The L-shaped association between superoxide dismutase levels and blood pressure in older Chinese adults: community-based, cross-sectional study.

BACKGROUND: As an antioxidant, serum superoxide dismutase (SOD) have been found to be associated with hypertension. METHODS: The data were derived from the Chinese Longitudinal Healthy Longevity Survey (CLHLS), a prospective cohort study in China. We explored the association between serum SOD and blood pressure (BP) using multivariable correction analysis in an older Chinese population. RESULTS: We observed a significantly gradual downward trend in the association between serum SOD levels and diastolic BP (DBP) in participants with lower serum SOD levels (< 58 IU/mL), while no associations were observed between serum SOD levels and DBP in participants with higher serum SOD levels (> 58 IU/mL). Similar results showed a significant gradual downward trend in associations between serum SOD levels and the risk of diastolic hypertension only at SOD < 58 IU/mL. Multiple linear regression analysis suggested that serum SOD was negatively correlated with DBP (Sß = -0.088,P < 0.001) but not with SBP (Sß = 0.013, P = 0.607). Multiple logistic regression analysis suggested that serum SOD was independently associated with the risk of diastolic hypertension (OR = 0.984, 95% CI: 0.973-0.996, P = 0.010) but not with the risk of systolic hypertension (OR = 1.001, 95% CI: 0.990-1.012,P = 0.836)) after adjusting for relevant confounding factors. Serum SOD levels (< 58 IU/mL, > 58 IU/mL) were an effect modifier of the association between serum SOD and DBP (interactionP = 0.0038) or the risk of diastolic hypertension (interaction P = 0.0050). CONCLUSIONS: Our study indicated for the first time that there was an L-shaped association between serum SOD levels and the risk of diastolic hypertension in the older Chinese population.

Low deceleration capacity is associated with higher stroke risk in patients with paroxysmal atrial fibrillation.

BACKGROUND: Deceleration capacity (DC) is a non-invasive marker for cardiac autonomic dysfunction; however, few studies have shown that the influence factors of cardiac autonomic dysfunction and the correlations between DC and stroke risk in paroxysmal atrial fibrillation (AF). We aimed to explore the influencing factors of abnormal DC and the relationships between DC and stroke risk in patients with paroxysmal AF. METHODS: The study included hospitalized paroxysmal AF patients with DC measurements derived from 24-h Holter electrocardiography recordings taken between August 2015 and June 2016. Multivariable regression analysis was performed to evaluate the associations between correlated variables and abnormal DC values. The relationship between DC and ischemic stroke risk scores in patients with paroxysmal AF was analyzed. RESULTS: We studied 259 hospitalized patients with paroxysmal AF (143 [55.2%] male, mean age 66.4 ±â€Š12.0 years); 38 patients of them showed abnormal DC values. In the univariate analysis, age, hypertension, heart failure, and previous stroke/transient ischemic attack (TIA) were significantly associated with abnormal DC values. Among these factors, a history of previous stroke/TIA (odds ratio = 2.861, 95% confidence interval: 1.356-6.039) were independently associated with abnormal DC values in patients with paroxysmal AF. The abnormal DC group showed a higher stroke risk with the score of congestive heart failure, hypertension, age >75 years, diabetes mellitus, previous stroke and TIA (CHADS2) (2.25 ±â€Š1.48 vs. 1.40 ±â€Š1.34, t = -4.907, P = 0.001) and CHA2DS2-vascular disease, age 65-74 years and female category (VASc) (3.76 ±â€Š1.95 vs. 2.71 ±â€Š1.87, t = -4.847, P = 0.001) scores. Correlation analysis showed that DC was negatively correlated with CHADS2 scores (r = -0.290, P < 0.001) and CHA2DS2-VASc scores (r = -0.263, P < 0.001). CONCLUSIONS: Lower DC is closely associated with previous stroke/TIA, and is also correlated negatively with higher stroke risk scores in patients with paroxysmal AF. It could be a potential indicator of stroke risk in paroxysmal AF patients.

[SCN5A mutation in patients with Brugada electrocardiographic pattern induced by fever].

OBJECTIVE: To explore the relationship between SCN5A, SCN1b, SCN3b and GPD1L genotypes and the risk of malignant arrhythmia in patients with Brugada electrocardiographic pattern induced by fever. METHODS: The clinical data and peripheral blood of patients with Brugada electrocardiographic pattern induced by fever were collected. Patients with depolarization abnormality associated with hypertension, coronary heart disease, drugs and other factors were excluded. The direct DNA sequencing was used to screen the mutation of candidate gene SCN5A, SCN1b, SCN3b and GPD1L. If gene variation was found, mutation or polymorphism was then determined by comparison with 200 control individuals. The relationship between genotype and phenotype as well as the risk of malignant arrhythmia were analyzed. RESULTS: Five eligible patients with fever-induced Brugada ECG pattern were included in this study. TypeI Brugada ECG was presented in all five patients in fibrile state and disappeared in normothermia. No sudden cardiac death (SCD) occurred and no ventricular arrhythmia was presented in Holter monitor during the 3 to 5 years follow-up period. Six gene variants were found including a novel missense mutation of base C to T, named Arg965 Cys (R965C), which located in 965 codon of the 17 exon in SCN5A, and five SCN5A polymorphisms including A29A (c.87A>G), R1193Q (c.3578G>A), D1819D (c.5457T>C), exon11 -24G>A, exon23 +4A>G. CONCLUSION: SCN5A mutation is related to fever-induced Brugada ECG pattern. However, individuals with Brugada ECG pattern induced by fever bear low risk of malignant arrhythmia and SCD during fibrile state and follow up in this small patient cohort.