Sacubitril/Valsartan Can Reduce Atrial Fibrillation Recurrence After Catheter Ablation in Patients with Persistent Atrial Fibrillation.

PURPOSE: This study compared the effectiveness of sacubitril/valsartan (SV) vs. valsartan (V) for treating persistent atrial fibrillation (AF) after radio-frequency catheter ablation (RFCA). METHODS: Patients with persistent AF who received RFCA were randomly assigned to the SV or V treatment group with the intervention lasting for 12 months. The primary outcome included any atrial arrhythmia episode lasting ≥ 30 s after a 3-month blanking period. The secondary outcome included any atrial arrhythmia episode lasting ≥ 24 h or requiring cardioversion after a 3-month blanking period. The H2FPEF score was used to assess the possibility of patients suffering from heart failure with preserved ejection fraction. RESULTS: A total of 143 patients with persistent AF who received RFCA were randomized for the study, with 5 patients failing to follow-up. Among them, 29 (42%) out of 69 patients receiving V and 15 (21.7%) out of 69 patients receiving SV reached the primary endpoint (P < 0.001). A total of 26 (37.7%) out of 69 patients receiving V and 7 (10.1%) out of 69 patients receiving SV reached the secondary endpoint (P < 0.001). A decrease in the H2FPEF score after a 1-year follow-up seemed to be related to the recurrence of AF (OR, 0.065; 95% CI: 0.018-0.238, P < 0.001). CONCLUSIONS: SV can decrease AF recurrence after catheter ablation in patients with persistent AF at the 1-year follow-up. The mechanism for this process may be related to the reduction in the H2FPEF score in patients with preserved ejection fraction heart failure.

Thymoquinone ameliorates pressure overload-induced cardiac hypertrophy by activating the AMPK signalling pathway.

Prolonged pathological myocardial hypertrophy leads to end-stage heart failure. Thymoquinone (TQ), a bioactive component extracted from Nigella sativa seeds, is extensively used in ethnomedicine to treat a broad spectrum of disorders. However, it remains unclear whether TQ protects the heart from pathological hypertrophy. This study was conducted to examine the potential utility of TQ for treatment of pathological cardiac hypertrophy and if so, to elucidate the underlying mechanisms. Male C57BL/6J mice underwent either transverse aortic constriction (TAC) or sham operation, followed by TQ treatment for six consecutive weeks. In vitro experiments consisted of neonatal rat cardiomyocytes (NRCMs) that were exposed to phenylephrine (PE) stimulation to induce cardiomyocyte hypertrophy. In this study, we observed that systemic administration of TQ preserved cardiac contractile function, and alleviated cardiac hypertrophy, fibrosis and oxidative stress in TAC-challenged mice. The in vitro experiments showed that TQ treatment attenuated the PE-induced hypertrophic response in NRCMs. Mechanistical experiments showed that supplementation of TQ induced reactivation of the AMP-activated protein kinase (AMPK) with concomitant inhibition of ERK 1/2, p38 and JNK1/2 MAPK cascades. Furthermore, we demonstrated that compound C, an AMPK inhibitor, abolished the protective effects of TQ in in vivo and in vitro experiments. Altogether, our study disclosed that TQ provides protection against myocardial hypertrophy in an AMPK-dependent manner and identified it as a promising agent for the treatment of myocardial hypertrophy.

The causal relationship between sleep traits and the risk of schizophrenia: a two-sample bidirectional Mendelian randomization study.

BACKGROUND: Observational studies suggest that sleep disturbances are commonly associated with schizophrenia. However, it is uncertain whether this relationship is causal. To investigate the bidirectional causal relation between sleep traits and schizophrenia, we performed a two-sample bidirectional Mendelian randomization (MR) study with the fixed effects inverse-variance weighted (IVW) method. METHODS: As genetic variants for sleep traits, we selected variants from each meta-analysis of genome-wide association studies (GWASs) conducted using data from the UK Biobank (UKB). RESULTS: We found that morning diurnal preference was associated with a lower risk of schizophrenia, while long sleep duration and daytime napping were associated with a higher risk of schizophrenia. Multivariable MR analysis also showed that sleep duration was associated with a higher risk of schizophrenia after adjusting for other sleep traits. Furthermore, genetically predicted schizophrenia was negatively associated with morning diurnal preference and short sleep duration and was positively associated with daytime napping and long sleep duration. CONCLUSIONS: Therefore, sleep traits were identified as a potential treatment target for patients with schizophrenia.

High-Normal Thyroid Function and Recurrence of Atrial Fibrillation after Catheter Ablation: A Prospective Observational Study.

BACKGROUND: Thyroid function is increasingly recognized as an important modifiable factor for atrial fibrillation (AF); however, it is unclear if the changes in thyroid hormones, even within the normal range, are associated with AF recurrence after catheter ablation. METHODS: Consecutive paroxysmal AF patients who underwent catheter ablation were enrolled. Patients with abnormal thyroid hormones or previous thyroid illnesses were excluded. Patients were followed for 12 months or until they presented with the first episode of atrial tachyarrhythmia after a blanking period. RESULTS: The study included 448 patients with a mean age of 61 (14) years, and 46% were women. After a 1-year follow-up, 104 (23.2%) patients experienced atrial tachyarrhythmia recurrences after an ablation procedure. Recurrence was significantly different among quartile groups of thyroid function, with highest FT4 and FT3 levels associated with the greatest risk of recurrence (p < 0.001 and p = 0.024, respectively). FT4 and FT3 levels were independent predictors of atrial tachyarrhythmia recurrence (hazard ratio 1.07 per 1 pmol/L increase in FT4, 95% confidence interval [CI] 1.01-1.15, p = 0.036 and 1.31 per 1 pmol/L increase in FT3, 95% CI 1.01-1.71, p = 0.032). CONCLUSIONS: High-normal FT3 and FT4 levels are associated with AF recurrence after catheter ablation in this Chinese population. Attention to thyroid hormones could be valuable to assist in the management of AF.

The Association Between Ambient Air Pollution and Atrial Fibrillation.

Atrial fibrillation (AF) is the most common cardiac arrhythmia; it has been known to increase the risk of stroke and heart failure. The association between air pollutants and AF has remained to be controversial. Thus, in this study, we sought to undertake a systematic review and meta-analysis in order to assess the short- and long-term effects of ambient air pollution on AF.We searched PubMed, Web of Science, Embase, and Ovid for all related studies up to October 2019. We used the random-effects model to estimate the excess risk percentage (ER%) and confidence intervals (CI) for particulate matter with diameter ≤ 2.5 (PM2.5) and ≤ 10 µm (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), ozone (O3), and carbon monoxide (CO). Results were further analyzed by subgroups according to location, age, outcome, and gender.In total, 18 studies were included in our meta-analysis: 5 evaluated for long-term effects, 12 for short-term effects, and 1 for both long- and short-term effects. For the short term, ER per 10 µg/m3 increase of pollutants was 1.8% (0%-3.7%) for PM2.5 and 1.1% (-0.2%-2.4%) for PM10; per 10 parts per billion (ppb) increment of gaseous pollutions was 3.2% (0.6%-5.8%) for NO2, 2.9% (0.3%-5.7%) for SO2, 0.5% (-3.4%-4.7%) for O3, and 2.0% (-1.3%-5.4%) for CO per 1000 ppb change. The subgroup analysis showed the short-term effect was significantly different by region, gender, outcome, and age. Meanwhile, in the long term, except for O3, a statistically significant association was noted between AF incidence and all pollutants.Our meta-analysis suggests that short-term exposure to part of pollutants (PM2.5, SO2, and NO2) increases AF attack. Further, long-term exposure to air pollution can significantly contribute to the incidence of AF in a healthy population.

The Effect of Renin-Angiotensin System Inhibitors on the Recurrence of Atrial Fibrillation After Catheter Ablation.

Atrial fibrillation (AF) is the most common sustained arrhythmia. Renin-angiotensin system (RAS) inhibitors were reported to modify the arrhythmia substrate and reverse atrial remodeling. However, the role of RAS inhibitors on AF recurrence after catheter ablation remains much more controversial. In this study, a meta-analysis was performed to explore the effect of RAS inhibitors on AF recurrence after catheter ablation.We searched PubMed, Cochrane Library, EMBASE, and Web of Science for all articles published up to July 2019 on the effect of RAS inhibitors on AF recurrence rate after ablation. We used the random-effects model to estimate the odds ratios (ORs) and confidence intervals (CI). The I2 statistic was used to evaluate statistical heterogeneity. A two-tailed P value of <0.05 was considered statistically significant. Results were further analyzed by subgroup according to the type of study design.We included 13 studies, including 3661 patients with AF, in this analysis, of which 4 were randomized controlled trials (RCTs) and the others were cohort studies. Overall, treatment with RAS inhibitors showed a significant reduction of AF recurrence after catheter ablation (OR, 0.61; 95% CI, 0.45-0.82). Additionally, both the RCT (OR, 0.35; 95% CI, 0.24-0.49) and non-RCT (OR, 0.76; 95% CI, 0.57-1.00) groups demonstrated that RAS inhibitors could reduce the AF recurrence rate after catheter ablation in the subgroup analysis.Our meta-analysis suggests that RAS inhibitors had significant benefit in reducing the recurrence rate of AF after catheter ablation.

U-Shaped Relationship Between Left Atrium Size on Echocardiography and 1-Year Recurrence of Atrial Fibrillation After Radiofrequency Catheter Ablation　- Prognostic Value Study.

BACKGROUND: The larger the left atrium anteroposterior dimension (LAD) and left atrium volume (LAV), the stronger the association with recurrent atrial fibrillation (AF) after radiofrequency catheter ablation (RFCA). Patients with a smaller left atrium (LA) size, however, also have increased AF recurrence.Methods and Results:In 521 patients, routine 48-h Holter electrocardiogram and echocardiography were obtained at each outpatient visit every 3 months for 12 months. On multivariate analysis, AF type, LAD, and LAV calculated using the ellipsoid model/body surface area (LAVe/BSA) were independent predictors of AF recurrence. Patients were divided into 7 groups at 0.4-cm increments of LAD: ≤3 cm, LAD≤3 cm, 3.05.0 cm. Compared with the 3.4-3.8-cm group, the adjusted HR were 3.88 (95% CI: 2.02-7.46, P<0.001), 1.03 (95% CI: 0.50-2.12, P=0.939), 0.96 (95% CI: 0.52-1.77, P=0.901), 1.36 (95% CI: 0.72-2.57, P=0.347), 3.04 (95% CI: 1.67-5.53, P<0.001), and 4.07 (95% CI: 1.93-8.60, P<0.001), respectively. Similarly, we divided LAVe/BSA into 8 groups and also observed a U-shaped curve for AF recurrence. CONCLUSIONS: Both larger and smaller LAD and LAVe/BSA were associated with a higher risk of AF recurrence 1 year after RFCA. The association of LA size and AF recurrence after RFCA is represented by a U-shaped curve.

Gramine protects against pressure overload-induced pathological cardiac hypertrophy through Runx1-TGFBR1 signaling.

BACKGROUND: Gramine, also named 3-(N,N-dimethylaminomethyl) indole, is a indole alkaloid. It is mainly extracted from various natural raw plants. Despite being the simplest 3-aminomethylindole, Gramine has broad pharmaceutical and therapeutic effects, such as vasodilatation, antioxidation, mitochondrial bioenergetics-related effects, and angiogenesis via modulation of TGFß signaling. However, there is little information available about Gramine's role in heart disease, especially pathological cardiac hypertrophy. PURPOSE: To investigate Gramine's effect on pathological cardiac hypertrophy and clarify the mechanisms behind its action. METHODS: In the in vitro experiment, Gramine (25 µM or 50 µM) was used to investigate its role in Angiotensin II-induced primary neonatal rat cardiomyocytes (NRCMs) hypertrophy. In the in vivo experiment, Gramine (50 mg/kg or 100 mg/kg) was administrated to investigate its role in transverse aortic constriction (TAC) surgery mice. Additionally, we explored the mechanisms underlying these roles through Western blot, Real-time PCR, genome-wide transcriptomic analysis, chromatin immunoprecipitation and molecular docking studies. RESULTS: The in vitro data demonstrated that Gramine treatment obviously improved primary cardiomyocyte hypertrophy induced by Angiotensin II, but had few effects on the activation of fibroblasts. The in vivo experiments indicated that Gramine significantly mitigated TAC-induced myocardial hypertrophy, interstitial fibrosis and cardiac dysfunction. Mechanistically, RNA sequencing and further bioinformatics analysis demonstrated that transforming growth factor ß (TGFß)-related signaling pathway was enriched significantly and preferentially in Gramine-treated mice as opposed to vehicle-treated mice during pathological cardiac hypertrophy. Moreover, this cardio-protection of Gramine was found to mainly involved in TGFß receptor 1 (TGFBR1)- TGFß activated kinase 1 (TAK1)-p38 MAPK signal cascade. Further exploration showed that Gramine restrained the up-regulation of TGFBR1 by binding to Runt-related transcription factor 1 (Runx1), thereby alleviating pathological cardiac hypertrophy. CONCLUSION: Our findings provided a substantial body of evidence that Gramine possessed a potential druggability in pathological cardiac hypertrophy via suppressing the TGFBR1-TAK1-p38 MAPK signaling axis through interaction with transcription factor Runx1.

Association of age at first sexual intercourse and lifetime number of sexual partners with cardiovascular diseases: a bi-directional Mendelian randomization study.

Background: Limited studies have explored the association between sexual factors [age at first sexual intercourse (AFS) and lifetime number of sexual partners (LNSP)] and cardiovascular diseases (CVDs), leaving the causality inconclusive. Methods: We performed a bi-directional Mendelian randomization (MR) study to investigate the causality between sexual factors and CVDs, including coronary artery disease, myocardial infarction, atrial fibrillation (AF), heart failure (HF), and ischemic stroke (IS). Single-nucleotide polymorphisms (SNPs) for sexual factors were extracted from the UK Biobank. Statistics for each CVD were derived from two different databases. MR estimates were calculated per outcome database and were combined through meta-analysis. Several complementary sensitivity analyses were also performed. Results: The primary analysis suggested that AFS was causally associated with the risk of CVDs; the odds ratios (ORs) ranged from 0.686 [95% confidence interval (CI), 0.611-0.770] for HF to 0.798 (95% CI, 0.719-0.886) for AF. However, the association between AFS and IS (OR, 0.844; 95% CI, 0.632-1.126) was not consistent in the meta-analysis after excluding SNPs related to confounders. Moreover, non-significant associations were found between LNSP and CVDs. Reverse direction MR analysis showed that CVDs were not associated with sexual factors. Conclusions: Genetic evidence suggested that AFS was causally associated with the risk of CVDs except for IS, whereas non-significant association of LNSP with CVDs was detected. Further investigation into AFS could be warranted in preventing the progression of CVDs.

Assessing Causal Associations of Atopic Dermatitis With Heart Failure and Other Cardiovascular Outcomes: A Mendelian Randomization Study.

Background and Aims: Observational epidemiological studies have suggested that atopic dermatitis (AD) was associated with an increased risk of cardiovascular diseases (CVDs). However, causality remains to be established. In the present study, Mendelian randomization (MR) analyses were used to evaluate whether AD and CVDs are causally associated. Methods: This study was based on summary statistics of genome-wide association studies (GWASs) for a set of cardiovascular outcomes including heart failure (HF), coronary artery disease (CAD), myocardial infarction (MI), atrial fibrillation (AF), stroke, and stroke subtypes. A total of 19 independent single nucleotide polymorphisms associated with AD were identified at a genome-wide significance threshold (P < 5 × 10-8) based on a large GWAS meta-analysis. MR estimates were pooled using the inverse variance weighted method. Complementary analyses further evaluated the robustness of the results. Results: Genetically determined AD was causally associated with HF [odds ratio (OR), 1.07; 95% confidence interval (CI), 1.03-1.10; P = 1.11 × 10-4]. However, there was no causal association between AD and the risk of AF, CAD, MI, stroke, and stroke subtypes. Complementary analyses returned similar results. No horizontal pleiotropy was found. Conclusion: This MR study provided evidence to support that AD exerted an effect contributing to HF. No significant associations were found for other cardiovascular outcomes. The study suggested that prevention and early diagnosis of AD may help prevent HF. Improved awareness of these associations is warranted for better management of CVDs in the future.

Cardiac Troponin I and Risk of Stroke: A Mendelian Randomization Study.

PURPOSE: Cardiac troponin I (cTnI) is a well-established biomarker for stroke prediction, especially in patients with heart diseases. However, the causal effect of circulating cTnI on stroke remains unclear. METHODS: We employed Mendelian Randomization (MR) analysis to determine the associations between genetically predicted circulating cTnI levels and stroke and its subtypes. Summary-level data for exposure and outcomes were generated from different genome-wide association studies. Single-nucleotide polymorphisms (SNPs) associated with circulating cTnI at genome-wide significance level (P < 5 × 10-8) were employed as instrumental variables (IVs). We used fixed-effect inverse-variance weighted (IVW) as the main method for pooling MR estimates. Sensitivity analyses and multivariable MR analyses were carried out to assess the robustness of the results. RESULTS: Using the fixed-effects IVW method, we found that genetically elevated plasma cTnI levels may have a causal effect on the risk of cardioembolic stroke (CES) (odds ratio (OR), 1.58; 95% confidence interval (CI), 1.17-2.13; P = 0.003). Additional analyses including multiplicative random-effects (mre) IVW, weighted median, MR-Egger and MR-PRESSO yielded similar results, but with broader CIs that span 1.0. The total effect of cTnI on CES was attenuated by adjusting for the effect of atrial fibrillation (OR,1.26; 95% CI, 0.76-2.11; P = 0.371) and smoking (OR,1.53; 95% CI, 0.87-2.66; P = 0.137). In addition, we found no causal effect of cTnI on the risk of any stroke and other stroke subtypes, including any ischemic stroke, large artery stroke, cardioembolic stroke, small vessel stroke, and intracerebral hemorrhage. These results were consistent across sensitivity analyses. CONCLUSION: This study provides little evidence that increased serum cTnI levels lead to a higher risk of stroke.

Assessment of causal associations between handgrip strength and cardiovascular diseases: A two sample mendelian randomization study.

Background: Several observational studies have identified that handgrip strength was inversely associated with cardiovascular diseases (CVDs). Nevertheless, causality remains controversial. We conducted Mendelian randomization (MR) analysis to examine whether handgrip strength and risk of CVDs are causally associated. Methods: We identified 160 independent single nucleotide polymorphisms (SNPs) for right-hand grip strength and 136 independent SNPs for left-hand grip strength at the genome-wide significant threshold (P < 5 × 10-8) from UK Biobank participants and evaluated these in relation to risk of CVDs. MR estimates was calculated using the inverse-variance weighted (IVW) method and multiple sensitivity analysis was further conducted. Results: Genetical liability to handgrip strength was significantly associated with coronary artery disease (CAD) and myocardial infarction (MI), but not stroke, hypertension, or heart failure. Additionally, there was significant association between right-hand grip strength and atrial fibrillation (OR, 0.967; 95% CI, 0.950-0.984; p = 0.000222), however, suggestive significance was found between left-hand grip strength and atrial fibrillation (OR, 0.977; 95% CI, 0.957-0.998; p = 0.033). Results were similar in several sensitivity analysis. Conclusion: Our study provides support at the genetic level that handgrip strength is negatively associated with the risk of CAD, MI, and atrial fibrillation. Specific handgrip strength interventions on CVDs warrant exploration as potential CVDs prevention measures.

Cannabis Use and the Risk of Cardiovascular Diseases: A Mendelian Randomization Study.

Several observational studies have shown that cannabis use has negative effects on the cardiovascular system, but the causality of this relationship has not been confirmed. The aim of the current study was to estimate the effects of genetically determined cannabis use on risk of cardiovascular diseases. Ten single-nucleotide polymorphisms related to cannabis use were employed as instruments to estimate the association between genetically determined cannabis use and risk of cardiovascular diseases using a two-sample Mendelian randomization (MR) method. Summary statistics data on exposure and outcomes were obtained from different genome-wide association meta-analysis studies. The results of this MR analysis showed no causal effects of cannabis use on the risk of several common cardiovascular diseases, including coronary artery disease, myocardial infarction, stroke and ischemic stroke subtypes, atrial fibrillation (AF), and heart failure. Various sensitivity analyses yielded similar results, and no heterogeneity and directional pleiotropy were observed. After adjusting for tobacco use and body mass index, multivariable MR analysis suggested a causal effect of cannabis use on small vessel stroke (SVS) [odds ratio (OR) 1.17; 95% CI 1.02-1.35; p = 0.03] and AF (OR 1.06; 95% CI 1.01-1.10; p = 0.01), respectively. This two-sample MR study did not demonstrate a causal effect of genetic predisposition to cannabis use on several common cardiovascular outcomes. After adjusting for tobacco use and body mass index, the multivariable MR analysis suggested a detrimental effect of cannabis use on the risk of SVS and AF, respectively.

Physical Activity and Risks of Cardiovascular Diseases: A Mendelian Randomization Study.

Background: Although some observational studies have shown that physical activity may have a positive relationship with cardiovascular diseases, the causal effect remains uncertain. We conducted a Mendelian randomization (MR) study to identify the potential causal effect between physical activity and cardiovascular diseases. Methods: Summary statistics of genome-wide association studies on four physical activity phenotypes and cardiovascular diseases were utilized. MR analysis was performed using inverse-variance weighted (IVW) and multivariable MR. Multiple sensitivity analysis was further conducted to identify the robustness of our results. Results: Genetically predicted self-reported vigorous physical activity (VPA) was significantly associated with lower risk of myocardial infarction (IVW OR: 0.24, 95% CI: 0.08-0.68, p-value: 0.007). Additionally, the causal effect of VPA with myocardial infarction was robust after adjusting for several cardiovascular risk factors through using the multivariable MR. There were no apparent causal associations between physical activity with other cardiovascular diseases. Results were consistent with the sensitivity analysis. Conclusion: The present study supports a protective role of self-reported vigorous physical activity in the initiation of myocardial infarction and highlights the importance of activity levels of physical activity. Further studies are required to elucidate the potential biological pathways of physical activity with cardiovascular diseases.

Association of Sleep Duration With Atrial Fibrillation and Heart Failure: A Mendelian Randomization Analysis.

Both short (<7 h per night) and long (≥9 h per night) sleep durations are related to atrial fibrillation (AF) and heart failure (HF), but their causality has not been confirmed. We applied Mendelian randomization (MR) approaches to estimate the causal association between genetically determined sleep duration and the risk of AF and HF. We performed two-sample MR analysis to obtain the effect of sleep duration on AF and HF. Instrumental variables were constructed using genetic variants known to be associated with continuous sleep duration, short sleep duration, and long sleep duration. MR estimates of the effect of sleep duration on AF and HF were derived based on two large meta-analyses of genome-wide association studies. The pooled MR estimate demonstrated a significant protective effect of continuous sleep duration on HF [odds ratio (OR) = 0.765, 95% confidence interval (CI) = 0.675-0.867; P = 2.64 × 10-5] and a suggestive inverse association of continuous sleep duration with AF (OR = 0.893, 95% CI = 0.804-0.991; P = 0.034). In addition, the results showed a suggestive detrimental effect of short sleep duration on the risk of AF (OR = 1.108, 95% CI = 1.017-1.207; P = 0.019) and HF (OR = 1.136, 95% CI = 1.025-1.258; P = 0.015). Conversely, there is no significant evidence for the causal protective effect of long sleep duration on AF (OR = 0.956, P = 0.410) and HF (OR = 0.921, P = 0.202). This MR study indicated that genetically determined continuous sleep duration has a significant protective effect on HF and a suggestive inverse association with AF. Short sleep duration is positively associated with the risk of AF and HF. Nevertheless, there is no significant evidence for the causal protective effect of long sleep duration on AF and HF. Larger intervention studies are required to confirm the effectiveness of improving sleep on reducing the incidence of AF and HF.

Blood lipid levels and recurrence of atrial fibrillation after radiofrequency catheter ablation: a prospective study.

PURPOSE: The relation between dyslipidemia and atrial fibrillation (AF) development remains controversial. We conducted a prospective study to investigate the association of lipids with the risk of recurrence of AF after radiofrequency catheter ablation (RFCA). METHODS: This study enrolled 287 consecutive patients who underwent initial circumferential pulmonary vein ablation (CPVA). Fasting levels of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG) were measured at baseline before ablation. Patients were classified according to lipid quartiles. AF recurrence was confirmed by 48-h electrocardiograms at follow-up visits. RESULTS: A total of 71 patients (24.7%) experienced AF recurrence during 3 to 12 months after ablation. By univariate Cox regression survival analysis, TC (HR, 0.63; 95%CI, 0.48-0.82), LDL-C (HR, 0.61; 95%CI, 0.44-0.84), non-paroxysmal AF type (HR, 2.56; 95%CI, 1.52-4.21), and left atrial diameter (HR, 2.18; 95%CI, 1.46-3.24) were significantly associated with AF recurrence. By multivariate Cox regression survival analysis, lower quartiles of TC (HR, 3.66; 95%CI, 1.56-8.56) and LDL-C (HR, 2.28; 95%CI 1.09-4.77) were associated with higher risk of AF recurrence compared with the highest quartiles. After adjustment by sex, lower TC (HR, 11.70; 95%CI, 2.79-49.13) and LDL-C (HR, 11.00; 95%CI, 2.77-43.72) levels were associated with the recurrence of AF in women, but not in men. HDL-C and TG levels showed no association with AF recurrence in both genders. CONCLUSIONS: TC and LDL-C levels were negatively correlated with AF recurrence after RFCA in women. HDL-C and TG were not independently associated with AF recurrence in both genders.

CHA2DS2-VASc and SAMe-TT2R2 scores as predictors of recurrence for nonvalvular atrial fibrillation patients on vitamin K antagonists after radiofrequency catheter ablation.

AIMS: Atrial fibrillation is the most common sustained arrhythmia in the general population, and circumferential pulmonary vein isolation has emerged as a cornerstone in the treatment of drug-resistant atrial fibrillation. However, there is a paucity of data regarding the CHA2DS2-VASc and SAMe-TT2R2 scores as predictors of outcomes among patients with nonvalvular atrial fibrillation on vitamin K antagonists after radiofrequency catheter ablation (RFCA). METHODS: The current prospective observational study enrolled 304 consecutive patients with atrial fibrillation who underwent RFCA. Warfarin was maintained for at least 3 months after RFCA. The 1-year atrial fibrillation recurrence rate was documented. RESULTS: Persistent atrial fibrillation (P = 0.003), heart failure (P < 0.001), an enlarged left atrium (P = 0.003), current smoking (P < 0.001), the CHA2DS2-VASc score (P = 0.001), and the SAMe-TT2R2 score (P < 0.001) were univariate associated with recurrent atrial fibrillation. Cutoff analysis showed that a CHA2DS2-VASc score at least 3 (areas under the curve = 0.612; 95% confidence interval 0.537-0.687) and a SAMe-TT2R2 score at least 5 (areas under the curve = 0.642, 95% confidence interval 0.575-0.708) had the highest predictive value for atrial fibrillation recurrence. Patients with a CHA2DS2-VASc score at least 3 (P < 0.001) and a SAMe-TT2R2 score at least 5 (P = 0.001) had a higher probability of experiencing atrial fibrillation recurrence after RFCA compared with patients with a CHA2DS2-VASc score less than 3 and a SAMe-TT2R2 score less than 5. CONCLUSION: CHA2DS2-VASc and SAMe-TT2R2 scores were associated with 1-year recurrence of atrial fibrillation in patients on vitamin K antagonists after RFCA. For CHA2DS2-VASc and SAMe-TT2R2 scores, a cutoff value of at least 3 and at least 5 had the highest predictive value for atrial fibrillation recurrence, respectively.

Investigation of proper home blood pressure with atrial fibrillation recurrence in patients undergoing radiofrequency catheter ablation.

BACKGROUND: Hypertension is an important target for interventions to improve ablation outcome in atrial fibrillation (AF) patients. No studies to date have determined the blood pressure level at which AF is less likely to recur in patients without hypertension. METHODS: A total of 503 AF patients undergoing radiofrequency catheter ablation (RFCA) (mean age, 59.6±9.6 years; 319 males [63.4%]) were identified for the study cohort and analysis. Patients received a pocket diary to record their home blood pressure (HBP) before RFCA and routine 48-hour Holter-ECGs to evaluate AF recurrence after RFCA. RESULTS: A total of 383 (76.1%) patients were free of AF recurrence one year after RFCA. Blood pressure (BP), including systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), and pulse pressure (PP), had different effects on AF recurrence one year after RFCA. A χ2 test showed that when SBP was <110 mmHg, it was associated with a lower AF recurrence in patients with hypertension (P=0.029). AF recurrence decreased (P=0.002) when SBP increased from <110 mmHg to >130 mmHg in patients without hypertension. Regression analysis indicated a significant linear correlation between BP and LAD in all patients. CONCLUSIONS: SBP should be strictly maintained at 110 mmHg after RFCA to minimize AF recurrence in patients with hypertension. Low SBP might be a risk factor for AF recurrence among patients without hypertension.