Cardiovascular Problems in Peritoneal Dialysis Patients: A Short Overview

cardiogram on starting dialysis. Forty-one percent had concentric left ventricular (LV) hypertrophy, 28% had LV dilatation, and 16% had systolic dysfunction. These results imply that the causes ofLV dysfunction occur in the predialysis phase of chronic renal failure. Two hundred and seventy-five patients had a f ollow-up echo cardiogram 17 months after starting dialysis therapy (12). Now the proportion of those who had a normal echocardiogram was 13%, the proportion with concentric LV hypertrophy was 40%, the proportion with LV dilatation was 26%, and the proportion with systolic dysfunction was 20% (12). In peritoneal dialysis patients, one might expect that blood flow would not increase as much as in hemodialysis patients, because no vascular access is required, and fluctuations in salt and water status are less variable. In 70 patients treated exclusively with peritoneal dialysis, LV cavity volume decreased by 5 mL/m2 during 1 year's follow-up (9). When compared to readings from hemodialysis patients, the differences in the changes in LV volume approached statistical significance (p = 0.06). In 55 normotensive CAPD patients who were on treatment for a mean of 28.8 ± 24.9 months, a high prevalence of left atrial dilatation and left ventricular hypertrophy was found (13). The latter was mainly the result of s eptal thickening. The degree ofventricular hypertrophy in these patients was related to the amount ofhypercirculation and to the quality of blood purification. Abnormal diastolic left ventricular filling in CAPD patients has been found in patients both with and without left ventricular hypertrophy (14,15). In these patients, a disturbed ratio exists between the ventricular rapid filling in protodiastole and the filling owing to atrial contraction, with a greater-thannormal atrial contribution. After init iation ofCAPD therapy, regression as well as progression in left ventricular hypertrophy has been described. Prospective studies did not show a deterioration in left ventricular function up to 2 years after the start of CAPD (16). Others did not observe changes in left ventricular mass, ejection fraction, or left ventricular telediastolic dimension, despite a fall in blood pressure