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Abstract
Abstract Background Hyperuricemia has been reported to accelerate the occurrence and worsening of cardiovascular disease, being a risk factor for coronary heart disease and cardiac mortality. Elevated uric acid (UA) is also associated with left ventricular (LV) hypertrophy and with LV diastolic dysfunction. The effect of hyperuricemia (HU) on LV systolic function is still unclear. Purpose Aim of our study was to evaluate the impact of elevated UA serum levels on LV systolic function, also evaluating longitudinal deformation, in a population of hypertensive patients. Methods We enrolled 160 treated hypertensive patients (M/F = 104/56, age 58.2 ± 13.3 years, blood pressure = 136.7 ± 16.8/81.3 ± 10.9 mmHg), who underwent standard echo-Doppler exam, including speckle tracking quantification of global longitudinal strain (GLS, considered in absolute value). HU was defined as UA≥7 mg/dL and the study population was divided in two groups: patients with (n = 63) and without (n = 97) HU. Exclusion criteria were coronary artery disease, overt heart failure, hemodynamically significant valve heart disease, primary cardiomyopathies, permanent atrial fibrillation and inadequate echo imaging. Results The two groups were comparable for sex prevalence, blood pressure and heart rate. Patients with HU were older and had higher body mass index (BMI) (both p < 0.0001). Prevalence of diabetes mellitus was higher in the group of patients with HU than in patients with normal UA (69% vs. 12% p < 0.0001). Fasting glycaemia was higher (p < 0.0001) and glomerular filtration rate (GFR) lower in HU hypertensives (both p < 0.0001). LV mass index (LVMi) was higher in patients with HU (p < 0.0001). Among diastolic parameters, transmitral E/A ratio (p < 0.0001) was lower, whereas E/e’ ratio (p < 0.0001), E velocity deceleration time and left atrial volume index (both p < 0.001) were higher in HU hypertensives. GLS resulted to be lower in patients with HU (20.8 ± 1.5 vs. 22.3 ± 2.2%, p < 0.0001). LV ejection fraction, despite still in normal range values, was also slightly lower in comparison with controls (60.6 ± 4.0 vs. 62.2 ± 3.9%, p < 0.01). Serum UA levels resulted to be negatively correlated with GLS (r=-0.28, p < 0.0001) (Figure), but not with ejection fraction. By a multiple linear regression analysis performed in the pooled hypertensive population, after adjusting for age, BMI, GFR, fasting glycaemia and LVMi, the association between UA levels and GLS remained significant (standardized beta coefficient =-0.25, p < 0.01), besides the significant impact of age (beta=-0.19 , p < 0.05). Conclusions In hypertensive patients with multiple cardiovascular risk factors, the presence of HU is associated with LV diastolic and systolic dysfunction. Serum UA levels and GLS resulted independently associated even after adjusting for several clinical and echo confounders. Acid uric might be considered as an independent marker of early LV dysfunction, able to identify hypertensive patients at increased risk for heart failure. Abstract P658 Figure. Relation between uric acid and GLS
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