Left Ventricular Global Longitudinal Strain (GLS) Is a Superior Predictor of All-Cause and Cardiovascular Mortality When Compared to Ejection Fraction in Advanced Chronic Kidney Disease

Abstract

Background: Echocardiographic global longitudinal strain (GLS) is increasingly recognised as a more effective technique than conventional ejection fraction (EF) in detecting subtle changes in left ventricular (LV) function. This study investigated the prognostic value of GLS over EF in patients with advanced Chronic Kidney Disease (CKD).

Methods: The study included 183 patients (57% male, 63% on dialysis) with CKD stage 4, 5 and 5Dialysis (D). 112 (61%) of patients died in a follow up of 7.8 ± 4.4 years and 41% of deaths were due to cardiovascular (CV) disease. GLS was calculated using 2-dimensional speckle tracking and EF was measured using Simpson's biplane method. Cox proportional hazard models were used to assess the association of measures of LV function and all- cause and CV mortality.

Results: The mean GLS at baseline was -13.6 ± 4.3% and EF was 45 ± 11%. GLS was a significant predictor of all-cause [Hazard Ratio (HR) 1.09 95%; Confidence Interval (CI) 1.02-1.16; p = 0.01] and CV mortality (HR 1.16 95%; CI 1.04-1.30; p = 0.008) following adjustment for relevant clinical variables including LV mass index (LVMI) and EF. GLS also had greater predictive power for both all- cause and CV mortality compared to EF. Impaired GLS (>-16%) was associated with a 5.6-fold increased unadjusted risk of CV mortality in patients with preserved EF.

Conclusions: In this cohort of patients with advanced CKD, GLS is a more sensitive predictor of overall and CV mortality compared to EF. Studies of larger populations in CKD are required to confirm that GLS provides additive prognostic value in patients with preserved EF.

Conflict of interest statement

Competing Interests: Associate Professor Carmel Hawley has received research funding from Baxter Healthcare Pty Ltd and Fresenius Medical Care. She has received travel grants from Amgen Australia. Associate Professor Isbel has received research funding from Baxter Healthcare Pty Ltd, Roche Pharmaceuticals and Amgen in the form of peer-reviewed grants. She has also received travel grants from Shire Australia, Alexion Pharmaceuticals and Pfizer. Dr Rathika Krishnasamy has received speaking honoraria from Shire Australia. Professor Thomas H. Marwick has received research support (equipment and software) from GE Medical Systems for studies of 2D strain. Associate Professor Tony Stanton has acted as a consultant to Medtronic and Novartis Pharmaceuticals. However, the current study was not supported by those grants. The remaining authors have no competing financial interests to declare. This does not alter the authors' adherence to PLOS ONE policies on sharing data and materials.

Figures

Fig 1. (a +b).

Kaplan Meier all-cause survival estimates according to GLS (a) and EF (b).

Fig 2. (a +b).

Kaplan Meier CV survival estimates according to GLS (a) and EF (b).

Fig 3. All-cause mortality: Comparing incremental value of EF and GLS to relevant demographic and biochemical variables (baseline model: age, diabetes mellitus, previous cardiovascular event, smoking history, systolic BP, diastolic BP, PTH).

Fig 4. CV mortality: Comparing incremental value of EF and GLS to relevant demographic and biochemical variables (baseline model: age, gender, diabetes mellitus, smoking history, previous cardiovascular events, systolic BP).

Fig 5. Kaplan Meier CV survival estimates according to GLS in patients with preserved EF.