Gender-Related Association of Serum Uric Acid Levels with Premature Ventricular Contraction

Abstract

In this study, we aim to investigate the association of serum uric acid (SUA) with the prevalence of premature ventricular contraction (PVC). The relationship between SUA and the prevalence of PVC in 98,965 subjects (79,034 male subjects, mean age: 51.9 ± 12.6 years old) in the Kailuan cohort study (n = 101,510, age range: 18-98 years) from June 2006 to October 2007 was investigated. These subjects were divided into five groups on the basis of their SUA levels. A multivariate logistic regression model was constructed to evaluate the association between SUA and the prevalence of PVC. The prevalence of PVC was 1.1% in all subjects, 1.1% in male subjects, and 1.0% in female subjects. Compared with the first quintile of SUA, the odds ratio (OR) and 95% confidence interval (95% CI) of other quintiles were 1.

Serum uric acid and the risk of ventricular arrhythmias: a systematic review

“…One study found a correlation between serum UA and PVCs in patients without myocardial infarction or stroke [19]. A gender-specific analysis found a significant correlation between elevated serum UA concentrations and PVC prevalence in men but not in women [4]. This is consistent with the report by Nakanishi et al that showed a positive correlation of serum UA with cardiovascular morbidity and mortality in a large male population, but not in women [20].…”

“…Thus, it is likely that a sexspecific mechanism may underlie the association between serum UA and cardiovascular disease. The difference between the findings from various studies can be related to ethnic and territorial specificity [4]. In addition, it is likely that the incidence of PVC may be associated with adverse ventricular remodeling associated with UA.…”

“…Greater production of angiotensin II will affect fibrogenic cytokine expression and increase perivascular and interstitial fibrosis, resulting in increased myocardial fibrosis. UA is also known to be involved in myocardial pathogenesis, where oxidative stress and inflammatory mediators induce electrophysiology and structural remodeling of the atrial and ventricular myocardium [4].…”