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To investigate the relationship between KCNN3 SNP (single-nucleotide polymorphism) rs13376333 and risk of atrial fibrillation (AF) and to provide evidence for prevention and treatment for AF.The PubMed, Embase, OVID, Cochrane library, CNKI, and Wan Fang databases were searched to identify studies on the relationship between KCNN3 SNP rs13376333 polymorphism and atrial fibrillation. Two authors performed independent article reviews and study quality assessment using the Newcastle-Ottawa Scale (NOS) checklist.Seven studies involving 24,339 individuals were included in the meta-analysis. The overall combined OR of rs13376333 polymorphism was observed for both lone AF (OR 1.58 [95%CI 1.37 to 1.82]; P less then 0.001; I(2) = 47.0%) and total AF (OR 1.33 [95%CI 1.14 to 1.54]; P less then 0.001; I(2) = 0). Further, when stratified by ethnicity, control sources, sample sizes, and genotyping method, similar results were observed in both subgroups. Sensitivity analysis revealed that the source of control was the source of the heterogeneity for lone AF. Omission of any single study had little effect on the combined risk estimate. No evidence of publication bias was found.This meta-analysis suggests that KCNN3 SNP rs13376333 polymorphism significantly increases the risk of lone AF and total AF, which suggests the rs13376333 polymorphism of the KCNN3 gene may play an important role in the pathogenesis of AF.Cell migration, proliferation, and differentiation of cardiac fibroblasts (CFs) play a central role in cardiac fibrosis. Factor Xa (FXa)-dependent protease-activated receptor (PAR)-1 and PAR-2 have been reported as important targets in proinflammatory and fibroproliferative diseases. From this viewpoint, we aimed to investigate whether treatment of rivaroxaban, an approved oral direct FXa inhibitor, attenuates functional changes in angiotensin (Ang) II-induced mouse CFs.Confluent cultured mouse CFs were pretreated with or without rivaroxaban. Ang II-induced cell migration was decreased by 73% in rivaroxaban induced cells. Rivaroxaban inhibited Ang II-induced cell proliferation by 27% at 0.01 μg/ mL, 69% at 0.1 μg/mL, 71% at 1 μg/mL, and 69% at 5 μg/mL. In mouse cytokine array measuring 40 cytokines, the productions of interleukin-16, TIMP-1, and tumor necrosis factor-α (TNF-α) were significantly reduced with 0.1 μg/mL of rivaroxaban pretreatment (all P less then 0.05). TIMP-1 levels in the culture supernatant measured by ELISA were also decreased by rivaroxaban pretreatment in Ang II-induced CFs (35% decrease at 0.01 μg/mL, 47% at 0.1 μg/mL, 47% at 1 μg/mL, and 57% at 5 μg/mL). In the dual reporter assay analysis, rivaroxaban inhibited various inflammatory signal pathways, including the nuclear factor-kappa B (NF-κB), active protein-1 (AP-1), and mitogen-activated protein kinase (MAPK) pathways (decreases of 82%, 78%, and 75%, respectively).These data suggest that rivaroxaban inhibits Ang II-induced functional activation in cultured mouse CFs via inhibiting NF-κB and MAPK/AP-1 signaling pathways, which may be a possible target of heart failure, through the antifibrotic and anti-inflammatory efficacy of rivaroxaban in Ang II-stimulated cardiac fibroblasts.Adaptive servo-ventilation (ASV) has been attracting attention as a novel respiratory support therapy for heart failure (HF). However, the acute hemodynamic effects have not been compared between ASV and continuous positive airway pressure (CPAP) in HF patients.We studied 12 consecutive patients with stable chronic HF. Hemodynamic measurement was performed by right heart catheterization before and after CPAP 5 cmH2O, CPAP 10 cmH2O, and ASV for 15 minutes each.Heart rate, blood pressure, pulmonary capillary wedge pressure (PCWP), and stroke volume index (SVI) were not changed by any intervention. Right atrial pressure significantly increased after CPAP 10 cmH2O (3.6 ± 3.3 to 6.7 ± 1.6 mmHg, P = 0.005) and ASV (4.1 ± 2.6 to 6.8 ± 1.5 mmHg, P = 0.026). Cardiac index was significantly decreased by CPAP 10 cmH2O (2.3 ± 0.4 to 1.9 ± 0.3 L/minute/m(2), P = 0.048), but was not changed by ASV (2.3 ± 0.4 to 2.0 ± 0.3 L/ minute/m(2), P = 0.299). There was a significant positive correlation between baseline PCWP and % of baseline SVI by CPAP 10 cmH2O (r = 0.705, P less then 0.001) and ASV (r = 0.750, P less then 0.001). ASV and CPAP 10 cmH2O had significantly greater slopes of this correlation than CPAP 5 cmH2O, suggesting that patients with higher PCWP had a greater increase in SVI by ASV and CPAP 10 cmH2O. The relationship between baseline PCWP and % of baseline SVI by ASV was shifted upwards compared to CPAP 10 cmH2O. Furthermore, based on the results of a questionnaire, patients accepted CPAP 5 cmH2O and ASV more favorably compared to CPAP 10 cmH2O.ASV had more beneficial effects on acute hemodynamics and acceptance than CPAP in HF patients.Tachyarrhythmias such as atrial fibrillation (AF) or atrial flutter (AFL) sometimes invoke life-threatening collapse of hemodynamics in patients with severe heart failure. Recently, landiolol, an ultra-short acting β1-selective antagonist, has been reported to be safe and useful for the treatment of supraventricular tachyarrhythmias with reduced left ventricular function. Here we report a case of advanced heart failure with severe hypotension who was treated successfully by landiolol for rapid AF. The patient was a 20-year old male with dilated cardiomyopathy. He presented with low output syndrome in spite of optimal medical therapy and was referred to our department to consider ventricular assist device implantation and heart transplantation. Soon after admission, he developed rapid atrial fibrillation at 180 beats per minute (bpm) followed by severe hypotension and liver enzyme elevation. Low dose landiolol at 2 μg/kg/minute was started because digoxin was not effective. After landiolol administration, his heart rate decreased to 110 bpm, and finally returned to sinus rhythm without hemodynamic deterioration. Intra-aortic balloon pumping was inserted soon after sinus recovery and he was discharged successfully with an implantable left ventricular assist device.The aim of this study was to provide a histopathological validation of cardiac late gadolinium enhancement (LGE) magnetic resonance imaging (MRI) for the assessment of left atrial (LA) substrate remodeling (SRM) in patients with rheumatic mitral valve disease and persistent atrial fibrillation (AF).Adult patients with rheumatic mitral valve disease and persistent AF undergoing open-heart surgery for mitral valve replacement were enrolled. Both two-dimensional (2D) sections and 3-dimensional (3D) full-volume LGE-MRI with different signal intensities were performed preoperatively to determine the extent of LA-SRM. Tissue samples were obtained intraoperatively from the LA roof and posterior lateral wall for pathological validation with Masson trichrome staining and immunostaining for collagen type I/III deposition. Ipatasertib concentration A linear regression model was used to determine the relationship between MRI-derived LA-SRM parameters and pathological results.Between February 2013 and March 2014, we successfully acquired LA tissue samples from 22 patients (13 men), with a mean age of 47 ± 8 years. All patients had rheumatic mitral valve stenosis, with a mean effective orifice area of 0.9 ± 0.2 cm(2) on echocardiography and a mean LA volume of 235 ± 85 mL on 3D-MRI. Multiple moderate linear associations were noted between the pathological results and LGE-MRI-derived LA-SRM parameters, with correlation indices (r(2)) of 0.194-0.385.LA-SRM measured by LGE-MRI showed moderate agreement with LA pathology in patients with rheumatic valve disease and persistent AF.Worsening of mitral regurgitation (MR) is sometimes observed after closure of an atrial septal defect (ASD). However, since the mechanism of this deterioration remains unclear, the aim of our study was to investigate the effect of left (LV) and right ventricular (RV) geometry on MR after transcatheter closure of ASD.We studied 27 patients with ASD who underwent transcatheter closure. Echocardiography was performed before and 6 ± 2 months after the procedure. In addition to conventional echocardiographic parameters, full volume data of the whole LV and RV heart was obtained with 3-dimensional echocardiography. MR was quantified by measuring the width of the vena contracta, and was graded as mild ( less then 3.0 mm), moderate (3.0 to 6.9 mm), or severe (≥ 7.0 mm).Ten patients (37%) were classified as having worsening MR and the remaining 17 (63%) as not having worsening MR. The two groups showed similar baseline characteristics, except for patients with worsening MR being more likely to be older (P = 0.009) and having a larger left-to-right shunt of pulmonary and systemic blood flow ratio (P = 0.02). It is noteworthy that the horizontal-to-vertical ratio of basal-RV at end-systole for patients with worsening MR was significantly smaller than that for patients without worsening MR (1.0 ± 0.2 versus 1.4 ± 0.2, P less then 0.0001). Furthermore, multivariate analysis showed that the horizontal-to-vertical ratio of basal-RV at end-systole was the independent predictor of worsening MR during follow-up (P less then 0.001).RV geometry may affect MR after closure of ASD. The pre-operative horizontal-to-vertical ratio of basal-RV is considered useful for predicting worsening of MR after closure of ASD.Autonomic dysfunction has been associated with paroxysmal atrial fibrillation (PAF). The head-up tilt test (HUTT) is an important diagnostic tool for autonomic dysfunction. The aim of this study was to examine atrial fibrillation recurrence after RFCA by performing HUTT. A total of 488 consecutive patients with PAF who underwent RFCA were prospectively enrolled. HUTT was positive in 154 (31.6%) patients after a mean follow-up of 22.7 ± 3.5 months, and 163 (33.4%) had a recurrence. HUTT positive was significantly higher in PAF patients with recurrence compared to those without (68 (41.7%) versus 86 (26.5%), P less then 0.001). Multivariate Cox regression analysis revealed that HUTT positive (HR 1.96; 95% CI 1.49-2.48, P less then 0.001), left atrial diameter (HR 1.77; 95%CI 1.15-2.11, P = 0.004), AF duration (HR 1.27; 95%CI 0.98-1.83, P = 0.014), and sleep apnea (HR 1.02; 95%CI 0.81-1.53, P = 0.032) were independent predictors of clinical recurrence after RFCA. The success rate of ablation was 70.4% in patients in the HUTT negative group compared with 58.4% in patients in the HUTT positive group (log-rank P = 0.006). Patients with a positive headup tilt test were at an increased risk of AF recurrence after catheter ablation. Our results suggest that HUTT was a significant predictor for AF recurrence after catheter ablation for PAF.Cardiac resynchronization therapy (CRT) reverses structural remodeling of the left ventricle. We investigated whether CRT reverses left-ventricular electrical remodeling.Eighty patients were enrolled and implanted with CRT-devices. Echocardiography and electrocardiography data were obtained from each patient prior to implantation and two years after implantation. At two years after implantation, the patients were classified into a responder group and a non-responder group based on echocardiography.Over the next 2 years, 75 patients completed follow-up, and 5 patients had died. Echocardiography results showed that 23 patients could be classified as non-responders and 52 as responders. Larger numbers of non-responders were diagnosed with either ischemic cardiomyopathy (ICM) or nonspecific intraventricular conduction delay (NICD). The intrinsic QRS duration was not changed in responders, patients with dilated cardiomyopathy, or in the patient categories of male and female. However, the intrinsic QRS duration was significantly prolonged in non-responders and patients with ischemic cardiomyopathy (P = 0.
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