[Analysis of risk factors of ventricular arrhythmia in patients with Brugada syndrome].

Objective: To investigate the risk factors of ventricular arrhythmias in patients with Brugada syndrome. Methods: Clinical data of 60 Brugada syndrome patients admitted in the department of cardiology of the First Affiliated Hospital of Nanjing Medical University from March 2003 to December 2016 were collected and retrospectively analyzed. The age at diagnosis was (43.2±13.1) years (0.6-83.0 years), 98.3% were males (n=59), and the patients were followed up to (92±41) months (12-169 months). The 12-lead surface electrocardiogram (ECG) recorded at the time of diagnosis and showing the highest type 1 ST elevation, either spontaneously or after provocative drug test, was used for the analysis. Patients were divided into ventricular arrhythmia (VA, n=12) group and non-ventricular arrhythmia (non-VA, n=48) group depending on the presence or absence of clinical VA event. The demographic data and ECG data of the 2 groups were compared, and the independent risk factors of VA events were analyzed by stepwise logistic regression. Results: Incidence of family history of sudden death (7/12 vs. 22.9% (11/48)) and percentage of type 1 ST elevation in the peripheral ECG leads (6/12 vs. 16.67% (8/48)) were significantly higher in VA group than in non-VA group (both P<0.05). Max Tpeak-Tend (Max-Tpe) interval ((144±53)ms vs. (110±16)ms) and dispersion of Tpe ((74±50)ms vs. (43±17)ms) were significantly higher in VA group than in non-VA group (both P<0.05). The area under receiver operating characteristic (ROC) curves for the Max-Tpe interval was 0.693 and Max-Tpe interval ≥140 ms was determined as an optimized cutoff point with increased risk of VA event, which had a sensitivity of 50.0%, a specificity of 98.0%, a positive predictive value of 85.7%, and a negative predictive value of 88.7% for predicting VA event. The ROC curves for the dispersion of Tpe was 0.775 and dispersion of Tpe ≥45 ms was determined as an optimized cutoff point for predicting VA event, which had a sensitivity of 91.7%, a specificity of 64.6%, a positive predictive value of 39.3%, and a negative predictive value of 96.9% for predicting VA event. In multivariate analysis, Max-Tpe interval ≥140 ms (OR=27.53, 95%CI 1.07-706.77, P=0.045) and family history of sudden death (OR=24.63, 95%CI 2.05-295.38, P=0.011) were found to be the independent risk factors of arrhythmic events. Conclusions: Max-Tpe interval ≥140 ms and family history of sudden death are risk factors of VA event in included patients with Brugada syndrome.

[Efficacy of biventricular pacing on preventing heart failure in patients with high degree atrioventricular block (BIVPACE-AVB Trial)].

OBJECTIVE: To investigate the long-term effect of biventricular (BIV) and right ventricular apical (RVA) pacing on cardiac function in patients with high-degree atrioventricular block (AVB) and left ventricular ejection fraction(LVEF)over 35%. METHODS: A total of 118 consecutive patients with high-degree AVB in six hospitals from East China between May 2009 and December 2012 were enrolled in this randomized, double-blind and parallel controlled study. Patients were randomly assigned to BIV and RVA pacing with or without LV lead on after one-week cardiac resynchronization therapy (CRT). Cardiac function including New York Heart Association(NYHA), 6 minute walking distance (6MWD), Minnesota living with heart failure (MLHF) score, LVEF, left ventricular end-diastolic volumes/diameters (LVEDV/LVEDD) and other echocardiography parameters, as well as N-terminal pro-B-type natriuretic peptide (NT-proBNP)were assessed at 6 months and 12 months. RESULTS: A total of 114 patients were successfully implanted with CRT. Cardiac function was significantly improved after one-week BIV pacing (n=57) compared with pre-CRT: rate of patients with NYHA Ⅲ (25.44%(29/114) vs. 9.65%(11/114)), MLHF score (17.1±13.6 vs. 26.9±21.6), 6MWD ((315.4±121.8)m vs. (291.8±102.9)m) and NT-proBNP (157.0(70.0, 639.0) ng/L vs. 444.7(144.0, 1 546.0)ng/L, all P<0.05). In BIV group, 6MWD extended from (314.8±142.7)m to (332.7±117.5)m at 6 months (P<0.05), LVEF increased from (60.7±7.9)% at 1 week to (56.6±10.7)% at 6 months(P<0.05), both LVEDV and LVEDD decreased at 12 months compared with at 1 week ((116.2±39.5)ml vs. (131.4±49.6)ml and (50.2±5.6)mm vs. (52.5±6.8)mm, P<0.05). In RVA group (n=57), 6MWD increased at 6 months compared that at 1week ((342.4±109.9)m vs. (310.2±105.1)m, P<0.05), NT-proBNP was higher at 12 months than that at 1 week (349.5(191.8, 884.3)ng/L vs. 127.0(70.3, 336.7)ng/L, P<0.05). Compared with RVA group, BIV group had a bigger shrink in LVEDV decrease at 12 months was more significant in BIV group ((-16.68±24.30)ml vs. (9.09±29.30)ml, P<0.05). CONCLUSIONS: Cardiac pacing could acutely improve the cardiac function in patients with high-degree AVB and LVEF over 35%. Improvements on cardiac function and remodeling are more significant after 12-month BIV pacing than that of RVA pacing. Clinical Trail Registry: Chinese Clinical Trial Registry, ChiCTR-TRC-10000832.

Renal sympathetic denervation improves cardiac dysfunction in rats with chronic pressure overload.

Varied causative and risk factors can lead to cardiac dysfunction. Cardiac dysfunction often evolves into heart failure by cardiac remodeling due to autonomic nervous system disturbance and neurohumoral abnormalities, even if the detriment factors are removed. Renal sympathetic nerve activity plays a pivotal regulatory role in neurohumoral mechanisms. The present study was designed to determine the therapeutic effects of renal sympathetic denervation (RSD) on cardiac dysfunction, fibrosis, and neurohumoral response in transverse aortic constriction (TAC) rats with chronic pressure overload. The present study demonstrated that RSD attenuated myocardial fibrosis and hypertrophy, and structural remodeling of the left atrium and ventricle, up-regulated cardiac beta adrenoceptor (beta-AR, including beta(1)AR and beta(2)AR) and sarco-endoplasmic reticulum Ca(2+)-ATPase (SERCA) while down-regulated angiotensin II type 1 receptor (AT(1)R), and decreased plasma B-type natriuretic peptide (BNP), norepinephrine (NE), angiotensin II (Ang II), and arginine vasopressin (AVP) levels in TAC rats with chronic pressure overload. We conclude that RSD attenuates myocardial fibrosis, the left atrial enlargement, and the left ventricular wall hypertrophy; inhibits the overdrive of the sympathetic nervous system (SNS), renin-angiotensin-aldosterone system (RAAS), and AVP system in TAC rats with chronic pressure overload. RSD could be a promising non-pharmacological approach to control the progression of cardiac dysfunction.