Journal Article

Aortic valve calcification is an independent factor of left ventricular hypertrophy in patients on maintenance haemodialysis

José E. Ventura, Norberto Tavella, Carlos Romero, Alicia Petraglia, Alvaro Báez and León Muñoz

in Nephrology Dialysis Transplantation

Published on behalf of European Renal Association - European Dialysis and Transplant Assoc

Volume 17, issue 10, pages 1795-1801
Published in print October 2002 | ISSN: 0931-0509
Published online October 2002 | e-ISSN: 1460-2385 | DOI: http://dx.doi.org/10.1093/ndt/17.10.1795
Aortic valve calcification is an independent factor of left ventricular hypertrophy in patients on maintenance haemodialysis

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Background. Calcification and dysfunction of aortic and mitral valves are frequently found in chronic dialysis patients, but their influence on the development of left ventricular hypertrophy (LVH) is not well defined.

Methods. Conventional echocardiography and Doppler measurement of trans‐aortic flow velocity were performed in 135 chronic haemodialysis patients, and left ventricular mass index (LVMI) and trans‐valve pressure gradients were calculated. Average values of systolic, diastolic and pulse pressure (PP), interdialytic weight gain, chronic overhydration (difference between mean post‐dialysis and dry weights), plasma calcium, phosphate, haemoglobin, and urea reduction ratio over the year preceding this study were obtained in every patient.

Results. Aortic valve calcification was present in 105 patients (78%), associated with stenosis in eight (6%); 39 patients (29%) had aortic regurgitation. Mitral annular calcification occurred in 35 (26%) cases and mitral regurgitation in 45 (33%). LVH was observed in 104 patients (77%). Logistic analysis revealed that only aortic valve calcification predicted LVH. LVMI was higher in patients with aortic valve calcification than in those without calcification: (mean±SD) 241±52 vs 154±64 g/m2, P=0.001. LVMI was not different between patients with normal, calcified, or regurgitating mitral valves. Patients with aortic valve calcification had higher trans‐valve peak flow velocities and pressure gradients than those with non‐calcified valves: 1.65±0.53 vs 1.37±0.33 m/s, P=0.01, and 12.1±8.9 vs 7.9±3.6 mmHg, P=0.01, respectively. The LVMI correlated directly with both variables (r=0.27 and r=0.24, P<0.005). Stepwise linear regression on nine covariates potentially influencing LVMI (age, body mass index, time on dialysis, systolic blood pressure, PP, chronic overhydration, haemoglobin concentration, trans‐aortic flow velocity, and urea reduction ratio) showed that LVMI was independently associated with (i) PP, (ii) haemoglobin (inverse correlation), (iii) peak aortic flow velocity, and (iv) chronic overhydration (r=0.502, R2=0.252, ANOVA F‐ratio=10.19, P<0.0005).

Conclusion. Our findings show that aortic valve calcification is associated with LVH in chronic haemodialysis patients, probably because valve resistance to ventricular outflow is increased as shown by trans‐aortic flow velocities and pressure gradients. The effect on LVMI is independent of PP, anaemia, and overhydration.

Keywords: aortic valve calcification; haemodialysis; left ventricular hypertrophy

Journal Article.  4473 words.  Illustrated.

Subjects: Nephrology

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