Renal failure is often associated with electrolyte imbalance, anemia, hypertension, volume overload, metabolic acidosis, increase in parathyroid hormone level, all of which may contribute to the development of left ventricular dysfunction. To evaluate the left ventricular function in chronic renal failure patients undergoing maintenance hemodialysis and to assess the effect of hemodialysis on cardiac function, 13 normal subjects, 11 essential hypertensive and 15 chronic renal failure patients were examined with two dimensional and targeted M-mode echocardiograms, Doppler echocardiogram and indirect carotid pulse tracing. In hemodialysis patients, these were recorded pre and post-hemodialysis.
The results were as follows : With hemodialysis, body weight decreased from 57.9 ± 9.2 to 552 ± 9.0 kg (p<0.05) without a change in heart rate. LV end-diastolic dimension, an index of preload, was larger in chronic renal failure patients than in control and hypertensive group (5.69 ± 0.78 vs. 5.00 ± 0.47 cm p=0.11, 5.30 ± 0.83 an ; p=0.25), decreased by 3.5 % with dialysis. Left ventricular end-systolic dimension was also larger in chronic renal failure patients than in control and hypertensive group (4.25 ± 0.74 vs. 3.52 ± 0.34 cm ; p<0.05, 3.63 ± 0.68 cm p<0.05, decreased by 6.0 % with dialysis. There was no difference in the thickness of ventricular septum among control, hypertensive and chronic renal failure groups.
End-systolic and end-diastolic LV posterior wall were thicker in chronic renal failure patients than in control and hypertensive group (1.22 ± 0.18 vs. 1.06 ± 6.10 cm ; p=0.12, 1.18 e 021 cm ; p=0 62 in end systolic wall thickness and 0.81 ± 0.15 . Vs. 0.58 ± 0.07 cm ; p=0.05, 0.66 ± 0.16 an ; p<0.05 in end diastolic wall thickness), increased by 4 %, 2 % with dialysis respectively. There was ventricular hypertrophy as demonstrated by an LVMI of 239.3 ± 80.4 g/m, which was significantly higher than control (123.5 ± 33.9 g/d) and hypertensive group (122.2 ± 36.1 9/m´). End-systolic wall stress, a measure of LV afterload, was greater in chronic renal failure and hypertensive group than in control (136.9 ± 51.0, 112.7 ± 26.5 vs. 91.7 ± 9.6 g/cm ; p<0.05, respectively) and decreased by 18.8 % with dialysis. Percent fractional shortening ´( % AD) and LV rate-corrected velocity of fiber shortening (mVcfc) were lower in chronic renal failure patients than in control and hypertensive group (24.4 ± 5.1 vs. 29.4 ± 4.8 % ; p=0.16, 32.6 t 4.5 % ; <0.05 in % iD and 0.84 ± 0.22 vs. 0.94 ± 0.17 circ/sec ; p=0.17, 1.06 ± 0.19 circ/sec ; p<0.05). There was small increase (8 %) in % L D with dialysis. In contrast, mVcfc increased significantly from 0.84 ± 0.22 to 1.04 ± 0.19 cire/sec(p<0.05) with the procedure. 6es was inversely related to end-systolic wall stress in linear fashion. A2D was the longest in the hypertensive group, longer in chronic renal failure patients than in control group (100. 7 ± 31.1 vs. 88.8 ± 22.7 msec ; p=027). There was no change in A2I) with hemodialysis. PE was faster in chronic renal failure parientss than control and hypertensive group (0.85 ± 0.19 vs. 0.70 ± 0.19 m/sec ; p<0.05, 0.63 ± 0.11 m/sec ; p<0.05), PA was faster in hypertensive group and chronic renal failure patients than in control group (0.68 ± 0.12, 0.79 ± O. 27 vs. 0.44 + 0.16m/sec p(0.05, respectively). With hemodialysis, there was significant decrease in PE (0.85 ± 0.19 vs. 0.71 ± 0.15 m/sec ; p(O.05), but no change in PA (0.79 ± 0.27 vs. 0.76 ± 0.20 ; p=0.97). E/A ratio was higher in control group than in chronic renal failure patients and hypertensive group (1.61 ± 0.45 vs. 0.93 ± 0.22 ; p<0.05, 1.15 ± O. 32 ; p<0.05); decreased from 1.15 ± 0.32 to 1.00 ± 0.27 ; p=0.17) with hemodialysis. There was no difference in decceleration time among groups. Parathyroid hormone level was higher in chronic renal failure patients than in control and hypertensive group (1.36 ± 1. 30 vs. 021 ± 0.07 ; .p<0.05, 021 ± 0.17 ; p<0.05).
As the results of above, left ventricular mass index(LVMI), end-diastolic dimension(preload) and end-systolic wall stress(afterload) were increased in chronic renal failure(CRF) patients. mVcfc, index of myocardial performance, was decreased in CRF patients, but the decrease in mVcfc in CRF patients was not so much as expected from the relation between 6es and mVcfc in control group. This suggest that left ventricular contractile state in CRF undergoing maintenance hemodialysis is preserved relatively well. With hemodialysis, mVcfc increased significantly. LV contractility, as determined by the load-independent relation between 8es and mVcfc, did not change. So this increase in mVcfc is thought to be due to the decrease in afterload rather than enhanced contractile state with hemodialysis. Viewed from the A2D and E/A ratio, left ventricular diastolic function was impaired in CRF patients, did not improved with dialysis.
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