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Updated: May 5, 2026

Evaluation of Left Ventricular Structure and Function using 3D Echocardiography
Published on: October 28, 2020
Correlates of left ventricular mass in chronic hemodialysis recipients
Ron Wald1, Marc B Goldstein, Rachel M Wald
1Division of Nephrology, St. Michael's Hospital, University of Toronto, 61 Queen Street East, Room 9-140, Toronto, ON, M5C 2T2, Canada, waldr@smh.ca.
Insights
Blood pressure and left ventricular volume overload are key factors driving left ventricular mass in hemodialysis patients. Managing these may improve heart health outcomes for dialysis recipients.
Area of Science:
- Nephrology
- Cardiology
- Biomedical Engineering
Background:
- Left ventricular hypertrophy (LVH) is prevalent in hemodialysis patients.
- LVH is linked to poor clinical outcomes in this population.
- Pathophysiology of LVH in dialysis patients requires further elucidation.
Purpose of the Study:
- To identify correlates of left ventricular mass index (LVMI) and left ventricular end-diastolic volume index (LVEDVI).
- To understand mechanisms of LVH in prevalent hemodialysis recipients.
Main Methods:
- Cross-sectional study of 56 hemodialysis patients.
- Cardiac magnetic resonance imaging (CMR) for LV mass and volume assessment.
- Multivariable linear regression analysis of clinical, biochemical, and dialysis-related parameters.
Main Results:
- Systolic blood pressure and LVEDVI were independently associated with LVMI.
- Post-dialysis weight, urea reduction, and permanent vascular access correlated with LVEDVI.
- Fibroblast growth factor-23 showed no association with LVMI or LVEDVI.
Conclusions:
- Elevated left ventricular mass in dialysis patients is determined by blood pressure and volume status.
- Strategies targeting blood pressure reduction and volume management may improve LVH and outcomes.
Abstract:
We aimed to clarify the correlates of left ventricular mass and secondarily, left ventricular volume, in a cohort of prevalent hemodialysis recipients. Left ventricular hypertrophy is common and left ventricular mass is a widely-accepted surrogate for clinical outcomes in dialysis recipients, who are often subjected to chronic pressure and volume overload. However, the precise pathophysiologic mechanisms of left ventricular hypertrophy in this unique population have not been well understood. This was a cross-sectional study of patients receiving conventional thrice-weekly dialysis in Toronto, Canada. Left ventricular mass and volume were assessed with cardiac magnetic resonance and indexed to the patient's height to the power of 2.7. Fibroblast growth factor-23 concentration was measured using a C-terminal enzyme-linked immunosorbent assay. Patient demographics, comorbidities, dialysis-associated blood pressures and ultrafiltration volumes, biochemical and hematologic parameters, vascular access and medications were extracted from clinical records. Multivariable linear regression was used to identify independent correlates of left ventricular mass index (LVMI) and the left ventricular end diastolic volume index (LVEDVI). We enrolled 56 patients, of whom 23 (41.1 %) were women with mean age 54 ± 12 years. Mean LVMI was 31.1 ± 6.8 g/m(2.7). In multivariable analyses, systolic blood pressure and LVEDVI were the only factors significantly associated with LVMI. Post-dialysis weight, percent reduction in urea and the presence of a permanent form of vascular access were associated with LVEDVI. Fibroblast growth factor-23 was not associated with either LVMI or LVEDVI. Blood pressure and left ventricular dilatation are independent determinants of elevated left ventricular mass. Aggressive blood pressure reduction and avoidance of volume overload may confer LVM regression and improve clinical outcomes.
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