Role of Arterial Hypertension in Left Ventricle Hypertrophy in Hemodialysis Patients: An Echocardiographic Study

Abstract

To assess the role of arterial hypertension in left ventricle (LV) hypertrophy among hemodialysis patients, echocardiographic evaluation was performed in 10 hypertensive and 13 normotensive hemodialysis subjects matched for age, sex, race, duration of dialysis treatment and degree of interdialytic volume expansion. We excluded from the latter group patients with previous hypertension since hypertensive heart disease may persist after adequate blood pressure control. We also studied 17 normal controls and 10 non-uremic patients with essential hypertension. Comparisons between the two uremic groups showed that the hypertensive patients had a higher mass index(222 ± 74 × 108 ± 26, p = 0.0001)andposteriorwallthickness(12 ± 2 X 9 ± 2, p = 0.0001) and a reduced LV radius/wall thickness ratio (4.4 ± 0.7 X 5.8 ± 1, p = 0.0001). There were no significant echocardiographic differences between normal controls and normotensive uremics. In contrast, compared to controls, hypertensive uremic patients showed an increased LV mass index (222 ± 74 X 83 ± 21, p = 0.0001) and posterior wall thickness (12 ± 2 X 7 ± 1, p = 0.0001) and a reduced LV radius/wall thickness ratio (4.4 ± 0.7 X 6.5 ± 1.1, p = 0.001), characterizing concentric hypertrophy. They also had ventricular dilation with larger LV dimensions than in controls (53 ± 5 X 47 ± 4, p = 0.004). In patients with essential hypertension, the mass index (135 ± 22), wall thickness (11 ± 1) and LV radius/wall thickness ratio (4.3 ± 0.7) significantly differed (p = 0.0001) from those in the controls. Hypertensive uremic patients and patients with essential hypertension had similar LV wall and interventricular septum thickness and LV radius/wall thickness ratio, suggesting that arterial hypertension was equally important in the genesis of hypertrophy in both groups. Systolic function was preserved in the three patient groups but hypertensive dialysis individuals had lower ejection fraction and fractional LV shortening than essential hypertensives. LV hypertrophy was found only in patients with arterial hypertension, whereas normotensive dialysis patients showed few echocardiographic abnormalities despite prolonged exposure to hyper-volemia and to the other hemodynamic and metabolic derangements of chronic uremia. It is concluded that arterial hypertension plays a central role in LV hypertrophy in hemodialysis patients.