Correlation between the elevated uric acid levels and circulating renin-angiotensin-aldosterone system activation in patients with atrial fibrillation.

Abstract

Background\nThe aim of the present study was to investigate the correlation between the elevated uric acid (UA) levels and activation of the circulating renin-angiotensin-aldosterone system (RAAS) in patients with atrial fibrillation (AF).\n\n\nMethods\nA total of 233 outpatients and inpatients of the Cardiology Department from January 1, 2019, to December 31, 2019, were selected and divided into the sinus rhythm group (SR) with 84 cases, the paroxysmal AF group (pAF) with 76 cases, and the persistent AF group (PAF) with 73 patients. The general clinical data and the serum levels of UA of the enrolled patients were collected, and the radioimmunoassay was adopted to detect the levels of renin (Renin), angiotensin II (Ang II), and aldosterone (Ald).\n\n\nResults\nRenin, AngII, Ald, and UA in the PAF group were significantly higher than those in the pAF group, and the levels of the above indicators in the pAF group were significantly higher than those in the SR group (P<0.001). The left atrium anteroposterior diameter (LAD) and the left ventricular end-diastolic diameter (LVEDD) were significantly increased in the PAF group (P<0.001). The Pearson correlation analysis showed that the levels of the high sensitivity C-reactive protein (hsCRP), AngII Renin, Ald, LVEDD, and LAD were positively correlated with the serum levels of UA (r=0.174, 0.273, 0.34, 0.385, 0.138, respectively, P<0.05 in all). The left ventricular ejection fraction (LVEF) was negatively correlated with the UA level (r=-0.177, P<0.05). Multiple linear regression analysis showed that UA (β=0.103) and LAD (β=2.162) were independent risk factors for Renin. The independent risk factor for Ang II was UA (β=0.167). The independent risk factor for Ald was UA (β=0.283) and LAD (β=8.721) (P<0.05).\n\n\nConclusions\nElevated UA might cause excessive activation of the RAAS, aggravate the oxidative stress, and participate in the atrial remodeling, thereby promoting the occurrence and persistence of AF.