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The findings on the relationship between marital status and hypertension are inconsistent. We aimed to explore age differences in their associations. We used Hainan Hypertension Survey data, including 13,088 individuals aged more than 25 years, as part of the China Hypertension Survey study, a population-based nationwide study. The marital status was classified as following three groups: the unmarried, the married, and those who formerly lived with his/her spouse. We examined the association between marital status and blood pressure levels and the odds of hypertension across different ages and sex. The participants' mean age was 49.9 ± 17 years, 49% were male, and 23% experienced hypertension. The multivariable logistic regression model showed among younger (

Yu Liu,1 Le-Feng Wang,1 Li-Hong Liu,1 Xin-Chun Yang,1 Zheng-Hong Ren,2 Kui-Bao Li,1 Mu-Lei Chen,1 Hong-Shi Wang,1 Jiu-Chang Zhong,1 Li Xu,1 Zhu-Hua Ni,1 Wei-Ming Li,1 Kun Xia,1 Da-Peng Zhang,1 Hao Sun,1 Zong-Sheng Guo,1 Yong-Hui Chi,1 Ji-Fang He,1 Zhi-Yong Zhang,1 Feng Jiang1 1Heart Center & Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing, People’s Republic of China; 2School of Public Health, Peking University Health Science Center, Beijing, People’s Republic of ChinaCorrespondence: Le-Feng WangHeart Center & Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, No. 8 of Gongtinan Road, Chaoyang District, Beijing, People’s Republic of ChinaTel/Fax +86 10 85231173Email wanglefeng_dr66@163.comObjective: Patients presenting with acute myocardial infarction (AMI) with prior digestive system disease are more likely to suffer from gastrointestinal (GI) bleeding than those without these diseases. However, few articles reported how the different conditions of the digestive tract produced different risks of GI bleeding.Methods: A single-center study on 7464 patients admitted for AMI from December 2010 to June 2019 in the Beijing Chaoyang Heart Center was retrospectively examined. Patients with major GI bleeding (n = 165) were compared with patients without (n = 7299). Univariate and multivariate logistic regression models were constructed to test the association between GI bleeding and prior diseases of the digestive tract, including gastroesophageal reflux disease, chronic gastritis, peptic ulcer, hepatic function damage, diseases of the colon and rectum, and gastroenterological tract tumors.Results: Of the 7464 patients (mean age, 63.4; women, 25.6%; STEMI, 58.6%), 165 (2.2%) experienced major GI bleeding, and 1816 (24.3%) had a history of digestive system disease. The risk of GI bleeding was significantly associated with peptic ulcer (OR = 4.19, 95% CI: 1.86– 9.45) and gastroenterological tumor (OR = 2.74, 95% CI: 1.07– 7.04), indicated by multivariate logistic regression analysis.Conclusion: Preexisting peptic ulcers and gastroenterological tract tumors rather than other digestive system diseases were indicators of gastrointestinal bleeding in patients with AMI who undergo standard antithrombotic treatment during hospitalization.Keywords: gastrointestinal bleeding, digestive system disease, acute myocardial infarction, peptic ulcer, gastroenterological tract tumor

Objectives To investigate the long-term outcome of patients with acute ST-segment elevation myocardial infarction (STEMI) and a chronic total occlusion (CTO) in a non-infarct-related artery (IRA) and the risk factors for mortality. Methods The enrolled cohort comprised 323 patients with STEMI and multivessel diseases (MVD) that received a primary percutaneous coronary intervention between January 2008 and November 2013. The patients were divided into two groups: the CTO group (n = 97) and the non-CTO group (n = 236). The long-term major adverse cardiovascular and cerebrovascular events (MACCE) experienced by each group were compared. Results The rates of all-cause mortality and MACCE were significantly higher in the CTO group than they were in the non-CTO group. Cox regression analysis showed that an age ≥ 65 years (OR = 3.94, 95% CI: 1.47–10.56, P = 0.01), a CTO in a non-IRA(OR = 5.09, 95% CI: 1.79 ~ 14.54, P P P = 0.01), stress ulcer with gastraintestinal bleeding (SUB) (OR = 6.36, 95% CI: (1.45 ~ 28.01, P = 0.01) were significantly related the 10-year mortality of patients with STEMI and MVD; an in-hospital Killip class ≥ 3 (OR = 2.97,95% CI:1.46 ~ 6.03, P P = 0.03) were significantly related to the 10-year mortality of patients with STEMI and a CTO. Conclusions The presence of a CTO in a non-IRA, an age ≥ 65 years, an in-hospital Killip class ≥ 3, and the presence of renal insufficiency, and SUB were independent risk predictors for the long-term mortality of patients with STEMI and MVD; an in-hospital Killip class ≥ 3 and renal insufficiency were independent risk predictors for the long-term mortality of patients with STEMI and a CTO.

Alternations of gut microbiota (GM) in atrial fibrillation (AF) with elevated diversity, perturbed composition and function have been described previously. The current work aimed to assess the association of GM composition with AF recurrence (RAF) after ablation based on metagenomic sequencing and metabolomic analyses and to construct a GM‐based predictive model for RAF. Compared with non‐AF controls (50 individuals), GM composition and metabolomic profile were significantly altered between patients with recurrent AF (17 individuals) and non‐RAF group (23 individuals). Notably, discriminative taxa between the non‐RAF and RAF groups, including the families Nitrosomonadaceae and Lentisphaeraceae, the genera Marinitoga and Rufibacter and the species Faecalibacterium spCAG:82, Bacillus gobiensis and Desulfobacterales bacterium PC51MH44, were selected to construct a taxonomic scoring system based on LASSO analysis. After incorporating the clinical factors of RAF, taxonomic score retained a significant association with RAF incidence (HR = 2.647, P = .041). An elevated AUC (0.954) and positive NRI (1.5601) for predicting RAF compared with traditional clinical scoring (AUC = 0.6918) were obtained. The GM‐based taxonomic scoring system theoretically improves the model performance, and the nomogram and decision curve analysis validated the clinical value of the predicting model. These data provide novel possibility that incorporating the GM factor into future recurrent risk stratification.

Background There is a paucity of evidence on the combination of the SYNTAX score II (SSII) and erythrocyte sedimentation rate (ESR) in assessing the long-term prognosis of patients with ST-elevated myocardial infarction (STEMI) and multivessel disease. The objective of this study was to investigate whether the ESR could enhance the predictive value of SSII on the long-term prognosis of STEMI patients. Methods A retrospective cohort study involving 483 STEMI and multivessel disease subjects receiving primary percutaneous coronary intervention was conducted. Major adverse cardiovascular events (MACE) included cardiovascular death, acute heart failure, recurrent myocardial infarction, revascularization, and nonfatal stroke. The predicted values of different models were estimated by a likelihood ratio test, Akaike’s information criteria (AIC), receiver operating characteristic (ROC) curves, net reclassification improvement (NRI), and integrated discrimination improvement (IDI). Results During the follow-up period of up to 52 months, both the SSII and ESR were independently associated with MACE (hazard ratio [HR] = 1.032, p p p p p = 0.04) compared to that of the model with SSII alone. The net reclassification and integrated discrimination of the SSII alone model improved significantly with ESR (NRI = 0.0319, p p Conclusions The prognostic model containing SSII, which is an independent risk factor of MACE, had a significantly enhanced predictive probability with the addition of ESR.

Background: Nicorandil prior to reperfusion by primary percutaneous coronary intervention (PCI) in patients with ST-segment elevated myocardial infarction (STEMI) has been suggested to be beneficial. However, results of previous randomized controlled trials (RCTs) were not consistent. We aimed to perform a meta-analysis to systematically evaluate the effect of periprocedural nicorandil in these patients. Methods: Related studies were obtained by searching PubMed, Embase and Cochrane's Library. Effects of perioperative nicorandil on the incidence of no-reflow phenomenon (NRP), corrected thrombolysis in myocardial infarction (TIMI) frame count (CTFC), wall motion score (WMS), left ventricular ejection fraction (LVEF), heart failure (HF) exacerbation of rehospitalization and incidence of major cardiovascular adverse events (MACE) were analyzed. Results: Eighteen RCTs with 2,055 patients were included. Treatment of nicorandil prior to PCI significantly reduced the incidence of NRP (risk ratio [RR]: 0.47, P

BACKGROUND: This study aims to analyze the in-hospital outcome of primary percutaneous coronary intervention (PCI) for patients with acute myocardial infarction (AMI) and prior coronary artery bypass grafting (CABG). METHODS: This was a retrospective study. From January 2011 to December 2018, the data of 78 consecutive patients (study group) with prior CABG, who received primary coronary angiography in the setting of ST-elevation myocardial infarction (STEMI) or non-ST-elevation myocardial infarction (NSTEMI), were screened. The study group was compared with another well-matched 78 patients without a history of CABG (control group). The information of the coronary angiograms and clinical data of both groups were analyzed. Multivariate conditional logistic regression models were constructed to test the association between PCI success rate and the prior CABG at age ≥65 and

There is scarce evidence that the erythrocyte sedimentation rate (ESR) could efficiently improve the prediction accuracy of the Global Registry of Acute Coronary Events (GRACE) risk score in cases of ST-elevation myocardial infarction (STEMI). A cohort of 1094 STEMI patients undergoing primary percutaneous coronary intervention was retrospectively recruited. Patients were categorized based on the ESR values. Final endpoints included cardiovascular death and major adverse cardiovascular event (MACE) occurrence. The predictive value of combined models with the GRACE score and ESR was assessed by receiver operating characteristic (ROC) analysis, net reclassification improvement (NRI), and integrated discrimination improvement. During the mean follow-up of 23 months, 34 patients died and 190 experienced MACEs, of which 23 patients died in the first year; both endpoints were more frequent in the higher group. The ESR and high-sensitivity C-reactive protein (hs-CRP) were independent risk factors of 1-year cardiovascular death, together with the GRACE score (ESR: hazard ratio = 1.03, P = .006 hs-CRP: hazard ratio = 1.00, P = .001; GRACE: 1.03, P = .012). Although no statistical improvement in the area under the ROC curve was observed in either the GRACE/ESR or the GRACE/hs-CRP model (GRACE/ESR models: 0. 8073 vs GRACE: 0.7714, P = .22; GRACE/ESR models: 0. 7815 vs GRACE: 0.7714, P = .61), the GRACE score and ESR together significantly improved the NRI (0.633; P

Chronic kidney disease (CKD) significantly increases the rate of adverse cardiovascular events in patients with coronary artery disease. In this study, we aimed to establish a risk score (RS) model to predict in-hospital mortality risk in patients with end-stage renal disease (ESRD) and acute myocardial infarction (AMI). A total of 113 consecutive patients with ESRD and AMI were retrospectively enrolled between January 1, 2015 and December 31, 2019. All patients received regular hemodialysis and were divided into two groups according to the prognosis during hospitalization. Univariable and multivariable logistic regression analyses were used to identify the risk factors of in-hospital mortality. A RS model was developed based on multiple regression analysis and was internally validated using 1000 bootstrap analysis. The receiver operating characteristic (ROC) curve was performed, and the area under curve (AUC) was analyzed to evaluate the performance of the RS model. AUCs were compared using the Z test. Thirty-three patients died during hospitalization, resulting in in-hospital mortality rate of 29.2%. After multivariate logistic regression, an RS model (0–8) was established based on five independent factors that were assigned with different points according to relative coefficients (coefficient of the index risk factor divided by the lowest coefficient among these five risk factors; rounded to closest integer): 1 for C-reactive protein (CRP) ≥ 14.2 mg/L and left ventricular ejection fraction (LVEF) ≤ V3%; 2 for age ≥ 65 years old, heart rate (HR) at admission ≥ 86 beats per minute (bpm) and d-dimer ≥ 2.4 mg/L FEU. The present RS model had a sensitivity of 85.7%, the specificity of 84%, and an accuracy of 78.1%. In ROC curve analysis, the model demonstrated a good discriminate power in predicting in-hospital mortality (AUC = 0.895, 95% CI 0.814–0.96; P

Atrial fibrillation has been identified to be associated with disordered gut microbiota. Notably, atrial fibrillation is a progressive disease and could be categorized as paroxysmal and persistent based on the duration of the episodes. The persistent atrial fibrillation patients are accompanied by higher risk of stroke and lower success rate of rhythm control. However, the microbial signatures of different categories of atrial fibrillation patients remain unknown. We sought to determine whether disordered gut microbiota occurs in the self-terminating PAF or intestinal flora develops dynamically during atrial fibrillation progression. We found that different types of atrial fibrillation show a limited degree of gut microbiota shift. Gut microbiota dysbiosis has already occurred in mild stages of atrial fibrillation, which might act as an early modulator of disease, and therefore may be regarded as a potential target to postpone atrial fibrillation progression., Dysbiotic gut microbiota (GM) and disordered metabolic patterns are known to be involved in the clinical expression of atrial fibrillation (AF). However, little evidence has been reported in characterizing the specific changes in fecal microbiota in paroxysmal AF (PAF) and persistent AF (psAF). To provide a comprehensive understanding of GM dysbiosis in AF types, we assessed the GM signatures of 30 PAF patients, 20 psAF patients, and 50 non-AF controls based on metagenomic and metabolomic analyses. Compared with control subjects, similar changes of GM were identified in PAF and psAF patients, with elevated microbial diversity and similar alteration in the microbiota composition. PAF and psAF patients shared the majority of differential taxa compared with non-AF controls. Moreover, the similarity was also illuminated in microbial function and associated metabolic alterations. Additionally, minor disparity was observed in PAF compared with psAF. Several distinctive taxa between PAF and psAF were correlated with certain metabolites and atrial diameter, which might play a role in the pathogenesis of atrial remodeling. Our findings characterized the presence of many common features in GM shared by PAF and psAF, which occurred at the self-terminating PAF. Preventative and therapeutic measures targeting GM for early intervention to postpone the progression of AF are highly warranted. IMPORTANCE Atrial fibrillation has been identified to be associated with disordered gut microbiota. Notably, atrial fibrillation is a progressive disease and could be categorized as paroxysmal and persistent based on the duration of the episodes. The persistent atrial fibrillation patients are accompanied by higher risk of stroke and lower success rate of rhythm control. However, the microbial signatures of different categories of atrial fibrillation patients remain unknown. We sought to determine whether disordered gut microbiota occurs in the self-terminating PAF or intestinal flora develops dynamically during atrial fibrillation progression. We found that different types of atrial fibrillation show a limited degree of gut microbiota shift. Gut microbiota dysbiosis has already occurred in mild stages of atrial fibrillation, which might act as an early modulator of disease, and therefore may be regarded as a potential target to postpone atrial fibrillation progression.

Although the CHADS2 and CHA2DS2-VASc scoring systems are commonly used as measures of thromboembolic risk in patients with nonvalvular atrial fibrillation (NVAF), data are inconsistent as to their value in predicting the presence of left atrial (LA) and/or left atrial appendage (LAA) thrombogenic milieu (TM). The present study aimed to establish a novel risk score to assess the risk of LA and/or LAATM in NVAF patients.This is a retrospective case-control study that included 125 consecutive patients with NVAF plus TM, as evidenced by transesophageal echocardiography (TEE) during a period from1 January 2010 to 1 February 2017. The controls were 1098 NVAF patients without TM during the same period. Risk factors for LA and/or LAATM were identified using univariable analysis and multivariable logistic regression. The risk score model was developed based on 10-fold validation and multiple regression. Risk model performance was evaluated using receiver operating characteristic (ROC) curves. Net reclassification improvement (NRI) was used for the comparison of C-statistics. The AUCs were compared using the Z test.Among all 1223 NVAF patients, 125 (10.22%) patients had LA and/or LAATM. A score system (0-12) was developed based on the following 6 independent variables identified by 10-fold validation with sequential methods. Different points were assigned for each variable, according to multivariable regression using relative coefficients (coefficient of the index risk factor divided by the lowest coefficient among the 6 risk factors; rounded to closest integer): 1 for blood type A and N-terminal B-type natriuretic peptide (NT-proBNP) ≥864.85 pg/mL; 2 for LAD ≥43.5 mm and age ≥ 73.5 years old; 3 for previous heart failure and previous stroke or TIA. The present risk score system had a sensitivity of 58.3%, specificity of 91.4 and accuracy of 81.6%. The area under the ROC curve (AUC) was 0.832, (95% CI: 0.784-0.881; P 0.001). The negative predictive value (NPV) was 92% when we set the cut-off point at 4; when the cut-off point was set at 8, the positive predictive value (PPV) was 85.7%. Compared with CHADS2 and CHA2DS2-VASc score, the present novel risk score has better predictive power [net reclassification improvement (NRI) +96.3% and +66.2%, respectively; all P 0.001].This study developed a novel risk score to help predicting LA and/or LAATM in NVAF patients, which had higher accuracy than CHADS2 and CHA2DS2-VASc score system.

Background Previous studies have identified ABO blood groups as predictors of thromboembolic diseases. In patients with atrial fibrillation (AF), however, potential association between ABO blood groups and the risk of left atrial (LA) and/or left atrial appendage (LAA) thrombogenic milieu (TM) has not been established. Methods This is a retrospective case-control study that included 125 consecutive patients with non-valvular atrial fibrillation (NVAF) plus TM, as evidenced by transesophageal echocardiography (TEE) during a period from1 January 2010 to 31 December 2016. The controls were selected randomly from 1072 NVAF without TM at a 1:2 ratio. Potential association between ABO blood groups and TM was analyzed using multivariate logistic regression analysis. Results The risk of TM was higher in patients with blood group A (33.6% vs. 20.2% in non-A blood groups, P = 0.005). After adjusting for age, sex, oral anticoagulant use, AF type and duration, and relevant functional measures (e.g., NT-pro BNP level, left atrium diameter, and left ventricular ejection fraction), blood group A remained associated with an increased risk of TM (OR = 2.99, 95% CI 1.4–6.388, P = 0.005). Conclusion Blood group A is an independent risk factor for TM in NVAF patients.

BACKGROUND The CHA2 DS2 -VASc score is a classic predictor of stroke in patients with atrial fibrillation (AF). Decreased left atrial appendage flow velocity (LAA-FV) reflects the blood stasis, and left atrial (LA) strain is a manifestation of atrial remodeling. This study aimed to explore the effects of AF rhythm and CHA2 DS2 -VASc score in the development of thrombogenesis and their potential correlation with LAA-FV and LA strain. HYPOTHESIS AF rhythm and high CHA2 DS2 -VASc score correlate independently with decreased LAA-FV, which can be predicted by LA strain. METHODS In 98 AF patients, LAA-FV was measured by transesophageal echocardiography and LA strain was measured by transthoracic echocardiography. RESULTS LAA-FV decreased sharply in the AF rhythm group (26.22 vs 61.87 mm/s; P < 0.001), and CHA2 DS2 -VASc score did not differ between the decreased and normal LAA-FV groups in all patients (P = 0.289). However, in sinus rhythm (SR), LAA-FV was associated with CHA2 DS2 -VASc score (coefficient = -0.317, P = 0.013), and the CHA2 DS2 -VASc score differed between the normal and decreased LAA-FV groups (2 [0-7] vs 3 [0-6], respectively; P = 0.038). Moreover, LA strain was a predictor of LAA-FV in both AF rhythm and SR, whereas a peak positive systolic strain divided by LA volume index

Objectives To examine whether the association between resting heart rate (RHR) and all-cause mortality and cardiovascular events differs according to age. Design Prospective cohort. Setting Community in Beijing, China. Participants Individuals aged 40 and older without cardiovascular disease at baseline (N = 6,209). Measurements Trained investigators interviewed participants using a standard questionnaire to obtain information on demographic characteristics, medical history and lifestyle risk factors in 1991. RHR was evaluated according to quartiles (

Background: The exact relationship between 25-hydroxyvitamin D [25(OH) D] levels and small vessel disease (SVD) are not clear in China. The aim of this study was to determine the association between 25(OH) D and SVD in China. Methods: We enrolled consecutive 106 patients with SVD and 115 controls in Beijing Chaoyang Hospital and Jinan City people’s hospital between Jan 2017 and Dec 2017. Vitamin D status was estimated by measuring serum 25-hydroxyvitamin D [25(OH) D]. The subjects were categorized into three subgroups: vitamin D deficiency (≤12ng/ml), insufficiency (12-20ng/ml) and sufficiency (≥20 ng/ml). Results: Among 106 stroke patients, 80 (75.5%) were men and mean age was 61.6±13.2 years. 25(OH) D deficiency was observed in 76 (71.7%) stroke patients and 47 (40.9%) controls (P=0.001). Comparing with controls, patients with SVD were correlated with higher proportion of male, the histories of stroke, smoking and hyperlipidemia; higher systolic blood pressure, diastolic blood pressure and low density lipoprotein; lower of 25(OH)D level. The logistic regression analysis showed the level of 25(OH)D was independently predicted the occurrence of SVD (OR 0.772, CI 0.691-0.862, P=0.001). Compared with those in sufficiency group (≥20ng/ml), the ORs of SVD in the deficiency (≤12ng/ml) and insufficiency group (12–20 ng/ml) of 25(OH)D were 5.609 [95% confidence interval (CI) 2.006-15.683] and 1.077 (95% CI: 0.338-3.428) after adjusting for potential confounders, respectively. We also found a significant effect modification of SVD risk by 25(OH)D status and hypertension interaction (P=0.001), and compared with those with sufficiency 25(OH)D levels, in hypertensives with vitamin D deficiency (≤12ng/ml) and insufficiency (12-20 ng/ml), the ORs were increased to 9.738 (2.398-39.540) and 1.108 (0.232-5.280), respectively (Pinteraction=0.001). Conclusion: Our findings showed patients with SVD were correlated with the deficiency of 25(OH)D. The combined presence of hypertension and vitamin D deficiency increased the probability of developing SVD. Our study raises the importance that vitamin D supplementation combined with monitoring hypertension are promising approaches in the management of SVD.

INTRODUCTION Advanced age is the foremost risk factor for atrial fibrillation (AF). Telomere length is a surrogate for biological aging, but the association between shortened leukocyte telomere length (LTL) and recurrence of AF (RAF) after ablation remains inconclusive. METHODS In this prospective analysis, 282 patients underwent an initial catheter ablation for paroxysmal or persistent AF. The association between RAF and LTL was analyzed by univariate and multivariate Cox regression, as well as time-dependent receiver operating characteristic (ROC) analysis and Kaplan-Meier analysis. RESULTS After a mean follow-up of 14.20 ± 5.04 months, RAF was documented in 78 of the 277 patients who completed the study (28.16%). In Cox proportional hazards models, LTL, age, diagnosis to ablation time (DTAT), N-terminal pronatriuretic peptide, and CHA2DS2-VASc score were significantly associated with RAF. After multivariable adjustment, LTL and DTAT were predicted as independent risk factors for RAF with hazard ratio (HR) of 3.17 (95% confidence interval [CI]: 1.23-8.15, P = 0.017) and 1.43 (95% CI: 1.10-1.86, P = 0.007), respectively. In addition, ROC analysis indicated the potential diagnostic value of LTL with an area under the curve of 0.64 (P

Objective: Atrial fibrosis plays a critical role in atrial fibrillation (AF). A key event in the pathogenesis of fibrosis is the activation of fibroblasts (FBs) into myofibroblasts (MFBs). Paracrine factors released from MFBs lead to ion channel expression changes in cardiomyocytes (CMs). Downregulation of L-type calcium channel Cav1.2 expression is a hallmark of AF-associated ionic remodeling. However, whether exosome (Exo)-mediated crosstalk between MFBs and CMs regulates Cav1.2 expression remains unknown. Methods: Atrial FBs and CMs were isolated and cultured from neonatal rats by enzymatic digestion. The activation of FBs into MFBs was induced by angiotensin II. Co-culture assay and in vitro Exo treatment were used to determine the effect of MFB-derived Exos on Cav1.2 expression. Confocal Ca2+ imaging was performed to examine the adrenergic stimulation-elicited Ca2+ influx signals. The levels of potential Cav1.2-inhibitory microRNAs (miRNAs) were measured by qRT-PCR. Results: Untreated FBs expressed limited amounts of alpha smooth muscle actin (α-SMA), while angiotensin II induced a significant upregulation of α-SMA-expressing MFBs. Co-cultures of MFBs and CMs resulted in downregulation of Cav1.2 expression in CMs, which was largely abolished by pretreatment of MFBs with exosomal inhibitor GW4869. More importantly, treatment with MFB-derived Exos caused repression of Cav1.2 expression in CMs. Additionally, the adrenergic receptor agonist-elicited Ca2+ influx signals in CMs were remarkably attenuated by pretreatment with MFB-derived Exos, corresponding to the paralleled change in Cav1.2 expression. Finally, miR-21-3p, a potential Cav1.2-inhibitory miRNA, was enriched in MFB-derived Exos and upregulated in CMs in response to MFB-derived Exos. Conclusion: We uncover an Exo-mediated crosstalk between MFBs and CMs, contributing to increased vulnerability to AF by reducing the expression of Cav1.2 in CMs.

Atrial remodeling plays a significant role during the progression of atrial fibrillation (AF). Left atrial wall thickness (LAT) is a subjective and easily acquirable indicator referring to structural remodeling. Therefore, we aimed to investigate the association between LAT and atrial remodeling substrate, and to explore the predictive role of LAT about strong maintenance substrate and poor response to catheter ablation. LAT was measured by cardiac computed tomography in 2 selected locations (roof and floor) in 100 persistent AF patients. Then the low-dose-ibutilide-facilitated catheter ablation was performed and atrial maintenance substrate was categorized as weak, mild, and strong, based on the response to circumferential pulmonary vein isolation or complex fractionated atrial electrograms ablation. During follow-up, the success rate was evaluated. LAT showed a progressive thickening tendency from weak, mild, to strong maintenance substrate (roof: 2.2 mm vs. 2.6 mm vs. 3.9 mm, P 3.10 mm might be the predictor to strong atrial maintenance substrate and poor response to ablation. LAT was associated with the remodeling extent of atrial maintenance substrate and might predict the response to catheter ablation. These findings could help the clinicians to select the appropriate ablative strategy and predict the complexity and prognosis before catheter ablation.

Background Accumulating studies have suggested that gut microbiota (GM) dysbiosis and vitamin D3 deficiency each play an important role during the progression of hypertension (HTN). However, few studies have characterized the underlying interaction between GM shift and vitamin D3 deficiency in HTN patients. Hypothesis This study aimed to evaluate the possible crosstalk between GM dysbiosis and vitamin D deficiency in the pathogenesis of HTN. Methods In a cohort of 34 HTN patients and 15 healthy controls, we analyzed the fecal microbiota products, GM composition, and the interaction between GM and vitamin D3. Results Vitamin D3 was significantly decreased in feces of HTN patients (P = .006, vs controls) and was correlated with altered GM, including decreased Shannon index (R 2 = 0.1296, P = .0111) and Pielou evenness (R 2 = 0.1509, P = .0058). Moreover, vitamin D3 positively correlated with HTN‐reduced bacterial genera, including Subdoligranulum (R 2 = 0.181, P = .0023), Ruminiclostridium (R 2 = 0.1217, P = .014), Intestinimonas (R 2 = 0.2036, P = .0011), Pseudoflavonifractor (R 2 = 0.1014, P = .0257), Paenibacillus (R 2 = 0.089, P = .0373), and Marvinbryantia (R 2 = 0.08173, P = .0464). Partial least squares structural equation modeling showed that 27.7% of the total effect of gut microbiome on HTN was mediated by limiting vitamin D production. Finally, receiver operating characteristic curve analysis revealed the predictive capacity of differential gut microbiome signatures and decreased vitamin D3 to distinguish HTN patients (AUC = 0.749, P = .006). Conclusions Our findings suggest that the GM dysbiosis contributing to the development of HTN might be partially mediated by vitamin D3 deficiency. Future studies involving the underlying mechanism and intervention strategies targeting microbiome composition and vitamin D3 to counteract the progression of HTN are warranted.

Acute myocardial infarction (AMI) due to unprotected left main coronary artery (ULMCA) disease is clinically catastrophic although it has a low incidence. Studies on the long-term prognosis of these patients are rare.From January 1999 to September 2013, 55 patients whose infarct-related artery was the ULMCA were enrolled. Clinical, angiographic and interventional data was collected. Short-term and long-term clinical follow-up results as well as prognostic determinants during hospitalisation and follow-up were analysed.Cardiogenic shock (CS) occurred in 30 (54.5%) patients. During hospitalisation, 22 (40.0%) patients died. Multivariate logistic regression analysis showed that CS (odds ratio [OR] 5.86; p = 0.03), collateral circulation of Grade 2 or 3 (OR 0.14; p = 0.02) and final flow of thrombolysis in myocardial infarction (TIMI) Grade 3 (OR 0.05; p = 0.03) correlated with death during hospitalisation. 33 patients survived to discharge; another seven patients died during the follow-up period of 44.6 ± 31.3 (median 60, range 0.67-117.00) months. The overall mortality rate was 52.7% (n = 29). Kaplan-Meier analysis showed that the total cumulative survival rate was 30.7%. Cox multivariate regression analysis showed that CS during hospitalisation was the only predictor of overall mortality (hazard ratio 4.07, 95% confidence interval 1.40-11.83; p = 0.01).AMI caused by ULMCA lesions is complicated by high incidence of CS and mortality. CS, poor collateral blood flow and failure to restore final flow of TIMI Grade 3 correlated with death during hospitalisation. CS is the only predictor of long-term overall mortality.

Background: Studies on the association between body mass index (BMI) and death risk among patients with hypertension are limited, and the results are inconsistent. We investigated the association between BMI and cardiovascular disease (CVD) and all-cause mortality among hypertensive patients in a population of Beijing, China. Methods: We conducted a prospective cohort study of 2535 patients with hypertension aged 40 to 91 years from Beijing, China. Participants with a history of CVD at baseline were excluded from analysis. Cox proportional hazards regression models were used to estimate the association of different levels of BMI stratification with CVD and allcause mortality. Results: During a mean follow-up of 8.1 years, 486 deaths were identified, including 233 cases of CVD death. The multivariable-adjusted hazards ratios for all-cause mortality associated with BMI levels ( 0.05 for all interactions). Regarding the association of BMI with CVD mortality, a U-shaped trend was also observed. Conclusions: The present study showed a U-shaped association of BMI with CVD and all-cause mortality among patients with hypertension. A lowest risk of all-cause mortality was found among hypertensive patients with BMI between 24 and 26 kg/m2.

Accumulating studies have suggested that epicardial adipose tissue (EAT) play an important role in the pathogenesis of atrial fibrillation (AF), but few have characterized the underlying mechanism between their interactions. Recent evidence suggested that bioactive molecules secreted from EAT, including exosomes carrying long non-coding RNAs (lncRNAs), may modulate atrial remodeling. LncRNAs are associated with cardiovascular disorders, including AF, but their roles in EAT remain elusive. The aim of the present study was to investigate the expression profile of lncRNAs in EAT with AF. Differentially expressed lncRNAs and nearby mRNAs interaction networks were constructed. Epicardial adipose samples were collected from patients with persistent non-valvular AF (n = 6) and sinus rhythm (SR) (n = 6), and the expression of lncRNAs and mRNAs were profiled using RNA-sequencing method. A total of 46,577 transcripts, including 35,552 protein-coding pattern, corresponding to 15,404 genes in EAT, among which, 655 mRNAs (265 upregulated and 390 downregulated) and 57 lncRNAs (17 upregulated and 40 downregulated) were differentially expressed between AF and SR (P 0.05; fold change1.5). GO enrichment, KEGG pathway analysis and interaction network construction showed that these differentially expressed lncRNAs were enriched in functional categories, including metabolism and stress response, which might contribute to the pathogenesis of AF. Our study demonstrated a differentially expressed lncRNA profile in EAT with AF, and provide a novel insight into the interactions between EAT and AF.

We have read enthusiastically and carefully the article authored by Atkins et al. [(1)][1] published in the Journal in June 2019. Based on their findings, the investigators concluded that despite the competing risk of cancer-specific death in these patients, cardiac radiation dose exposure is a

Given both smoking and vitamin D are associated with coronary heart disease (CHD) via inflammation and smoking may interfere with the local antiinflammatory effects of vitamin D. We hypothesized that the relationship between smoking and severity of CHD may be modified by vitamin D. A cross-sectional study was conducted. 25-OH vitamin D values were determined in 348 consecutive patients (mean age 62.4 ± 10.5 years; 56.3% male) undergoing coronary angiography at the Heart Center of Chaoyang Hospital affiliated to Capital Medical University between the period of September 2014 and May 2015. We categorized the patients into 2 groups based on 25-OH vitamin D levels, that is, severe hypovitaminosis D (25-OH vitamin D = 10 ng/mL). Multivariable logistic regression models were used to estimate odds ratios (ORs) of severe coronary stenosis or higher Gensini score across three smoking status, that is, never smokers, former smokers, and current smokers in severe hypovitaminosis D and higher vitamin D groups, respectively. Of these patients, we identified 212 (60.9%) cases of severe CHD and 161 (46.3%) cases of severe hypovitaminosis D. Multivariable logistic regression model showed the ORs of severe CHD were 1.94 (95% confidence interval [CI]: 0.47, 7.98) for former smokers and 2.62 (95% CI: 0.83, 8.24) for current smokers, compared with never smokers in group with severe hypovitaminosis D (P-trend = 0.005). In contrast, smoking was not found to be significantly associated with severe CHD in group with higher 25-OH vitamin D (P-trend = 0.115). We found a significant interaction between smoking status and vitamin D on presence of severe CHD (P-interaction = 0.015). In terms of Gensini score as a dependent variable, similar results were identified. Our finding indicated the association between smoking and severity of CHD appeared to be substantially stronger among patients with severe hypovitaminosis D as compared with those with higher vitamin D levels. This suggests vitamin D sufficiency may have a protective effect against the damaging effects of smoking on coronary artery. Future cohort studies are warranted to confirm this finding.

Given both lipoprotein (Lp)(a) and vitamin D have been found to be associated with coronary heart disease (CHD) risk and a biochemical link between vitamin D and cholesterol on atherosclerosis has been proposed, we hypothesised there could exist an interaction between Lp(a) and vitamin D on the severity of CHD.Lp(a) and 25-OH vitamin D were measured in the plasma of 348 consecutive patients (mean age 62.4±10.5 years; 56.3% male) undergoing coronary angiography at our Heart Center. A multivariate logistic regression model was used to estimate the odds ratios (ORs) of CHD.Of these patients, CHD was identified in 212 (60.9%). A multivariable logistic regression model showed multivariable-adjusted ORs (95% CI) of CHD for patients with Lp(a)≧30mg/dl and vitamin D10 ng/ml, Lp(a)30mg/dl and vitamin D10 ng/ml, and Lp(a)≧30mg/dl and vitamin D ≧10 ng/ml were 4.62 (2.04-10.46), 1.79 (1.00-3.17), and 1.70 (0.88-3.31), respectively, compared with those with Lp(a)30mg/dl and vitamin D ≧10 ng/ml; the multivariable-adjusted ORs of a higher Gensini Score for the above three corresponding groups were 3.48 (1.84-6.60), 1.59 (0.96-2.65), and 1.55 (0.86-2.79), respectively. The interaction term between Lp(a) and vitamin D in each of the above two models was significant (p=0.004 and p=0.005, respectively).Among patients undergoing coronary angiography, there existed an interaction between Lp(a) and vitamin D on the severity of CHD. Future cohort studies are warranted to confirm this finding.

Intensive atorvastatin may be beneficial for patients with ST segment elevated myocardial infarction (STEMI). However, its effects on endothelial and residual platelet function remain uninvestigated in these patients.This single-center single-blinded prospective randomized controlled trial included STEMI patients undergoing PCI, aiming to investigate the acute effects of intensive atorvastatin (40mg) vs. standard atorvastatin (20mg) on serum endothelin-1 (ET-1) and ADP-induced platelet clot strength (MA-ADP), which were measured before and after 7days of atorvastatin treatment respectively. MA-ADP was measured by thromboelastography. The tolerance and safety of intensive atorvastatin therapy in these patients were also observed.A total of 120 patients (60 patients in the intensive group and 60 patients in the standard group) with STEMI, who are undergoing primary PCI, were included into this study (mean age, 63.5years). Patients from these two groups were matched for baseline characteristics. Atorvastatin did not significantly affect the serum level of LDL-C or CRP in either the standard or intensive group. Furthermore, ET-1 did not significantly change following treatment with atorvastatin in the standard group. However, intensive treatment with atorvastatin significantly reduced ET-1 serum level (0.65±0.38pmol/L vs. 0.49±0.21pmol/L, P0.05) and achieved a greater reduction of MA-ADP (49.2±12.1 vs. 38.4±17.4mm, P0.05). In addition, although not statistically significant, patients assigned to the intensive group appeared to suffer from less major adverse cardiovascular events.Periprocedural intensive atorvastatin is associated with improved endothelial function and platelet inhibition, and is well-tolerated in STEMI patients undergoing PCI.

Cigarette smoking is the leading preventable cause of death worldwide. Few studies, however, have examined the modified effects of age on the association between smoking and all-cause mortality.In the current study, the authors estimated the association between smoking and age-specific mortality in adults from Beijing, China. This is a large community-based prospective cohort study comprising of 6209 Beijing adults (aged ≥40 years) studied for approximately 8 years (1991-1999). Hazard ratios (HRs) and attributable fractions associated with smoking were estimated by Cox proportional hazard models, adjusting for age, sex, alcohol intake, body mass index, systolic blood pressure, hypertension, and heart rate.The results showed, compared with nonsmokers, the multivariable-adjusted HRs for all-cause mortality were 2.7(95% confidence interval (CI):1.56-4.69) in young adult smokers (40-50 years) and 1.31 (95% CI: 1.13-1.52) in old smokers (>50 years); and the interaction term between smoking and age was significant (P = 0.026). Attributable fractions for all-cause mortality in young and old adults were 63% (95% CI: 41%-85%) and 24% (95% CI: 12%-36%), respectively. The authors estimated multivariate adjusted absolute risk (mortality) by Poisson regression and calculated risk differences and 95% CI by bootstrap estimation. Mortality differences (/10,000 person-years) were 15.99 (95% CI: 15.34-16.64) in the young and 74.61(68.57-80.65) in the old. Compared with current smokers, the HRs of all-cause deaths for former smokers in younger and older adults were 0.57 (95% CI: 0.23-1.42) and 0.96 (95% CI: 0.73-1.26), respectively.The results indicate smoking significantly increases the risks of all-cause mortality in both young and old Beijing adults from the relative and absolute risk perspectives. Smoking cessation could also reduce the excess risk of mortality caused by continuing smoking in younger adults compared with older individuals.