Abstract

BackgroundHigher left ventricular mass (LV) strongly predicts cardiovascular mortality in hemodialysis patients. Although several parameters of preload and afterload have been associated with higher LV mass, whether these parameters independently predict LV mass, remains unclear.MethodsThis study examined a cohort of 391 adults with incident hemodialysis enrolled in the Predictors of Arrhythmic and Cardiovascular Risk in End Stage Renal Disease (PACE) study. The main exposures were systolic and diastolic blood pressure (BP), pulse pressure, arterial stiffness by pulse wave velocity (PWV), volume status estimated by pulmonary pressures using echocardiogram and intradialytic weight gain. The primary outcome was baseline left ventricular mass index (LVMI).ResultsEach systolic, diastolic blood, and pulse pressure measurement was significantly associated with LVMI by linear regression regardless of dialysis unit BP or non-dialysis day BP measurements. Adjusting for cardiovascular confounders, every 10 mmHg increase in systolic or diastolic BP was significantly associated with higher LVMI (SBP β = 7.26, 95 % CI: 4.30, 10.23; DBP β = 10.05, 95 % CI: 5.06, 15.04), and increased pulse pressure was also associated with higher LVMI (β = 0.71, 95 % CI: 0.29, 1.13). Intradialytic weight gain was also associated with higher LVMI but attenuated effects after adjustment (β = 3.25, 95 % CI: 0.67, 5.83). PWV and pulmonary pressures were not associated with LVMI after multivariable adjustment (β = 0.19, 95 % CI: −1.14, 1.79; and β = 0.10, 95 % CI: −0.51, 0.70, respectively). Simultaneously adjusting for all main exposures demonstrated that higher BP was independently associated with higher LVMI (SBP β = 5.64, 95 % CI: 2.78, 8.49; DBP β = 7.29, 95 % CI: 2.26, 12.31, for every 10 mmHg increase in BP).ConclusionsAmong a younger and incident hemodialysis population, higher systolic, diastolic, or pulse pressure, regardless of timing with dialysis, is most associated with higher LV mass. Future studies should consider the use of various BP measures in examining the impact of BP on LVM and cardiovascular disease. Findings from such studies could suggest that high BP should be more aggressively treated to promote LVH regression in incident hemodialysis patients.Electronic supplementary materialThe online version of this article (doi:10.1186/s12882-015-0131-4) contains supplementary material, which is available to authorized users.

Highlights

  • Higher left ventricular mass (LV) strongly predicts cardiovascular mortality in hemodialysis patients

  • The relative importance of various modifiable risk factors in predicting Left ventricular hypertrophy (LVH) in incident dialysis patients, in particular, remains unclear, as the majority of studies have included prevalent dialysis patients, predominantly Europeans, with potential survivor and selection bias as well as small sample sizes limiting analyses

  • Cardiovascular risk factors are common: 57 % with diabetes, 33 % with coronary artery disease (CAD), 41 % with congestive heart failure (CHF), 20 % with peripheral vascular disease (PVD), and 62 % has a history of smoking

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Summary

Introduction

Higher left ventricular mass (LV) strongly predicts cardiovascular mortality in hemodialysis patients. Left ventricular hypertrophy (LVH) is the most frequently observed cardiac abnormality in end-stage renal disease (ESRD), and strongly predicts cardiovascular mortality in hemodialysis patients [1]. Despite past findings demonstrating associations between various cardiac parameters and LVH [2,3,4], independent, modifiable, and clinically relevant predictors of left ventricular mass (LVM) in ESRD patients remain difficult to define. Hypertension is a major risk factor for LVH, and the role of blood pressure (BP) in the progression of LVM and mortality of patients receiving hemodialysis has been well documented [6]. The timing of BP measurements, has been controversial in dialysis patients, as BP levels are highly variable and BP measurements at a single time point may not be a reliable estimate of the arterial pressure load [7, 8]

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