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Aims The current study aimed to evaluate the associations between general and abdominal obesity with left ventricular (LV) structure and function and whether these associations differed by sex. Methods and results This is a community‐based cross‐sectional study, and 971 hypertensive individuals without overt cardiovascular disease were included. General obesity was defined as body mass index (BMI) ≥ 28 kg/m2, and abdominal obesity was defined as waist circumference (WC) ≥ 90 cm for men and ≥85 cm for women. The associations between general and abdominal obesity with LV structure and function were examined using linear regression analysis, and the interaction by sex was performed. The mean age was 66.5 ± 11.4 years, and women accounted for 62%. General obese individuals (n = 205) were more likely to have concentric remodelling, LV hypertrophy, and worse diastolic function. Similar differences were observed in abdominal obese individuals (n = 593). General obesity was associated with LV end‐diastolic volume, LV mass, left atrial volume, and septal E/e' ratio after adjusting for WC and clinical covariates; and abdominal obesity was associated with septal e' velocity after adjusting for BMI and clinical covariates. The associations between general obesity with LV structure and function did not differ by sex, while the magnitudes of the associations between abdominal obesity with LV mass and septal e' velocity were greater in men. Conclusions General and abdominal obesity were associated with different patterns of LV structural and functional alterations, stressing the importance of incorporating BMI and WC measurements into assessing obesity‐related LV alterations.

Aims The aims of the current study were to evaluate the association between anaemia and all‐cause mortality according to chronic kidney disease (CKD) status and to explore at what level of haemoglobin concentration would the all‐cause mortality risk increase prominently among CKD and non‐CKD patients, respectively. Methods and results This is a prospective cohort study, and 1559 patients with ischaemic heart failure (IHF) were included (mean age of 63.5 ± 11.0 years, 85.8% men) from December 2015 to June 2019. Patients were divided into the CKD (n = 481) and non‐CKD (n = 1078) groups based on the estimated glomerular filtration rate of 60 mL/min/1.73 m2. In the CKD group, the incidence rate of all‐cause mortality in anaemic and non‐anaemic patients was 15.4 per 100 person‐years and 10.8 per 100 person‐years, respectively, with an incidence rate ratio of 1.42 (95% confidence interval: 1.00–2.02; P‐value = 0.05). In the non‐CKD group, the incidence rate of all‐cause mortality in anaemic and non‐anaemic patients was 9.8 per 100 person‐years and 5.5 per 100 person‐years, respectively, with an incidence rate ratio of 1.78 (95% confidence interval: 1.20–2.59; P‐value = 0.005). After a median follow‐up of 2.1 years, the cumulative incidence rate of all‐cause mortality in anaemic and non‐anaemic patients was 41.5% and 44.1% (P‐value = 0.05) in the CKD group, and 30.9% and 18.1% (P‐value

Nonvalvular atrial fibrillation (NVAF) is the most common arrhythmia. It is of a high disability and death rate, and seriously affects quality of life. Although New oral anticoagulants (NOACs) are recommended for anticoagulation therapy of atrial fibrillation, they are not widely used for the high cost and limited availability. Warfarin is effective and economical. The risk of thromboembolism and anticoagulant hemorrhage is higher in patients >65 years with NVAF. So, it is of great clinical significance to explore the optimal anticoagulation intensity of warfarin in patients >65 years of China, and other ethnicities. Some studies suggested that low-intensity international normalized ratio (INR) has similar antithrombotic efficacy comparing to standard-intensity INR, whereas bleeding risk was significantly reduced. But others showed conflicting results. We pooled the efficacy and safety data of low- and standard-intensity warfarin therapy for patients over 65 years with NVAF by meta-analysis, as to evaluate optimal INR intensity of warfarin therapy in patients over 65 years. We identified 18 studies providing data of 2105 patients receiving anticoagulation therapy with warfarin. On meta-analysis (odds ratio [OR] [95% confidence interval {CI}]), low-intensity INR conferred similar efficacy to standard intensity INR on all thrombosis (1.28 [0.90 to 1.81]), stroke (1.09 [0.67 to 1.77]), other thromboembolism ([peripheral and pulmonary embolism] 2.26 [0.89 to 5.79]), and all cause death (1.38 [0.94 to 2.02]). Low-intensity INR conferred better safety profile than standard intensity INR in major bleeding (intracranial and gastrointestinal hemorrhage) (0.32 [0.19 to 0.52]), minor bleeding (gum, nasal cavity and conjunctival hemorrhage, skin ecchymosis, hematuria, hemoptysis) (0.30 [0.20 to 0.45]), and all bleeding (0.30 [0.22 to 0.40]). In conclusion, low-intensity INR (1.5 to 2.0) of warfarin therapy is as effective as standard intensity INR (2.0 to 3.0) therapy in reducing thromboembolic risk in patients>65 years with NVAF, and has a safer profile of bleeding.

The purpose of the current study was to determine whether aortic blood pressure (BP) and arterial stiffness are greater in patients with controlled resistant hypertension (RHTN) than controlled non‐resistant hypertension (non‐RHTN) despite similar clinic BP level. Participants were recruited from University of Alabama at Birmingham (UAB) Hypertension Clinic. Controlled hypertension was defined as automated office BP measurement with BP

Impaired response to P2Y12 receptor antagonists, such as clopidogrel and prasugrel, can have devastating consequences for patients that require prolonged or indefinite therapy with these agents, including those with a left ventricular assist device (LVAD). While loss-of-function (LOF) alleles in CYP2C19 have been elucidated as contributing to high on treatment platelet reactivity (HTPR) during clopidogrel therapy, genetic variations in the metabolic pathway of prasugrel have not been shown to elicit this same effect. Moreover, limited studies have assessed the effect of coexisting genetic variations in pharmacokinetic and pharmacodynamic pathways. Herein, we report a left ventricular assist device patient exhibiting high on treatment platelet reactivity during clopidogrel and prasugrel therapy. Genotyping revealed variants in pharmacokinetic ( CYP2B6), and pharmacodynamic pathways, with multiple variants in P2Y12, the target receptor.

The study was to compare age‐related alterations in cardiac and arterial structure and function by sex and to explore the impacts of achieved systolic blood pressure (SBP

Background Lipoprotein(a) is genetically determined and increasingly recognized as a major risk factor for arteriosclerotic cardiovascular disease. We examined whether plasma lipoprotein(a) concentrations were associated with intraplaque neovascularization (IPN) grade in patients with carotid stenosis and in terms of increasing plaque susceptibility to haemorrhage and rupture. Methods We included 85 patients diagnosed with carotid stenosis as confirmed using carotid ultrasound who were treated at Guangdong General Hospital. Baseline data, including demographics, comorbid conditions and carotid ultrasonography, were recorded. The IPN grade was determined using contrast-enhanced ultrasound through the movement of the microbubbles. Univariate and multivariate binary logistic regression analyses were used to evaluate the association between lipoprotein(a) and IPN grade, with stepwise adjustment for covariates including age, sex, comorbid conditions and statin therapy (model 1), total cholesterol, triglyceride, low-density lipoprotein cholesterol calculated by Friedwald's formula, high-density lipoprotein cholesterol, apolipoprotein A and apolipoprotein B (model 2), maximum plaque thickness and total carotid maximum plaque thickness, degree of carotid stenosis and internal carotid artery (ICA) occlusion (model 3). Results Lipoprotein(a) was a significant predictor of higher IPN grade in binary logistic regression before adjusting for other risk factors (odds ratio [OR] 1.238, 95% confidence interval [CI] (1.020, 1.503), P = 0.031). After adjusting for other risk factors, lipoprotein(a) still remained statistically significant in predicting IPN grade in all model. (Model 1: OR 1.333, 95% CI 1.074, 1.655, P = 0.009; Model 2: OR 1.321, 95% CI 1.059, 1.648, P = 0.014; Model 3: OR 1.305, 95% CI 1.045, 1.628, P = 0.019). Lp(a) ≥ 300 mg/L is also significantly related to IPN compare to P = 0.039) as well as in model 1, while in model 2 and model 3 there are not significant difference. Conclusions Plasma lipoprotein(a) concentrations were found to be independently associated with higher IPN grade in patients with carotid stenosis. Lowering plasma lipoprotein(a) levels may result in plaque stabilization by avoiding IPN formation.

Background Distinct populations differ in LVH prevalence and impaired LV geometry. Currently, the prevalence of and risk factors for LV geometric patterns in Chinese hypertensives administered irbesartan have not been specifically addressed in large studies. Methods Totally 10,883 patients (6623 men and 4260 women) completed the survey, including 1181 hypertensives administered irbesartan (488 males and 693 females) that were finally enrolled. Based on LVMI and RWT derived from comprehensive echocardiography, the LV geometric patterns of irbesartan‐treated hypertensive individuals were classified into four types, including the normal, concentric remodeling, and concentric and eccentric hypertrophy groups. Logistic regression analysis was applied in males and females, respectively, for determining odds ratios (ORs) and 95% confidence intervals (CIs) for various potential risk factors for abnormal LV geometrical patterns in irbesartan‐treated hypertensives. Results The clinical and echocardiographic data differed significantly between males and females. The prevalence rates of concentric remodeling, concentric hypertrophy, and eccentric hypertrophy were 36.3%, 15.4%, and 6.1% in males, respectively, and 23.5%, 20.3%, and 23.8% in females, accordingly. Gender, daily dose of irbesartan, BMI, SBP, WtHR, and neck‐circumference were significantly associated with LV geometric patterns. After adjustment for confounding factors, risk factors for LVH and impaired LV geometry included SBP, WtHR in males, and MAU‐Cr and WtHR in females. Conclusions LVH and impaired LV geometric patterns are more prevalent in females (67.7%) compared with that in males (57.8%) among hypertensives upon irbesartan administration. For such population, risk factors beyond elevated blood pressure may be involved in the progression of LVH and impaired LV geometric patterns in both genders., Prevalence of and risk factors for abnormal left ventricular geometrical patterns in hypertensive subjects with irbesartan treatment.

Major adverse cardiac event (MACE) and bleeding risks following percutaneous coronary intervention (PCI) for acute coronary syndromes (ACS) are not well defined in individuals with heart failure (HF). We followed 1,145 individuals in the Pharmacogenomic Resource to improve Medication Effectiveness Genotype Guided Antiplatelet Therapy cohort for MACE and bleeding events following PCI for ACS. We constructed Cox proportional hazards models to compare MACE and bleeding in those with versus without HF, adjusting for sociodemographics, comorbidities, and medications. We also determined predictors of MACE and bleeding events in both groups. 370 (32%) individuals did and 775 (68%) did not have HF prior to PCI. Mean age was 61.7 ± 12.2 years, 31% were female, and 24% were African American. After a median follow-up of 0.78 years, individuals with HF had higher rates of MACE compared to those without HF (48 vs. 24 events per 100 person years) which remained significant after multivariable adjustment (hazard ratio [HR] 1.31, 95% confidence interval [CI] 1.00 to 1.72). Similarly, bleeding was higher in those with versus without HF (22 vs. 11 events per 100 person years), although this was no longer statistically significant after multivariable adjustment (HR 1.29, 95% CI 0.86 to 1.93). Diabetes and peripheral vascular disease were predictors of MACE, and end-stage renal disease was a predictor of bleeding among participants with HF. MACE risk is higher in individuals with versus without HF following PCI for ACS. However, the risk of bleeding, especially among those with end-stage renal disease , must be considered when determining post-PCI anticoagulant strategies.

Introduction To investigate the association between blood pressure components and microalbuminuria (MAU) in newly diagnosed and treatment-naive hypertensive patients. Material and methods A total of 1858 newly diagnosed and treatment-naive hypertensive patients were enrolled. Based on 24 h urine albumin concentration, all patients were divided into MAU and normo-albuminuria groups. The associations between blood pressure (BP) components, namely systolic/diastolic BP (SBP/DBP) and pulse pressure (PP) and MAU, as well as the sensitivity and specificity of each BP component in predicting MAU, were evaluated. Results Compared to the normo-albuminuria group, patients in the MAU group were older and had significantly higher SBP and PP (p < 0.05). Serum levels of fasting blood glucose, total protein and creatinine were significantly higher in the MAU group (p < 0.05). 24-hour urine albumin excretion was significantly higher in the MAU group than the normo-albuminuria group (182.5 ±156.5 mg vs. 17.6 ±7.1 mg, p < 0.001). Logistic regression analyses revealed that SBP and PP were significantly associated with MAU, with an odds ratio (OR) of 1.010 (95% confidence interval (CI): 1.005-1.016, p < 0.001) in SBP and OR of 1.009 (95% CI: 1.003-1.015, p = 0.003) in PP. The receiver operating characteristic curve showed that the area under the curve for SBP to predict MAU was 0.541 ±0.013, and PP was 0.536 ±0.013. The difference in predicting MAU by SBP or PP was non-significant. Conclusions In newly diagnosed and treatment-naive hypertensive patients, increased SBP and PP were independently associated with MAU.

Background Data on racial disparities in major adverse cardiovascular events ( MACE ) and major hemorrhage ( HEM ) after percutaneous coronary intervention are limited. Factors contributing to these disparities are unknown. Methods and Results PR i ME ‐GGAT (Pharmacogenomic Resource to Improve Medication Effectiveness–Genotype‐Guided Antiplatelet Therapy) is a prospective cohort. Patients aged ≥18 years undergoing percutaneous coronary intervention were enrolled and followed for up to 1 year. Racial disparities in risk of MACE and HEM were assessed using an incident rate ratio. Sequential cumulative adjustment analyses were performed to identify factors contributing to these disparities. Data from 919 patients were included in the analysis. Compared with white patients, black patients (n=203; 22.1% of the cohort) were younger and were more likely to be female, to be a smoker, and to have higher body mass index, lower socioeconomic status, higher prevalence of diabetes mellitus and moderate to severe chronic kidney disease, and presentation with acute coronary syndrome and to undergo urgent percutaneous coronary intervention. The incident rates of MACE (34.1% versus 18.2% per 100 person‐years, P HEM (17.7% versus 10.3% per 100 person‐years, P =0.02) were higher in black patients. The incident rate ratio was 1.9 (95% CI, 1.3–2.6; P MACE and 1.7 (95% CI , 1.1–2. 7; P =0.02) for HEM . After adjustment for nonclinical and clinical factors, black race was not significantly associated with outcomes. Rather, differences in socioeconomic status, comorbidities, and coronary heart disease severity were attributed to racial disparities in outcomes. Conclusions Despite receiving similar treatment, racial disparities in MACE and HEM still exist. Opportunities exist to narrow these disparities by mitigating the identified contributors.

This study aims to investigate the association of tissue Doppler E/e' with cardiac events in hypertension patients, independent of and incremental to clinical and left ventricular geometric patterns.We retrospectively enrolled 222 asymptomatic nonischemic patients with hypertension who had echocardiogram in 2012 to evaluate tissue Doppler E/e'. Patients were followed up for cardiac events (cardiac events were defined as myocardial infarction, coronary revascularization procedures, new-onset angina (stable or unstable), heart failure). A cox regression was used to assess the association of the ratio of transmitral Doppler early filling velocity to tissue Doppler early diastolic mitral annular velocity (E/e') with cardiac events.A total of 222 patients were included in analysis. There were 10 primary cardiac events during 3.2 ± 0.4 years follow-up. The E/e' ratio was the strongest predictor of cardiac events in Cox-proportional hazards models. Following adjustment for covariates, a unit rise in the E/e' ratio was associated with a 26% increment in risk of a cardiac event (HR 1.26, CI 1.06-1.50, p = 0.008). When E/e' ＞14 the hazard ratio of cardiac event was significantly increased compared with E/e' ≤ 14 in Kaplan-Meier analysis (log-rank ratio, 16.26; p ＜ 0.001).E/e', a non-invasive estimate of left ventricular filling pressure, predicts cardiac events in hypertensive population with preserved left ventricular ejection fraction, independent of and incremental to clinical and left ventricular geometric patterns. E/e' represents an early, effective tool for cardiovascular risk stratification in hypertension population.

Background/Aims: Although it is widely acknowledged that atherosclerosis is mainly a chronic inflammatory process, in which both miR-29b and interleukin-6 (IL-6) play multifaceted roles, the association between miR-29b and IL-6 remains unknown. The aim of the present study was to explore the relationship between miR-29b and IL-6 and to test whether circulating levels of miR-29b and IL-6 could predict atherosclerosis. Methods: A total of 170 participants were divided into two groups according to carotid intima-media thickness (CIMT): study group (CIMT ≥ 0.9mm) and control group (CIMT < 0.9mm). Levels of circulating miR-29b and IL-6 were measured by quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. The association of miR-29b and IL-6 levels with CIMT was assessed using Spearman correlation analysis and multiple linear regression analysis. Results: The study group showed higher miR-29b levels (31.61 ± 3.05 vs. 27.91 ± 1.71 Ct, p < 0.001) and IL-6 levels (3.40 ± 0.67 vs. 2.99 ± 0.37 pg/ml, p < 0.001), compared with the control group. CIMT was positively correlated with miR-29b (r = 0.587, p < 0.001) and IL-6 (r = 0.410, p < 0.001), and miR-29b levels were also correlated with IL-6 (r = 0.242, p = 0.001). Multiple linear regression analysis also showed that CIMT was positively correlated with miR-29b and IL-6. After adjustment for age, body mass index, systolic blood pressure, total cholesterol and C-reactive protein, CIMT was still closely correlated with miR-29b and IL-6. The combination of miR-29b and IL-6 (AUC = 0.901, p < 0.001) offered a better predictive index for atherosclerosis than either miR-29b (AUC = 0.867, p < 0.001) or IL-6 (AUC = 0.747, p < 0.001) alone. Conclusion: Circulating levels of miR-29b and IL-6 may be independently correlated with subclinical atherosclerosis, and may serve as novel biomarkers for the identification of atherosclerosis.

Previous studies have suggested that prolonged electrocardiogram QTc duration was independent risk factor for both increased cardiovascular and all-cause mortality, but there was no dating about the relationship between central aortic systolic blood pressure (CASP) and QTc duration. The aim of this study was to analyze the relationship between CASP and QTc duration, and assess whether CASP can predict prolonged QTc duration more than BSBP.A total of 500 patients were enrolled in this study, central and brachial aortic blood pressure and electrocardiogram QTc duration were measured. Pearson correlation was assessed for determining the associations of QTc duration with clinical conditions. Multivariate logistic regression analyses were performed to determine the independent predictor of prolonged QTc duration. Receiver operating characteristic (ROC) curve was used to evaluate the utility of blood pressure for prolonged QTc duration.We found QTc durations were significantly positive with CASP (r = 0.308, p 0.001), BSBP (r = 0.227, p 0.001), and age (r = 0.154, p = 0.010), but negatively related to heart rate (r = -440, p 0.001). A multiple logistic regression analysis demonstrated that the CASP was an independent determinant of prolonged QTc (OR = 1.648; 95%CI: 1.032, 2.101; p 0.001). CASP had a better predictive value for prolonged QTc duration than (AUC: 0.771 vs. 0.646, p 0.001) BSBP.Our results suggested that the non-invasive CASP is independently correlated with QTc duration, and CASP can predict prolonged QTc duration more than BSBP.

Introduction The effects of statins on lipoprotein-associated phospholipase A2 (Lp-PLA2) are controversial, and the present study aimed to investigate whether atorvastatin could reduce Lp-PLA2 in rats with dyslipidemia. Material and methods A high-fat and high-cholesterol diet was prescribed to produce a dyslipidemia model. Thereafter, low-dose atorvastatin (5 mg/kg/day), high-dose atorvastatin (20 mg/kg/day) or saline (without-treatment group) was prescribed for 14 days. At 6 weeks after dyslipidemia model establishment and 14 days of atorvastatin treatment, fasting venous blood was drawn for biochemical analysis. Between-group differences and Pearson correlation analysis were conducted. Results Compared to the normal-control group, fasting plasma total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) levels were significantly increased in dyslipidemia groups, while plasma nitric oxide (NO) levels were significantly decreased with attendant elevation of plasma C-reactive protein (CRP) and rho-associated kinase 1 (ROCK1) levels (p < 0.05). At 14 days of atorvastatin treatment, compared to the without-treatment group, plasma levels of TC and LDL-C in the high-dose group were significantly reduced (p < 0.05); and compared to low-dose and without-treatment groups, NO up-regulation (1.8 ±1.1 μmol/l), and CRP (-0.8 ±0.4 ng/ml), ROCK1 (-124 ±65 mmol/l) and Lp-PLA2 (-3.8 ±1.2 ng/ml) reduction were more significant in the high-dose group (p < 0.05). Pearson correlation analysis showed that TC (r = 0.365), LDL-C (r = 0.472), CRP (r = 0.501) and ROCK1 (r = 0.675) were positively correlated with Lp-PLA2, while NO (r = -0.378) and atorvastatin (r = -0.511) were negatively correlated with Lp-PLA2. Conclusions Atorvastatin treatment is beneficial for reducing the Lp-PLA2 level in rats with dyslipidemia, which may be related to reduced ROCK1 expression in a dose-dependent manner.

BACKGROUND Omentin-1 is one of the adipokines associated with obesity, diabetes, and coronary heart disease development. We determined to investigate whether serum omentin-1 concentrations were correlated with the presence of atrial fibrillation (AF). MATERIAL AND METHODS Serum omentin-1 concentrations were examined in a cross-sectional population that included 220 patients with AF (70 with paroxysmal AF, 78 with persistent AF, and 72 with permanent AF) and 115 healthy controls. RESULTS Reduced serum omentin-1 concentrations were found in AF patients compared to the controls. In addition, patients with permanent AF had lower serum omentin-1 concentrations compared to patients with persistent AF and patients with paroxysmal AF. Significantly decreased serum omentin-1 concentrations were observed in persistent AF patients compared to paroxysmal AF patients. Spearman correlation analysis suggested that serum omentin-1 concentrations were negatively correlated with left atrial diameter in AF patients. CONCLUSIONS Serum omentin-1 concentrations were correlated with the presence of AF and atrial remolding.

Our objective was to evaluate the associations of the systolic and diastolic blood pressure night-to-day ratios (SBP-NDR and DBP-NDR) with composite atherosclerotic cardiovascular diseases (ASCVDs) comprising coronary heart disease (CHD) and ischemic stroke (IS) cases, respectively. The clinical conditions associated with SBP-NDR and DBP-NDR were also evaluated. A total of 401 patients who underwent 24-h ambulatory BP monitoring were enrolled. In general, the mean age was 59.7±14.7 years and male subjects accounted for 59.1% of the study subjects. Regarding the ASCVD risk factors, 17.0% of the study subjects smoked, 5.2% abused alcohol, 2.0% had a family history of ASCVD, 23.3% had diabetes and 96.0% had dyslipidemia. Fifty (12.5%) and 128 (31.9%) study subjects had a previous diagnosis of CHD and IS, respectively. Dipper and non-dipper pattern-specific differences in clinical characteristics between the SBP-NDR and DBP-NDR categories were observed. The multiple linear regression analysis showed that advanced age, smoking, CHD and IS were positively associated with SBP-NDR and statins were inversely associated with SBP-NDR; only IS was positively associated with DBP-NDR. The logistic regression analysis showed that after adjusting for the covariates of age, smoking, alcohol abuse, diabetes, hypertension, dyslipidemia, and SBP and DBP at admission, only DBP-NDR remained significantly associated with composite ASCVD, with an odds ratio of 1.029 (95% confidence interval 1.002-1.056, P=0.038). There were significant differences in the associations of SBP-NDR and DBP-NDR with composite ASCVD. Clinical conditions independently associated with SBP-NDR and DBP-NDR were also somewhat different. In a specific population group, DBP-NDR may be superior to SBP-NDR with respect to screening for ASCVD.

Obstructive sleep apnea (OSA) is a major modifiable risk factor of hypertension and hypertensive patients with OSA are at increased risk for cardiovascular diseases. A substantial number of studies have revealed that OSA and hypertension have synergistic effects on the cardiovascular system and, therefore, it is clinically important and relevant to increase our understanding of the pathophysiological interactions between OSA and hypertension. In our present review, after briefly reviewing the characteristics and pathophysiological effects of OSA, we focus on the current understanding of OSA-associated hypertension, the potential approaches for treatment of OSA and the effect of OSA treatment on hypertension management. We hope our present review will shed light for future studies that investigate effective therapeutic strategies to simultaneously improve the management of OSA and hypertension.

Background/Aims: Atherosclerosis is a chronic inflammatory condition associated with a variety of vascular diseases. Previous studies showed that both miR-29a and oxidized low density lipoprotein (ox-LDL) were vital in the development of atherosclerosis. However, the relationship between miR-29a and ox-LDL remains unknown. This study was designed to investigate the association of miR-29a and ox-LDL and to test whether circulating miR-29a and ox-LDL levels could predict atherosclerosis. Methods: In 170 participants, plasma levels of miR-29a were assessed by quantitative real-time polymerase chain reaction (qRT-PCR) while plasma ox-LDL levels were determined using enzyme-linked immunosorbent assay (ELISA) kits. The relationship between miR-29a level and ox-LDL and carotid intima-media thickness (cIMT) was assessed using the Spearman correlation coefficient and multiple liner regression. Results: Compared with the normal cIMT group, the increased cIMT group had higher levels of ox-LDL (0.47 ± 0.08 vs 0.29 ± 0.06 ng/ml, p = 0.003) and miR-29a (32.93 ± 4.26 vs 26.37 ± 1.04, p < 0.001). A positive correlation was found between ox-LDL and miR-29a (r = 0.695, p < 0.001), and both the ox-LDL (r = 0.857, p < 0.001) and the miR-29a (r = 0.753, p < 0.001) were positively related to cIMT. Furthermore, multiple liner regression indicated that a significant correlation between ox-LDL and cIMT (β = 0.768, p < 0.001), as well as between miR-29a and cIMT (β = 0.686, p

Background: Despite the improvement in the health care industry, the rates of undetected, untreated, and uncontrolled hypertension (HTN) are still very high, especially in rural areas of China. The aim of this study was to investigate the efficacy and efficiency of a guideline-based HTN management (novel therapy) in population of rural areas of Guangdong Province. Methods: Totally, 3113 patients with essential HTN in a rural area of Guangdong Province were enrolled and assigned to two groups, named traditional (n = 372) and novel therapeutic (n = 2741) groups, respectively. Patients in the traditional group were treated routinely, and patients in the novel group were treated in a novel model characterized by regular educational programs for hypertensive populations, close monitoring of blood pressure in combination with finely tuned antihypertensive medications, strict implementation of lifestyle modification and improving medical knowledge and skill of local medical staff efficiently. After 2 years of follow-up, primary endpoints including magnitude of systolic and diastolic blood pressures (SBP and DBP) decrease, treated and controlled rates, as well as secondary endpoints, were evaluated in both groups. Results: Initially, the treated rate was significantly higher in traditional group than that of novel group (71.15% vs. 64.99%, P < 0.05), while the controlled rates were comparable and insignificant difference between baseline BP in both groups (31.07% vs. 26.88%, P > 0.05). Four variables were significantly different, namely smoking rate, daily vegetable consumption (VC), and serum levels of low-density lipoprotein-cholesterol and fasting blood glucose between these two groups. After 2 years of follow-up, decreases in SBP and DBP were more prominent in the novel group (P < 0.001). Treated and controlled rates in both groups were both increased. Nevertheless, in comparison to the traditional group, controlled rate increased more significantly in the novel group (64.31% vs. 37.85%, P < 0.001). Variables indicating lifestyle modification such as high sodium consumption, percentages of alcohol abuse, daily VC were profoundly improved in the novel group. Conclusions: The guideline-based HTN management implemented in the current study was beneficial for HTN control in rural areas of Guangdong Province.

To evaluate the relationship between pulse pressure index (PPI) and carotid intima-media thickness (CIMT).Observational trial was design and 342 patients newly diagnosed as hypertension without anti-hypertensive therapy were enrolled. According to the cut-off value of CIMT, 342 participants were divided into normal ( 0.9mm) and increased CIMT groups (≥ 0.9mm). Baseline characteristics were compared, logistic regression analysis and receiver operating characteristic curve (ROC) were performed.Approximately 34.2% of participants (n = 117) were with CIMT ≥ 0.9 mm and participants in increased CIMT group were more elderly. Diastolic blood pressure was lower in increased CIMT group than normal group (79.3 ± 10.8 mm Hg versus 83.8 ± 9.4 mm Hg, p 0.001), whereas pulse pressure (PP) (59.3 ± 20.2 mm Hg versus 53.6 ± 15.5 mm Hg, p = 0.004) and PPI (0.43 ± 0.09 versus 0.38 ± 0.08, p 0.001) were significantly higher in increased CIMT group. CIMTs were 1.11 ± 0.11 mm and 0.76 ± 0.12 in increased group and normal group respectively (p 0.001). After adjusted for the traditional risk factors, only PPI was found an independent determinant for CIMT increase, and the odd ratio was 1.644 (95% interval confidence 1.280-2.112, p 0.001). The ROC evaluations showed that area under the curve for PP to predict CIMT increase was 0.591 ± 0.034, and PPI was 0.664 ± 0.033. PPI was more powerful than PP in discriminating CIMT increase (p = 0.006).PPI is a valuable parameter for the preliminary screening of hypertensive patients who have an increased risk of atherosclerosis.

Aim The pressure study was carried out to evaluate the hypotheses that ambulatory blood pressure (ABP) is superior to clinic blood pressure for ischemic stroke and that ABP is important to refine risk stratification. Patients and methods A total of 889 hospitalized patients who had undergone ABP monitoring were enrolled. Baseline data were compared between diabetic and nondiabetic subgroups. Area under receiver operating characteristics curve for each blood pressure (BP) component with ischemic stroke was evaluated. Each BP component was entered separately into a logistic regression basic model. The predictive performance of each model was compared using the Akaike Information Criterion and Schwartz's Bayesian Information Criterion, and a lower value indicated better performance. Results The mean age of the patients was 58 years, 56.2% were men, and 63.0, 30.6, and 27.7% had hypertension, diabetes, and ischemic stroke, respectively. The diabetic subgroup had significantly higher systolic blood pressure (SBP) profiles than the nondiabetic subgroup. Compared with patients without ischemic stroke, those with ischemic stroke had significantly higher 24-h SBP and daytime-SBP, whereas no differences in clinic-SBP were observed in both subgroups. Compared with clinic-SBP, the area under receiver operating characteristics curve values for predicting ischemic stroke were significantly higher for 24-h SBP and daytime-SBP in both subgroups. The results of predictive performance showed that logistic regression models including 24-h SBP and daytime-SBP had lower Akaike Information Criterion and Schwartz's Bayesian Information Criterion values than that with clinic-SBP in both subgroups. However, no significant improvement in predictive performance was observed when the BP variable was added to the basic model. Conclusion Our study showed that in a hospital setting, 24-h SBP and daytime-SBP were superior to clinic-SBP in relation to ischemic stroke.

Background Obstructive sleep apnea (OSA) and resistant hypertension (RHTN) are two major risk factors of chronic heart failure (CHF) and limited information is available about the joint effects of OSA and RHTN on CHF. Methods Baseline data of participants who had completed polysomnography were used in the current study. The relative excess risk due to interaction (RERI) and attributable proportion due to interaction (AP) were calculated, and RERI >0 or AP >0 indicates joint effect of OSA and RHTN on CHF is greater than the sum of estimated effects of OSA alone and RHTN alone. Due to significant interaction between coronary heart disease (CHD) and both OSA and RHTN, participants were stratified into with and without CHD subgroups. Results Among 1157 participants, 33.1% had OSA. The prevalence of RHTN in OSA participants was 18.3%. The apnea–hypopnea index (AHI), pulse pressure and CHF were significantly associated with RHTN. In the CHD subgroup, participants with OSA and RHTN were associated with >3-fold increased odds of prevalent CHF. RERI was 2.66 and AP was 0.75. The odds of prevalent CHF with left ventricular ejection fraction (LVEF) ≥45% in participants with OSA+RHTN were >2-fold higher compared to those without, or with either OSA or RHTN, and RERI was 1.50 and AP was 0.72. Conclusion Presence of CHF, increased AHI and pulse pressure are independently associated with RHTN. OSA and RHTN have significant joint effects on CHF, especially in patients with concurrent CHD and preserved LVEF.

An estimated 10% to 30% of hypertensive patients can be considered to be resistant to treatment defined as controlled or uncontrolled blood pressure (BP) with use of ≥4 medications, including a diuretic.1–4 A large number of cross-sectional and longitudinal studies have demonstrated that patients with treatment-resistant hypertension compared with patients with more easily controlled hypertension have increased cardiovascular risk, including coronary artery disease, congestive heart failure, stroke, and chronic kidney disease (CKD). Since publication of the first Scientific Statement on the Diagnosis, Evaluation, and Treatment of Resistant Hypertension by the American Heart Association in 2008, which coincided with development of device-based strategies for treating resistant hypertension, resistant hypertension has become a major focus of intensive experimental and clinical investigation.1 In that context, this review highlights scientific advances specific for resistant hypertension that have occurred in the last 2 years, including important findings related to prognosis, medication adherence, clinical use of aldosterone antagonists, and application of device-based therapies. Multiple cross-sectional studies have related resistant hypertension to prevalent cardiovascular and renal diseases.2–8 Recent analyses have strengthened those associations with use of longitudinal or prospective assessments. From a secondary analysis of the ALLHAT (Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial) results, which included 1870 participants with resistant hypertension, Muntner et al9 reported that compared with study participants without resistant hypertension, participants with resistant hypertension had a 44%, 57%, 23%, 88%, 95%, and 30% higher risk of incident coronary heart disease, stroke, peripheral artery disease, heart failure, end-stage renal disease, and all-cause mortality, respectively, during the almost 5-year duration of the study after adjustment for multiple traditional risk factors, such as age, smoking, diabetes mellitus, and low-density lipoprotein cholesterol. Because of the ALLHAT study design, diuretic use in this analysis was not required to …

Background: Patients with chronic rheumatic heart disease (CRHD) have concomitant coronary artery disease (CAD), but the model to detect coexistent coronary artery stenosis prior to surgery has not been validated. Our study investigated whether the Framingham Risk Score (FRS) is a valid predictor of CAD in patients undergoing surgery for CRHD. Methods: A total of 989 rheumatic patients were enrolled between 2005 and 2010. They were subdivided into two groups according to coronary angiography (CAG) results to identify potential factors in the development of CAD. Finally, all patients were assessed using the FRS to examine the association between the 10-year cardiovascular disease (CVD) risk and CAD. Results: There were statistically significant inter-group differences in terms of age, sex, smoking, hypertension, bypass surgery and cardiac function in the New York Heart Association (NYHA) classification status (p Conclusions: The FRS model can accurately predict the prevalence of significant CAD and can reliably identify low-risk patients in whom routine pre-surgical angiography could be avoided.

Objective— Nicotinic acid (also known as niacin or vitamin B3), widely used to treat dyslipidemias, represents an effective and safe means to reduce the risk of mortality from cardiovascular disease. Nonetheless, a substantial fraction of patients discontinue treatment because of a strong side effect of cutaneous vasodilation, commonly termed flushing. In the present study, we tested the hypothesis that nicotinic acid causes flushing partially by activating the capsaicin receptor TRPV1, a polymodal cellular sensor that mediates the flushing response on consumption of spicy food. Approach and Results— We observed that the nicotinic acid–induced increase in blood flow was substantially reduced in Trpv1 –/– knockout mice, indicating involvement of the channel in flushing response. Using exogenously expressed TRPV1, we confirmed that nicotinic acid at submillimolar to millimolar concentrations directly and potently activates TRPV1 from the intracellular side. Binding of nicotinic acid to TRPV1 lowers its activation threshold for heat, causing channel opening at physiological temperatures. The activation of TRPV1 by voltage or ligands (capsaicin and 2-aminoethoxydiphenyl borate) is also potentiated by nicotinic acid. We further demonstrated that nicotinic acid does not compete directly with capsaicin but may activate TRPV1 through the 2-aminoethoxydiphenyl borate activation pathway. Using live-cell fluorescence imaging, we observed that nicotinic acid can quickly enter the cell through a transporter-mediated pathway to activate TRPV1. Conclusions— Direct activation of TRPV1 by nicotinic acid may lead to cutaneous vasodilation that contributes to flushing, suggesting a potential novel pathway to inhibit flushing and to improve compliance.

Background and Aim. Incidence of coronary restenosis after stent placement is high. Our study was going to investigate whether Lp(a) elevation was potential for predicting coronary restenosis and whether the effects of Lp(a) elevation on coronary restenosis were dependent on LDL-C level.Methods and Results. Totally 832 participants eligible for stent placement were enrolled and followed up for monitoring clinical end points. Baseline characteristics were collected. According to the cut point of Lp(a), participants were divided into low Lp(a) group (Lp(a) < 30 mg/dL) and high Lp(a) group (Lp(a) ≥ 30 mg/dL). Furthermore, based on baseline LDL-C level, participants were divided into LDL-C < 1.8 mmol/L and ≥1.8 mmol/L subgroups. Clinical end points including major adverse cardiovascular events (MACE), cardiovascular death, nonfatal myocardial infarction, ischemic stroke, and coronary revascularization (CR) were compared. Patients in high Lp(a) groups more frequently presented with acute coronary syndrome and three vessel stenoses. In subgroup of LDL-C < 1.8 mmol/L, no significant differences of cardiovascular outcomes were found between low and high Lp(a) groups. While in the subgroup of LDL-C ≥ 1.8 mmol/L, incidences of MACE and CR were significantly higher in high Lp(a) group, and odds ratio for CR was 2.05.Conclusion. With baseline LDL-C and Lp(a) elevations, incidence of CR is significantly increased after stent placement.

Atherosclerotic cardiovascular diseases (CVD) are still the leading cause of morbidity and mortality worldwide, although optimal medical therapy has been prescribed for primary and secondary preventions. Residual cardiovascular risk for some population groups is still considerably high although target low density lipoprotein-cholesterol (LDL-C) level has been achieved. During the past few decades, compelling pieces of evidence from clinical trials and meta-analyses consistently illustrate that lipoprotein(a) (Lp(a)) is a significant risk factor for atherosclerosis and CVD due to its proatherogenic and prothrombotic features. However, the lack of effective medication for Lp(a) reduction significantly hampers randomized, prospective, and controlled trials conducting. Based on previous findings, for patients with LDL-C in normal range, Lp(a) may be a useful marker for identifying and evaluating the residual cardiovascular risk, and aggressively lowering LDL-C level than current guidelines’ recommendation may be reasonable for patients with particularly high Lp(a) level.

MicroRNAs (miRs) are key posttranscriptional regulators of gene expression in all eukaryotic cells and have a vital role in the evolution of hypertension and cardiovascular remodelling and, therefore, have emerged as potential biomarkers for cardiovascular disease. We assessed 240 participants, including 60 healthy volunteers with normal carotid intima-media thickness (nCIMT), 60 healthy volunteers with increased CIMT (iCIMT), 60 hypertensive patients with nCIMT and 60 hypertensive patients with iCIMT. All patients underwent measurements of CIMT, carotid-femoral pulse wave velocity (cfPWV) and ambulatory blood pressure (BP) monitoring. Plasma miR-92a expression was quantified by real-time reverse transcription PCR. Correlations between miR-92a expression and BP parameters, CIMT and cfPWV were assessed using the Spearman correlation coefficient. We observed the lowest miR-92a expression (24.59±1.30 vs 27.76±2.13 vs 29.29±1.89 vs 33.76±2.08; P

Objective: To explore the effects of insulin-like growth factor-1 (IGF-1) on migration, proliferation and differentiation of mesenchymal stem cells (MSCs). Methods: MSCs 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). Results: The 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. Conclusions: IGF-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.

In past decades, growing evidence from basic and clinical researches reveal that small guanosine triphosphate binding protein ras homolog gene family, member A (RhoA) and its main effector Rho-associated kinase (ROCK) play central and complex roles in cardiovascular systems, and increasing RhoA and ROCK activity is associated with a broad range of cardiovascular diseases such as congestive heart failure, atherosclerosis, and hypertension. Favorable outcomes have been observed with ROCK inhibitors treatment. In this review, we briefly summarize the pathophysiological roles of RhoA/ROCK signaling pathway on cardiovascular system, displaying the potential benefits in the cardiovascular system with controlling RhoA/ROCK signaling pathway.

3‐Hydroxy‐methylglutaryl‐coenzyme A (HMG‐CoA) reductase inhibitors or statins are a class of medications with potent effects on reducing serum cholesterol level, and currently have been widely used in the primary and secondary prevention of atherosclerotic cardiovascular diseases (ASCVD).

Background Asymmetric Dimethylarginine (ADMA) is an inhibitor of endogenous nitric oxide synthase, which is the key synthase for nitric oxide (NO) production. Whether statins could protect endothelium by reducing ADMA concentration is unclear, and whether this effect is associated with the dose of statins usage is also needed further studied. Methods Dyslipidemia rat model was produced by giving high-fat and high-cholesterol diet for 8 weeks. Thereafter, low-dose (5 mg/kg body weight/day) and high-dose (20 mg/kg body weight/day) atorvastatin were orally prescribed for 4 weeks. Parameters of interest including lipid profiles, inflammatory and oxidative markers, NO production and plasma levels of ADMA and ADMA concentration of myocardium were evaluated. Liver enzymes and creatinine kinase (CK) were also detected for safety concern. Results At baseline, all parameters were comparable between the sham and the dyslipidemia groups. At 8 weeks of dyslipidemia establishment, as compared to the sham group, body weight and lipid profiles were significantly elevated, and plasma levels of C-reactive protein (CRP), malondialdehyde (MDA) and ADMA were concomitantly increased in accompanying with NO reduction in the dyslipidemia groups. With 4 weeks of atorvastatin therapy, as compared to the control group, lipid disorders and NO production were improved, and plasma levels of CRP, MDA and ADMA were significantly decreased in the high-dose atorvastatin group. ADMA concentration of cardiac tissues was also significantly reduced in the high-dose atorvastatin group. Notably, there was a trend to similar effects which did not reach statistical significance in the low-dose atorvastatin group when compared to the control group. Liver enzyme and CK were comparable after 4 weeks of atorvastatin therapy between groups. Conclusion In rats with dyslipidemia, atorvastatin therapy could reduce plasma level of ADMA and ADMA concentration in cardiac tissues, and these effects are associated with the dose of atorvastatin therapy.

Background Lipoprotein-associated phospholipase A2 (Lp-PLA2) plays complex and adverse roles on atherosclerosis. Current study was to investigate whether increased plasma Lp-PLA2 level is independently associated with the severity of coronary artery diseases (CAD). Methods Totally 781 participants were enrolled and performed coronary angiography (CAG) to figure out the number of coronary artery stenosis. According to clinical presentation, electrocardiography, cardiac biomarker, and CAG result, participants were divided into control (excluded CAD), stable angina (SA), unstable angina (UA) and acute myocardial infarction (AMI) groups. Baseline characteristics were recorded. Statistical analyses were performed to evaluate the relationship between Lp-PLA2 level and CAD severity. Results Plasma levels of Lp-PLA2 in control, SA, UA and AMI groups were 7.38(3.33-9.26) μg/L, 5.94(2.89-8.55) μg/L, 8.56(5.34-11.95) μg/L and 8.68(5.56-13.27) μg/L respectively (P

Background Lipoprotein associated phospholipase A2 (Lp-PLA2) is a novel biomarker for cardiovascular risk prediction. Whether increased Lp-PLA2 level is associated with re-stenosis after stent-placement is unclear. Methods Totally 326 participants eligible for stent-placement were enrolled and divided into two groups according to baseline Lp-PLA2 levels (named normal and elevated groups). Baseline characteristics and clinical outcomes were compared between normal and elevated groups. The relationships between Lp-PLA2 and other risk factors with re-stenosis were evaluated. Results Only the between-group difference of Lp-PLA2 was significant (123.2 ± 33.6 ng/mL vs 336.8 ± 85.4 ng/mL, P

Benign metastasizing leiomyoma (BML) is a rare clinical condition predominantly occurring in reproductive women with a history of uterine leiomyoma resection or hysterectomy. Oftentimes, it is easy to be misdiagnosed as a malignant tumor when nodules are found in multiple tissues. In order to raise clinicians' awareness of BML, we present a short review of the literature in combination with an unusual case.

Background The effects of atorvastatin on SDF-1α expression under acute myocardial infarction (AMI) are still unclear. Therefore, our present study is to investigate the roles and mechanisms of atorvastatin treatment on SDF-1α expression in rats with AMI. Methods Male Sprague–Dawley rats were underwent permanent coronary artery ligation and randomly assigned into four groups as follow: blank control (B), atorvastatin (A), atorvastatin plus L-NAME (A+L-NAME), and atorvastatin plus AMD3100 (A+AMD3100). Rats underwent similar procedure but without ligation were used as group sham operated (S). Atorvastatin (10mg/Kg/d body weight) was administrated by gavage to rats in three atorvastatin treated groups, and L-NAME (40mg/Kg/d body weight) or AMD3100 (5mg/Kg/d body weight) was given to group A+L-NAME or A+AMD3100, respectively. Results Comparing with group B, NO production, SDF-1α and CXCR4 expression were significantly up-regulated in three atorvastatin treated groups at the seventh day. However, the increments of SDF-1α and CXCR4 expression in group A+L-NAME were reduced when NO production was inhibited by L-NAME. Anti-inflammatory and anti-apoptotic effects of atorvastatin were offset either by decrease of SDF-1α and CXCR4 expression (by L-NAME) or blockage of SDF-1α coupling with CXCR4 (by AMD3100). Expression of STAT3, a cardioprotective factor mediating SDF-1α/CXCR4 axis induced cardiac protection, was up-regulated most significantly in group A. The effects of atorvastatin therapy on cardiac function were also abrogated either when SDF-1α and CXCR4 expression was diminished or the coupling of SDF-1α with CXCR4 was blocked. Conclusion SDF-1α upregulation by atorvastatin in rats with AMI was, at least partially, via the eNOS/NO dependent pathway, and SDF-1α upregulation and SDF-1α coupling with CXCR4 conferred anti-inflammatory and anti-apoptotic effects under AMI setting which we speculated that ultimately contributed to cardiac function improvement.

To investigate the effects and mechanisms of levorotatory (L)-amlodipine combined fluvastatin treatment on endothelium-mesenchymal transition (EndMT), a process related to hypertension development. Human umbilical vein endothelial cells (HUVECs) were used and divided to six groups based on different therapeutic strategies as follows: Blank Control, angiotensin-II (Ang-II), Ang-II+ rho-associated kinase (ROCK) inhibitor, Ang-II+ L-amlodipine, Ang-II+ fluvastatin, and Ang-II +L-amlodipine + fluvastatin groups. Twenty-four hours later, HUVECs were collected for immunofluorescence staining and western blot analyses to evaluate EndMT, and for flow cytometry to analyze cells apoptosis. Compared to Blank Control group, ROCK1 expression was significantly increased and phosphorylated endothelial nitric oxide synthase (p-eNOS) and eNOS expressions were profoundly reduced in Ang-II group. Immunofluorescence staining revealed that CD31 expression was down-regulated and α-SMA expression was up-regulated in HUVECs in Ang-II group. Western blot showed that endothelium-specific markers (CD31 and VE-cadherin) were significantly diminished and fibroblasts-specific markers (α-SMA and FSP-1) were significantly increased by Ang-II stimulation. Both L-amlodipine and fluvastatin were beneficial to improve these adverse changes, and these favorable effects were further enhanced by L-amlodipine combined fluvastatin treatment. HUVECs apoptosis induced by Ang-II were mitigated by both L-amlodipine and fluvastatin, and this benefit was further promoted by L-amlodipine combined fluvastatin treatment. Notably, all these improvements achieved by L-amlodipine combined fluvastatin treatment were comparable to those of ROCK1 inhibitor. Ang-II is a significant contributor to EndMT via increasing ROCK1 expression and L-amlodipine combined fluvastatin treatment confers additive effects on improving EndMT and endothelium apoptosis, which may be beneficial for preventing hypertension development.

Current study sought to evaluate the associations of obstructive sleep apnea (OSA) plus hypertension (HTN) and prevalent cardiovascular diseases (CVD).This was a cross-sectional study and a total of 1889 subjects were enrolled. The apnea-hypopnea index (AHI) was measured by polysomnography and OSA degree was classified as mild (AHI 5-14.9) and moderate-severe (AHI ≥ 15), and AHI < 5 was considered no-OSA. Mean and lowest oxyhemoglobin saturation (SaO2) was detected by pulse oximetry. Between-group differences were assessed and logistic regression analysis was used to analyze the association of OSA plus HTN and prevalent CVD.Compared to normotensive subjects, hypertensive subjects were older and had higher body mass index (BMI), neck girth, waist-hip ratio, AHI, and low-density lipoprotein cholesterol (LDL-C) level. Conversely, mean and lowest SaO2 levels were significantly lower. Logistic regression analysis showed that in an unadjusted model, compared to subjects with no-OSA and no-HTN (reference group), the association of HTN plus moderate-severe-OSA and prevalent CVD was the most prominent (odds ratio [OR]: 2.638 and 95% confidence interval [CI]: 1.942-3.583). In normotensive subjects, after adjusted for potential covariates, the associations of OSA (regardless of severity) and prevalent CVD were attenuated to nonsignificant. In hypertensive subjects, however, the associations remained significant but were reduced. Further adjusted for mean and lowest SaO2, the associations remained significant in HTN plus no-OSA (OR: 1.808, 95% CI: 1.207-2.707), HTN plus mild-OSA (OR: 2.003, 95% CI: 1.346-2.980), and HTN plus moderate-severe OSA (OR: 1.834, 95% CI: 1.214-2.770) groups.OSA plus HTN is associated with prevalent CVD, and OSA may potentiate the adverse cardiovascular effects on hypertensives patients but not normotensives.

Current study sought to evaluate the effects of obstructive sleep apnea (OSA) plus hypertension (HTN) on prevalent cardiovascular diseases (CVD). This was a cross-sectional study and a total of 1889 subjects were enrolled. The apnea-hypopnea index (AHI) was measured by polysomnography and OSA degree was classified as mild (AHI 5-14.9) and moderate-severe (AHI ≥ 15), and AHI

The aim of the present study was to evaluate the association between HDL cholesterol level and all-cause mortality in patients with ejection fraction reduced heart failure (EFrHF) complicating coronary heart disease (CHD). A total of 323 patients were retrospectively recruited. Patients were divided into low and high HDL cholesterol groups. Between-group differences and associations between HDL cholesterol level and all-cause mortality were assessed. Patients in the high HDL cholesterol group had higher HDL cholesterol level and other lipid components (P

Mesenchymal stem cells (MSCs) have been extensively applied for the restoration of cardiomyocytes loss after acute myocardial infarction (AMI). However, the optimal therapeutic efficacy of MSCs in ischemic heart diseases has been hampered by their poor survival and low differentiated rates. Therefore, the improvement of MSC survival and differentiated rates is warranted and critical for the efficacy of MSCs in AMI. In this paper, MSCs isolated from rat inguinal fat tissues were termed as adipose-derived mesenchymal stem cells (ASCs), and the fourth passage of ASCs was pre-specified by co-culturing with cardiomyocytes in a transwell system termed as co-ASCs. Fourteen days later, GATA-4 (a transcription factor) and cardiac troponin-I were detected by cellular immunofluorescence. Atorvastatin (Ator group) or vehicle (control group) was administrated for the first 24 h after AMI production in rats. Fourteen days later, inflammatory parameters and cardiac function were evaluated. The other surviving rats were injected with a total of 1 × 10(6) co-ASCs/100 μl phosphate-buffered saline (PBS), 1×10(6) ASCs/100 μl PBS, or 100 μl PBS. Twenty-eight days after cell injection, survival and differentiated rates of transplanted cells and cardiac function were evaluated. The percentage of GATA-4 expression in co-ASCs was 28.5% ± 5.6% and of cardiac troponin-I was 22.8% ± 3.2%. Compared with the control group, the number of infiltrating inflammatory cells, myeloperoxidase activity, inflammatory cytokines (VCAM-1, TNF-α, Hs-CRP) mRNA expression, and Bax protein expression were significantly reduced in the three Ator groups, accompanied by a significant improvement of Bcl-2 protein expression and cardiac function (P< 0.05). Compared with the Ator2 + ASCs group and Con + co-ASCs group, the number of 4-6-diamidino-2-phenylindole-stained cells and cardiac troponin-I-positive transplanted cells, concomitant with cardiac function, were improved most prominently in the Ator3 + co-ASCs group (P< 0.05). Pre-amelioration of the cardiac milieu, in conjunction with pre-specification of ASCs, was beneficial for enhancing ASCs' therapeutic efficacy on cardiac function after AMI.

Background Obstructive sleep apnea (OSA) is associated with an increase in the prevalence and incidence of hypertension and cardiovascular diseases. Data about epidemiological characteristics of OSA in Chinese hypertensive populations is limited. Methods Hypertensive subjects without a prior diagnosis of OSA were recruited, and the apnea-hyponea index (AHI) was assessed by polysomnography. Comparisons were performed between subjects without OSA and with different degrees of OSA. Gender-specific differences in epidemiological characteristics of OSA were also analyzed. Univariate and multivariate regression analyses were conducted to evaluate the associations between OSA and other variables. Results A total of 971 hypertensive subjects were enrolled and 685 (70.5%) were diagnosed with OSA. Compared to those without OSA, subjects with OSA were more likely male (78.4% versus 71.7%, P = 0.016) and at higher cardiovascular risk in subjects with moderate-severe OSA. Among the 685 OSA subjects, 79.4% (537 cases) were males. Gender-specific differences in epidemiological characteristics of OSA were observed. Multivariate regression analyses revealed that after adjusting for covariates, only body mass index positively correlated with OSA in males (odds ratio (OR): 1.064, 95% confidence interval (CI): 1.008–1.123, P = 0.024). In female subjects, after adjusting for covariates, only age positively correlated with OSA (OR: 1.071, 95% CI: 1.029–1.116, P = 0.001). Conclusion In summary, in a Chinese hypertensive population, OSA prevalence is strikingly high. Hypertensive subjects with the most severe OSA are at greater cardiovascular risk. There are significant differences in epidemiological characteristics of OSA between male and female.

Background To investigate relationship between glycated hemoglobin (HbA1c) level and coronary artery disease (CAD) severity. Methods Observational study was conducted and 573 participants were enrolled and baseline characteristics were collected. Clinical presentations in terms of stable angina, unstable angina or acute myocardial infarction were diagnosed. All participants were performed coronary angiography to figure out the numbers of coronary artery stenosis in terms of none-stenosis (< 50% stenosis), single or multiple vessels stenoses (≥ 50% stenosis). All participants were divided into subgroups according to two categories in terms of severity of clinical presentation (stable angina, unstable angina, or acute myocardial infarction) and the number of coronary artery stenosis (none, single, and multiple vessels). Primary endpoint was to evaluate relationship between baseline HbA1c value and CAD severity. Results Consistent to previous studies, participants with CAD had more risk factors such as elderly, smoking, low HDL-C and high CRP levels. Notably, HbA1c level was more prominent in CAD group than that without CAD. As compared to stable angina subgroup, HbA1c levels were gradually increased in unstable angina and acute myocardial infarction groups. Similar trend was identified in another category in terms of higher HbA1c level corresponding to more vessels stenoses. Multivariate regression analyses showed that after adjusted for traditional risk factors as well as fasting blood glucose, HbA1c remained strongly associated with the severity of CAD. Nonetheless, there was no significant association when CRP was accounted for. Conclusion HbA1c may be a useful indicator for CAD risk evaluation in non-diabetic adults.