Left ventricular global longitudinal strain across the spectrum of heart failure stages and its prevalence, correlates and prognostic relevance in heart failure with preserved ejection fraction

Abstract

LV global longitudinal strain (GLS) is significantly altered in HFpEF and is a powerful predictor of outcome according to a recent meta-analysis. We sought to determine the evolution of GLS across the spectrum of AHA HF stages and to analyze the correlation of GLS with other clinical, biological and imaging variables and its prognostic value in HFpEF. GLS was assessed by 2D speckle-tracking echocardiography in 172 patients with HFpEF stage C (78 ± 10 yrs, 38%men), 22 stage B (73 ± 10 yrs, 32%men), 56 stage A (63 ± 16 yrs, 52% men) and 20 healthy volunteers (38 ± 12 yrs, 55% men). Impaired GLS was defined as −16.6%, corresponding to 2 SD below the mean value of age and sex matched controls. All patients underwent 2D echo and cMR. Patients were followed up for a composite outcome of mortality and first HF hospitalization. Mean GLS was −20.1 ± 1.0%, −19.8 ± 1.6%, −19.1 ± 2.6% and −16.6 ± 3.0% in volunteers, stage A, stage B and stage C respectively ( P for trend < 0.001), showing the worsening of GLS across the stages ( Fig. 1 ). In HFpEF stage C, 86 patients (50%) had an impaired GLS. They had higher NTproBNP ( P = 0.002), higher sST2 ( P = 0.023), higher incidence of AF (55% vs. 36%, P = 0.014), lower LVEF ( P < 0.001), higher indexed RA volume ( P = 0.041) and impaired RV systolic function (lower FAC, P = 0.002; lower TAPSE, P < 0.001 and lower cMR RVEF, P < 0.001). In multivariate logistic analysis, only RVEF (OR 0.94 [0.89–0.98], P = 0.005) and NTproBNP (OR 1.91 [1.26–2.88], P = 0.003) were associated with impaired GLS in HFpEF stage C, even after adjustment for other variables. During a mean follow up of 19 ± 9months, 85 patients (49%) reached the combined endpoint. In univariate Cox analysis, GLS was not associated with outcome. There is a continuum in GLS impairment across the spectrum of AHA HF stages confirming the role of a subclinical myocardial dysfunction in HFpEF. Impaired GLS was associated with RV dysfunction and NTproBNP but not with clinical outcomes in HFpEF.