International urology and nephrology · 2008
Relationship between aortic valve sclerosis and left ventricular hypertrophy in chronic haemodialysis patients.
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Turkmen Funda, Emre Ayse, Ozdemir Ali, Sevinc Can, Erisken Emre, Yesilcimen Kemal
Аннотация
BACKGROUND: Cardiac valve calcification is a frequent finding in chronic haemodialysis patients. Left ventricular hypertrophy (LVH) is a significant predictor of cardiovascular mortality in patients with end-stage renal disease. We evaluated the influence of aortic valve sclerosis (AVS) on the development of LVH in chronic haemodialysis patients.
METHODS: A total of 82 consecutive patients (52 male, mean age 48 +/- 12 years) undergoing chronic haemodialysis treatment for > 1 year were subjected to echocardiography for the screening of AVS and the assessment of transaortic flow velocity and the left ventricular mass index (LVMI). The absence (group 1, n = 42) and presence of AVS (group 2, n = 40) was established. The average values of systolic, diastolic and pulse pressure were obtained. Plasma calcium, phosphorus, intact parathyroid hormone, C-reactive protein, haemoglobin and lipid levels were also measured.
RESULTS: LVH was detected in 59 (72%) of the study patients. The LVMI was higher in the AVS group (171 +/- 39 vs. 132 +/- 41 g/m2, p < 0.001). Patients with AVS also had higher transaortic flow velocities (1.64 +/- 0.36 vs. 1.21 +/- 0.21 m/s, p < 0.01) and maximal pressure gradients (10.8 +/- 7.1 vs. 5.9 +/- 3.4 mmHg, p < 0.01). The LVMI showed a direct correlation with transaortic flow velocity in the AVS group (r = 0.60, p < 0.01). Stepwise linear regression analysis revealed transaortic flow velocity (p = 0.02), pulse pressure (p = 0.01) and haemoglobin levels (inverse relationship) (p = 0.02) to be independent predictors of the LVMI.
CONCLUSION: These data suggest that AVS is strongly and independently interrelated with LVH in chronic haemodialysis patients. The underlying mechanism might be the valve resistance to left ventricular outflow, as shown by increased transaortic flow velocities and maximal pressure gradients in AVS patients.
METHODS: A total of 82 consecutive patients (52 male, mean age 48 +/- 12 years) undergoing chronic haemodialysis treatment for > 1 year were subjected to echocardiography for the screening of AVS and the assessment of transaortic flow velocity and the left ventricular mass index (LVMI). The absence (group 1, n = 42) and presence of AVS (group 2, n = 40) was established. The average values of systolic, diastolic and pulse pressure were obtained. Plasma calcium, phosphorus, intact parathyroid hormone, C-reactive protein, haemoglobin and lipid levels were also measured.
RESULTS: LVH was detected in 59 (72%) of the study patients. The LVMI was higher in the AVS group (171 +/- 39 vs. 132 +/- 41 g/m2, p < 0.001). Patients with AVS also had higher transaortic flow velocities (1.64 +/- 0.36 vs. 1.21 +/- 0.21 m/s, p < 0.01) and maximal pressure gradients (10.8 +/- 7.1 vs. 5.9 +/- 3.4 mmHg, p < 0.01). The LVMI showed a direct correlation with transaortic flow velocity in the AVS group (r = 0.60, p < 0.01). Stepwise linear regression analysis revealed transaortic flow velocity (p = 0.02), pulse pressure (p = 0.01) and haemoglobin levels (inverse relationship) (p = 0.02) to be independent predictors of the LVMI.
CONCLUSION: These data suggest that AVS is strongly and independently interrelated with LVH in chronic haemodialysis patients. The underlying mechanism might be the valve resistance to left ventricular outflow, as shown by increased transaortic flow velocities and maximal pressure gradients in AVS patients.