SERUM URIC ACID AND LONGITUDINAL CHANGES IN LEFT VENTRICULAR STRUCTURE AND FUNCTION IN THE GENERAL POPULATION

Abstract

Objective: Previous studies showed that serum uric acid as a marker of increased xanthine oxidase activity may be a useful prognosticator for incident heart failure particularly in patients with hypertension. However, population data on the longitudinal changes in left ventricular (LV) structure and function in relation to serum uric acid are sparse. We, therefore, assessed in the general population whether hyperuricemia predicts longitudinal changes in echocardiographic indexes reflecting LV structure and function. Design and method: In 641 randomly recruited Flemish participants (mean age 50.6 years, 50.9% women), we assessed echocardiographic indexes of LV structure and diastolic function at baseline and after 4.7 years. We regressed longitudinal changes in these indexes on baseline uric acid, and reported standardized effect sizes as a percentage of the SD of LV changes associated with a 1-SD of serum uric acid. Results: In multivariable-adjusted cross-sectional analyses, higher serum uric level correlated (P < 0.0018) with greater LV mass index (LVMI) and E/e′ ratio measured at follow-up. From examination 1 to 2, LVMI and E/e′ ratio increased by +3.6 ± 13.2 g/m2 and +0.37 ± 1.46, respectively (P < 0.0001). In longitudinal analyses, after full adjustment, higher baseline serum uric acid independently predicted a greater increase in LVMI (effect size: +14.8%; P = 0.0021) and E/e′ ratio (+21.6%; P < 0.0001) during follow-up. Compared to participants who had normal level of serum uric acid over time (n = 497), subjects with hyperuricemia at both visits (n = 65) experienced worse temporal changes in LVMI (+7.2 g/m2 vs +2.4 g/m2; P = 0.011) and E/e′ ratio (+0.97 vs +0.27; P = 0.0008). Conclusions: Hyperuricemia at baseline predicted worsening of LV diastolic function and LV remodeling over time. These findings suggest the importance of management of hyperuricemia in order to delay or prevent progression of adverse LV remodeling and dysfunction.