CLINICAL PATTERNS OF STRUCTURAL AND FUNCTIONAL LEFT VENTRICULAR DYSFUNCTION IN PATIENTS WITH GOUT ASSOCIATED WITH ARTERIAL HYPERTENSION

Aim. To study the patterns of structural and functional left ventricular dysfunction in men with gout.

Methods. 114 men with gout with either an intermittent course (n = 80, mean age 46.34±6.14 years) or chronic (n = 34, mean age 49.03± 5.66 years) were enrolled in the study. All patients underwent daily monitoring of blood pressure (DMBM), echocardiography (Echo-CG) with the further identification of the architectonic pattern of the left ventricle and estimation of diastolic function with the Doppler Echo-CG.

Results. The main study group consisted of 98 patients (85.9%) with arterial hypertension. The comparison group was composed of 16 (14.1%) patients without elevated blood pressure (BP). Left ventricular dysfunction was found in 67.6% of patients with gout. Importantly, its prevalence increased with the presence of arterial hypertension and its course duration. 52% of men with gout associated with hypertension had concentric left ventricular hypertrophy. Patients with extreme-dipping of nocturnal blood pressure were more frequently found among normotonics (39.2% vs. 13.8%), whereas patients without nocturnal blood pressure dipping and nocturnal BP elevation (nondippers and night-peakers, 41.6% vs. 18.9%) among those suffering from arterial hypertension. Positive correlations between serum uric acid and the LV myocardial mass index (r = 0.32, p<0.05), left ventricular posterior wall thickness (r = 0.42, p<0.001) and interventricular septum thickness (r = 0,38, p<0.001), as well as between the mean daily readings of systolic blood pressure (r = 0.31, p<0.05), diurnal and nocturnal indices of systolic and diastolic blood pressure (r = 0.29; p<0.05 and r = 0.33, p<0.001 and r = 0.29, p<0.05 and r = 0.41, p<0.001, respectively) have been found.

Conclusion. The correlations between severe clinical course of gout, left ventricular remodeling pattern and alterations in its diastolic filling have been established. The presence of arterial hypertension contributes to the development of hemodynamically unfavorable left ventricular pattern, such as concentric hypertrophy, and pathological 24-hour blood pressure profile (nocturnal blood pressure elevation). Alterations of left ventricular diastolic filling interplay with left ventricular myocardial mass, left ventricular architectonic pattern and uric acid levels.

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