), impaired glucose tolerance (2 hour plasma glucose concentration 7.8-11.0 mmol/L during an oral glucose tolerance test), or raised haemoglobin A1c (HbA1c) of 39-47 mmol/mol(5.7-6.4%) according to ADA criteria or 42-47 mmol/mol (6.0-6.4%) according to the National Institute for Health and Care Excellence (NICE) guideline. The relative risks of all cause mortality and cardiovascular events were calculated and reported with 95% confidence intervals. Results 53 prospective cohort studies with 1 611 339 individuals were included for analysis. The median follow-up duration was 9.5 years. Compared with normoglycaemia, prediabetes (impaired glucose tolerance or impaired fasting glucose according to IFG-ADA or IFG-WHO criteria) was associated with an increased risk of composite cardiovascular disease (relative risk 1.13, 1.26, and 1.30 for IFG-ADA, IFG-WHO, and impaired glucose tolerance, respectively), coronary heart disease (1.10, 1.18, and 1.20, respectively), stroke (1.06, 1.17, and 1.20, respectively), and all cause mortality (1.13, 1.13 and 1.32, respectively). Increases in HBA1c to 39-47 mmol/mol or 42-47 mmol/mol were both associated with an increased risk of composite cardiovascular disease (1.21 and 1.25, respectively) and coronary heart disease (1.15 and 1.28, respectively), but not with an increased risk of stroke and all cause mortality. Conclusions Prediabetes, defined as impaired glucose tolerance, impaired fasting glucose, or raised HbA1c, was associated with an increased risk of cardiovascular disease. The health risk might be increased in people with a fasting glucose concentration as low as 5.6 mmol/L or HbA1c of 39 mmol/mol.

Prehypertension and incidence of cardiovascular disease: a meta-analysis

BackgroundProspective cohort studies of prehypertension and the incidence of cardiovascular disease (CVD) are controversial after adjusting for other cardiovascular risk factors. This meta-analysis evaluated the association between prehypertension and CVD morbidity.MethodsDatabases (PubMed, EMBASE and the Cochrane Library) and conference proceedings were searched for prospective cohort studies with data on prehypertension and cardiovascular morbidity. Two independent reviewers assessed the reports and extracted data. The relative risks (RRs) of CVD, coronary heart disease (CHD) and stroke morbidity were calculated and reported with 95% confidence intervals (95% CIs). Subgroup analyses were conducted on blood pressure, age, gender, ethnicity, follow-up duration, number of participants and study quality.ResultsPooled data included the results from 468,561 participants from 18 prospective cohort studies. Prehypertension elevated the risks of CVD (RR = 1.55; 95% CI = 1.41 to 1.71); CHD (RR = 1.50; 95% CI = 1.30 to 1.74); and stroke (RR = 1.71; 95% CI = 1.55 to 1.89). In the subgroup analyses, even for low-range prehypertension, the risk of CVD was significantly higher than for optimal BP (RR = 1.46, 95% CI = 1.32 to 1.62), and further increased with high-range prehypertension (RR = 1.80, 95% CI = 1.41 to 2.31). The relative risk was significantly higher in the high-range prehypertensive populations than in the low-range populations (χ2= 5.69, P = 0.02). There were no significant differences among the other subgroup analyses (P>0.05).ConclusionsPrehypertension, even in the low range, elevates the risk of CVD after adjusting for multiple cardiovascular risk factors.

Association of all-cause and cardiovascular mortality with prehypertension: A meta-analysis

BACKGROUND Studies of prehypertension and mortality are controversial after adjusting for other cardiovascular risk factors. This meta-analysis sought to evaluate the association of prehypertension with all-cause and cardiovascular disease (CVD) mortality. METHODS The PubMed, EMBASE, Cochrane Library databases, and conference proceedings were searched for studies with data on prehypertension and mortality. The relative risks (RRs) of all-cause, CVD, coronary heart disease (CHD), and stroke mortality were calculated and presented with 95% CIs. Subgroup analyses were conducted according to blood pressure, age, gender, ethnicity, follow-up duration, participant number, and study characteristics. RESULTS Data from 1,129,098 participants were derived from 20 prospective cohort studies. Prehypertension significantly increased the risk of CVD, CHD, and stroke mortality (RR 1.28, 95% CI 1.16-1.40; RR 1.12, 95% CI 1.02-1.23; and RR 1.41, 95% CI 1.28-1.56, respectively), but did not increase the risk of all-cause mortality after multivariate adjustment (RR 1.03, 95% CI 0.97-1.10). The difference between CHD mortality and stroke mortality was significant (P < .001). Subgroup analyses showed that CVD mortality was significantly increased in high-range prehypertension (RR 1.28, 95% CI 1.16-1.41) but not in low-range prehypertension (RR 1.08, 95% CI 0.98-1.18). CONCLUSION Prehypertension is associated with CVD mortality, especially with stroke mortality, but not with all-cause mortality. The risk for CVD mortality is largely driven by high-range prehypertension.

Prehypertension and the risk of stroke A meta-analysis

Objective: In this meta-analysis, we sought to evaluate the association between prehypertension and the risk of stroke. Methods: We searched PubMed and EMBASE databases for studies with data on prehypertension and stroke. Two independent reviewers assessed the reports and extracted data. Prospective studies were included if they reported multivariate-adjusted relative risks (RRs) with 95% confidence intervals (CIs) for the associations between stroke and prehypertension or its 2 subranges (low-range prehypertension: 120–129/80–84 mm Hg; high-range prehypertension: 130–139/85–89 mm Hg). We conducted subgroup analyses according to blood pressure ranges, stroke type, endpoint, age, sex, ethnicity, and study characteristics. Results: Pooled data included the results of 762,393 participants from 19 prospective cohort studies. Prehypertension increased the risk of stroke (RR 1.66; 95% CI 1.51–1.81) compared with optimal blood pressure (<120/80 mm Hg). In the secondary outcome analyses, even low-range prehypertension increased the risk of stroke (RR 1.44; 95% CI 1.27–1.63), and the risk was greater for high-range prehypertension (RR 1.95; 95% CI 1.73–2.21). The RR was higher with high-range than with low-range prehypertension (p < 0.001). There were no significant differences in any of the subgroup analyses (all p > 0.05). Conclusions: After adjusting for multiple cardiovascular risk factors, prehypertension is associated with stroke morbidity. Although the increased risk is largely driven by high-range prehypertension, the risk is also increased in people with low-range prehypertension.

Prehypertension and Incidence of ESRD: A Systematic Review and Meta-analysis

BACKGROUND Studies of the association of prehypertension with the incidence of end-stage renal disease (ESRD) after adjusting for other cardiovascular risk factors have shown controversial results. STUDY DESIGN Systematic review and meta-analysis of prospective cohort studies. SETTING & POPULATION Adults with prehypertension. SELECTION CRITERIA FOR STUDIES Studies evaluating the association of prehypertension with the incidence of ESRD identified by searches in PubMed, EMBASE, and Cochrane Library databases and conference proceedings, without language restriction. PREDICTOR Prehypertension. OUTCOMES The relative risks (RRs) of ESRD were calculated and reported with 95% CIs. Subgroup analyses were conducted according to blood pressure (BP), age, sex, ethnicity, and study characteristics. RESULTS Data from 1,003,793 participants were derived from 6 prospective cohort studies. Compared with optimal BP, prehypertension significantly increased the risk of ESRD (RR, 1.59; 95% CI, 1.39-1.91). In subgroup analyses, prehypertension significantly predicted higher ESRD risk across age, sex, ethnicity, and study characteristics. Even low-range (BP, 120-129/80-84 mm Hg) prehypertension increased the risk of ESRD compared with optimal BP (RR, 1.44; 95% CI, 1.19-1.74), and the risk increased further with high-range (BP, 130-139/85-89 mm Hg) prehypertension (RR, 2.02; 95% CI, 1.70-2.40). The RR was significantly higher in the high-range compared with the low-range prehypertensive population (P = 0.01). LIMITATIONS No access to individual patient-level data. CONCLUSIONS Prehypertension is associated with incident ESRD. The increased risk is driven largely by high-range prehypertension.

Poor sleep quality, stress status, and sympathetic nervous system activation in nondipping hypertension.

ObjectiveIt has been reported that poor sleep quality is associated with nondipping hypertension, but the underlying mechanisms were not reported. This study was carried out to evaluate whether poor sleep quality is associated with stress status and sympathetic nervous system activation in nondippers. Materials and methodsA total of 307 Chinese essential hypertensive patients were defined as dippers or nondippers by ambulatory blood pressure monitoring. Sleep quality was assessed by Pittsburgh Sleep Quality Index (PSQI), and stress status was assessed by Perceived Stress Scale (PSS). The levels of epinephrine and norepinephrine were examined to investigate the underlying mechanisms. ResultsA total of 204 (66.4%) and 103 cases (33.6%) were found to be dippers and nondippers, respectively. Nondippers were with poorer sleep quality (P<0.05), more stressful status (P<0.05), and with an increased activity of sympathetic nervous system (P<0.01). The decline of systolic BP (SBP) and diastolic BP (DBP) at night was inversely related with the PSQI score (r=−0.469, P<0.01 and r=−0.421, P<0.01), PSS score (r=−0.432, P<0.01 and r=−0.404, P<0.01), epinephrine (r=−0.304, P<0.05 and r=−0.293, P<0.05), and norepinephrine (r=−0.321, P<0.05 and r=−0.357, P<0.05). Multiple logistic regression analyses showed that older age [odds ratio (OR): 1.69; 95% confidence interval (CI): 1.22–2.43], PSQI score (OR: 2.78; 95% CI: 1.65–6.87), and PSS score (OR: 2.43; 95% CI: 1.56–5.93) were independently correlated with the nondipping pattern. ConclusionPoor sleep quality and stressful status were closely associated with higher activation of sympathetic nervous system, and they are independent predictors of nondipping hypertension.

Lipoprotein-associated phospholipase A2 (Lp-PLA(2)): a novel and promising biomarker for cardiovascular risks assessment.

Atherosclerosis and its manifestations namely cardiovascular diseases (CVD) are still the leading cause of morbidity and mortality worldwide. Although intensified interventions have been applied, the residual cardiovascular (CV) risks are still very high. Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a novel and unique biomarker highly specific for vascular inflammation and atherosclerosis. Both pro-atherogenic property of Lp-PLA2 and positive correlation with CV events have already been demonstrated by a large number of scientific and clinical studies. Currently, in the Adult Treatment Panel III (ATP III) guideline, Lp-PLA2 has been recommended as an adjunct to traditional risk factors in assessing future CV risks. Encouragingly, darapladib, an orally Lp-PLA2 specific inhibitor, has been tested in basic research and preclinical trials and the outcomes are quite striking. Additionally, there are two phase III ongoing clinical trials in evaluating the efficacy and safety of darapladib on cardiovascular outcomes. With regard to the potential values of Lp-PLA2 in risk stratification, therapeutic regimen establishment and prognosis evaluation in patients with moderate or high risk, our present review is going to summarize the relevant data about the bio-chemical characteristics of Lp-PLA2, the actions of Lp-PLA2 on atherosclerosis and the results of Lp-PLA2 in scientific research and clinical studies.

White-coat hypertension is a risk factor for cardiovascular diseases and total mortality

Background: Whether white-coat hypertension (WCH) is an innocent phenomenon is controversial. Method: In this study, we evaluated the association of WCH and the risk of cardiovascular diseases (CVDs) and mortality, stratified by baseline antihypertensive treatment status. Databases (PubMed, EMBASE, CINAHL Plus, Scopus, and Google Scholar) were searched for prospective studies with data on CVD and total mortality associated with WCH. The primary outcomes were the risk of CVD and total mortality associated with WCH stratified by antihypertensive treatment status. The relative risks of events compared with normotension were calculated. Results: A total of 23 cohorts (20 445 individuals), 11 cohorts (8656 individuals), and 12 cohorts (21 336 individuals) were included for analysis of cardiovascular risk associated with WCH in patients without baseline antihypertensive treatment (untreated), or under antihypertensive treatment (treated) or mixed population (including both untreated and treated patients), respectively. In untreated cohorts, WCH was associated with a 38 and 20% increased risk of CVD and total mortality compared with normotension, respectively. In the mixed population, WCH was associated with a 19 and 50% increased risk of CVD and total mortality. However, in the treated patients, neither the risk of CVD, nor total mortality was increased in WCH. Meta-regression analyses indicated that neither differences of clinic blood pressure, nor out-of-office blood pressure variables were correlated with risk of CVD in WCH. Conclusion: We concluded that WCH is associated with long-term risk of CVD and total mortality in patients without antihypertensive treatment. Close follow-up should be performed in WCH patients.

Effects of insulin-like growth factor-1 on the properties of mesenchymal stem cells in vitro.

ObjectiveTo explore the effects of insulin-like growth factor-1 (IGF-1) on migration, proliferation and differentiation of mesenchymal stem cells (MSCs).MethodsMSCs were obtained from Sprague-Dawley rats by a combination of gradient centrifugation and cell culture techniques and treated with IGF-1 at concentrations of 5–20 ng/ml. Proliferation of MSCs was determined as the mean doubling time. Expression of CXC chemokine receptor 4 (CXCR4) and migration property were determined by flow cytometry and transwell migration essay, respectively. mRNA expression of GATA-4 and collagen II was determined by reverse transcription-polymerase chain reaction (RT-PCR).ResultsThe mean doubling time of MSC proliferation was decreased, and the expression of CXCR4 on MSCs and migration of MSCs were increased by IGF-1, all in a dose-dependent manner, while the optimal concentration of IGF-1 on proliferation and migration was different. IGF-1 did not affect the expression of GATA-4 or collagen II mRNA.ConclusionsIGF-1 dose-dependently stimulated the proliferation of MSCs, upregulated the expression of CXCR4, and accelerated migration. There was no apparent differentiation of MSCs to cardiomyocytes or chondrocytes after culturing with IGF-1 alone.

The effect of zolpidem on sleep quality, stress status, and nondipping hypertension

OBJECTIVE Poor sleep quality and stress status have previously been shown to be closely associated with higher activation of the sympathetic nervous system and to be independent predictors of nondipping hypertension. This study aimed to evaluate the effects of the non-hypotensive sedative zolpidem on sleep quality, stress status, and nondipping hypertension. METHODS A total of 103 nondippers were defined as poor or good sleepers by the Pittsburgh Sleep Quality Index. They were randomized to receive zolpidem or placebo treatment for 30 days. Stress status was assessed by the Perceived Stress Scale, and levels of epinephrine and norepinephrine were examined to investigate the underlying mechanisms. RESULTS Poor sleepers treated with zolpidem for 30 days showed significant improvements in sleep quality and stress levels (P<0.01). More nondippers were converted to dippers in the group of poor sleepers treated with zolpidem (11 of 22 patients, 50.0%) than in the placebo (2 of 23, 8.7%) (P<0.01). Epinephrine and norepinephrine levels were significantly reduced in poor sleepers treated with zolpidem (P<0.05). CONCLUSION The results of this study suggest that zolpidem can improve sleep quality and stress status, and can convert nondippers with poor sleep quality into dippers. It may be an option for treating nondipping hypertensive patients with poor sleep quality.