Sex differences in the association between green tea consumption and hypertension in elderly Chinese adults.

BACKGROUND: Green tea has been one of the most popular beverages in China since ancient times. Mixed results concerning the effect of green tea consumption on the incidence of hypertension have been published over the past decades. However, no previous studies have focused on longevous individuals in China and the sex differences in the association between habitual green tea intake and hypertension. METHODS: The data extracted from the database of the Chinese Longitudinal Healthy Longevity Survey (CLHLS) in 2018 were used for a secondary analysis. Logistic regression models were employed to examine the odds ratio (OR) of daily green tea consumption on the incidence of hypertension by sex. RESULTS: A total of 9277 individuals were included in the analysis (39.8% were men). The included individuals had a mean age of 80.9 and 84.8 years for those who drank green tea daily and those who had never, respectively (p <  0.001). The incidence of hypertension varied at baseline according to green tea drinking habit and sex. For women who had a habitual green tea intake or had never drunk green tea, the incidence of hypertension was 47.3 and 43.9%, respectively (p = 0.241), whereas it was 51.6 and 39.7% for men (p <  0.001). After adjusting for potential confounders, a 38% increase in the risk of hypertension was observed in men who consumed green tea daily (OR, 1.38; 95% CI, 1.15-1.67; p <  0.001). CONCLUSIONS: Chinese longevous men had a 38% higher risk of developing hypertension when drinking green tea daily. However, no effect of green tea consumption on the incidence of hypertension in women was found. More attention should be paid to the lifestyle of longevous individuals for health promotion, and a sex-specific approach to deliver care for very elderly people is warranted.

Right atrial diameter and outcome of catheter ablation of atrial fibrillation.

PURPOSE: While AF is considered more like a left atrial (LA) disease, to what extent the right atrium contributes to the pathogenesis and ablation outcome of AF remains unclear. This study aimed to identify if right atrial diameter (RAD) could predict arrhythmia recurrence after catheter ablation of atrial fibrillation (AF). METHODS: Four hundred and seventy patients with drug-resistant AF [paroxysmal AF (PAF) 196; non-PAF 274] who underwent primary catheter ablation were enrolled. Ablation strategy included complete bilateral pulmonary vein isolation (PVI) in all patients and additional linear ablation across mitral isthmus, LA roof, and tricuspid isthmus in non-PAF cases. Risk factors associated with recurrence were determined by a Cox regression model, and the predictive power was evaluated by using receiver operating characteristic curve. RESULTS: After 24.3 ± 18.0 months, 284 patients (60.6%) experienced atrial tachyarrhythmia recurrence (111 in PAF, 173 in non-PAF). RAD was moderately associated with LA diameter (r = 0.371, P < 0.001), left ventricular ejection fraction (r = -0.205, P < 0.001), and left ventricular end-diastolic diameter (r = 0.319, P < 0.001). Multivariate Cox regression analysis demonstrated that RAD was an independent predictor for recurrence only in PAF patients with LAD ≥35 mm (HR 1.044, 95% CI 1.007-1.082, P = 0.021). The RAD cutoff value of 35.5 mm predicts atrial tachyarrhythmia recurrence with 85.4% sensitivity and 29.2% specificity. Kaplan-Meier analysis indicated that RAD over 35.5 mm is associated with more recurrence after PAF ablation (log-rank P = 0.034), comparing to those with RAD <35.5 mm. CONCLUSIONS: RAD predicts outcome of ablation only in patients with PAF and concurrent LA enlargement. Under this condition, RAD <35.5 mm is associated with a more favorable recurrence-free survival at over 2-year follow-up.

hERG Blockade by Iboga Alkaloids.

The iboga alkaloids are a class of naturally occurring and synthetic compounds, some of which modify drug self-administration and withdrawal in humans and preclinical models. Ibogaine, the prototypic iboga alkaloid that is utilized clinically to treat addictions, has been associated with QT prolongation, torsades de pointes and fatalities. hERG blockade as IKr was measured using the whole-cell patch clamp technique in HEK 293 cells. This yielded the following IC50 values: ibogaine manufactured by semisynthesis via voacangine (4.09 ± 0.69 µM) or by extraction from T. iboga (3.53 ± 0.16 µM); ibogaine's principal metabolite noribogaine (2.86 ± 0.68 µM); and voacangine (2.25 ± 0.34 µM). In contrast, the IC50 of 18-methoxycoronaridine, a product of rational synthesis and current focus of drug development was >50 µM. hERG blockade was voltage dependent for all of the compounds, consistent with low-affinity blockade. hERG channel binding affinities (K i) for the entire set of compounds, including 18-MC, ranged from 0.71 to 3.89 µM, suggesting that 18-MC binds to the hERG channel with affinity similar to the other compounds, but the interaction produces substantially less hERG blockade. In view of the extended half-life of noribogaine, these results may relate to observations of persistent QT prolongation and cardiac arrhythmia at delayed intervals of days following ibogaine ingestion. The apparent structure-activity relationships regarding positions of substitutions on the ibogamine skeleton suggest that the iboga alkaloids might provide an informative paradigm for investigation of the structural biology of the hERG channel.

Pharmacological enhancement of cardiac gap junction coupling prevents arrhythmias in canine LQT2 model.

Gap junctions contribute to the transmural heterogeneity of repolarization in the normal heart and under conditions of prolonged QT interval in the diseased heart. This study examined whether enhancing of gap junction coupling can reduce transmural dispersion of repolarization (TDR) and prevent torsade de pointes (TdP) in a canine LQT2 model. Canine left ventricular wedge preparations were perfused with delayed rectifier potassium current (IKr) blocker d-sotalol to mimic LQT2 and the antiarrhythmic peptide 10 (AAP10) was used as a gap junction coupling enhancer. As compared with the control group, the LQT2 group had significantly augmented TDR and higher incidence of TdP associated with increased nonphosphorylated connexin 43 (Cx43). AAP10 prevented augmentation of TDR and induction of TdP while rescuing Cx43 phosphorylation. There was no significant change in the quantity and spatial distribution of Cx43. These data indicate that gap junction enhancer AAP10 can prevent augmentation of TDR and suppress TdP by preventing dephosphorylation of Cx43 in a LQT2 model.