Blood pressure and the risk of complex arrhythmia in renal insufficiency, hemodialysis, and renal transplant patients.

Complex arrhythmia is frequent in hemodialysis patients but it is not clear if this is a consequence of dialysis or uremia or is secondary to the hemodynamic and cardiovascular alterations often associated with chronic renal failure. The incidence of complex ventricular arrhythmia (frequent multiform premature beats, couplets, and runs) in 31 subjects who had their uremic status recently corrected by renal transplant (Group 1) and in 23 predialysis (Group 2) and 73 hemodialysis (Group 3) chronic renal failure patients were studied with 24-h Holter monitoring. Patients were not receiving antiarrhythmic drugs or digitalis and significant coronary artery disease was excluded by clinical and noninvasive methods. Complex arrhythmia was two times more frequent in dialysis patients but the difference did not reach statistical significance (Group 1: 16%; Group 2: 17%; Group 3: 34%; chi2 4.9, P = .086). The stepwise model of logistic regression analysis identified systolic blood pressure (odds ratio 1.015, 95% confidence interval [CI] 1.001-1.027, P = .03) and left ventricular systolic dysfunction (odds ratio 7.04, 95% CI 1.3-36.7, P = .02) as the only factors that independently influenced the probability of complex arrhythmia. Age, gender, race, diabetes, smoking status, body mass index, diastolic blood pressure, serum creatinine, hematocrit, left ventricular mass index, and use of diuretics, beta-blockers, angiotensin converting enzyme (ACE) inhibitors, sympatolytics, and calcium channel blockers did not influence the occurrence of complex arrhythmia. The data indicate that blood pressure and myocardial dysfunction are more important determinants of complex arrhythmia than dialysis or uremia in chronic renal disease patients.

Cardiac effects of persistent hemodialysis arteriovenous access in recipients of renal allograft.

In hemodialysis patients, large arteriovenous (AV) fistulas for vascular access may cause ventricular hypertrophy and high-output cardiac failure. The long-term cardiac consequences of functional AV fistulas in renal transplant patients are unclear. A precise knowledge of these consequences is important to decide if and when such fistulas should be closed in successfully transplanted patients. In this retrospective study including 61 stable renal transplant patients with adequate renal function (serum creatinine <2.0 mg/100 ml), echocardiography was performed in 39 patients with a functional AV fistula (group 1) and in 22 whose fistulas had been closed, for esthetic reasons, within 2 months postoperatively (group 2). The volume flow of the fistulas, measured in 22 randomly selected individuals of group 1, was 900 +/- 350 ml/min (range 500-1,600). Patients of group 1 were older (40 +/- 12 vs. 33 +/- 12 years, p < 0.05), had longer duration of the fistula (62 +/- 31 vs. 36 +/- 30 months, p < 0.05), higher body mass index (24 +/- 4 vs. 22 +/- 3 kg/m2, p < 0.05), systolic (154 +/- 24 vs. 138 +/- 18 mm Hg, p < 0.05) and diastolic (96 +/- 12 vs. 89 +/- 11 mm Hg, p < 0.05) blood pressure and increased left ventricular (LV) end-diastolic dimension (53 +/- 5 vs. 49 +/- 5 mm, p < 0.01). LV mass, cardiac index, ejection fraction and the proportion of patients with LV hypertrophy were comparable in the two groups. LV end-diastolic dimension was positively and independently influenced only by the presence of the AV fistula (p < 0.01) after adjusting for age, duration of the fistula, body mass index, systolic and diastolic blood pressure and the nature of the antihypertensive drugs used. In conclusion, the persistence of large, high-flow AV fistulas for prolonged periods of time had little impact on cardiac morphology and function of stable renal transplant patients with adequate renal function. The data do not support routine closure of these fistulas in all renal transplant patients.

Carotid arterial compliance in patients with congestive heart failure secondary to idiopathic dilated cardiomyopathy.

Conduit artery distensibility affects the pulsatile component of afterload and may contribute to impaired left ventricular function in patients with congestive heart failure (CHF). The objectives of this study were to (1) determine whether arterial distensibility is reduced in patients with CHF, and (2) determine whether decreased arterial compliance is related to an abnormality in vascular wall structure (i.e., wall thickness or excessive levels of circulating neurohumoral vasoconstrictors, or both). The study participants included 40 patients with CHF secondary to idiopathic dilated cardiomyopathy and 33 age-matched healthy volunteers. High-resolution ultrasonography was performed to directly visualize the common carotid artery and measure its diameter and wall thickness. Its elastic properties were determined by relating changes in arterial diameter to changes in pressure generated with each heart beat. Carotid artery distensibility was less (14.1 +/- 1.1 vs 25.3 +/- 1.6 10(-6).N-1.m2, p < 0.001) and Young's modulus of elasticity was greater (3.99 +/- 0.51 vs 2.29 +/- 0.23 10(5).N.m-2, p < 0.005) in patients with CHF than in normal subjects. Also, carotid artery wall thickness was increased in patients with CHF. When the entire population was considered, age, wall thickness, and plasma norepinephrine and aldosterone concentrations correlated inversely with distensibility, whereas age and plasma norepinephrine concentration correlated directly with elasticity. Among normal subjects, only age correlated inversely with distensibility; among patients with CHF, only plasma norepinephrine concentration correlated with elasticity. It is concluded that carotid artery distensibility is reduced in patients with CHF.(ABSTRACT TRUNCATED AT 250 WORDS)