Left ventricular concentric remodeling and impaired cardiorespiratory fitness in patients with heart failure and preserved ejection fraction.

Background: Left ventricular (LV) concentric remodeling refers to a process by which increased LV relative wall thickness alters myocardial geometry, resulting in reduced LV end-diastolic volume (LVEDV) and stroke volume (SV). While the degree of concentric remodeling is a negative prognostic factor in heart failure with preserved ejection fraction (HFpEF), it is not known how it contributes to cardiorespiratory fitness (CRF).

Methods: We performed a retrospective analysis of patients with HFpEF who underwent treadmill single-photon emission computed tomography myocardial perfusion imaging (SPECT-MPI) and cardiopulmonary exercise testing (CPX). From exercise SPECT-MPI, we recorded postexercise LVEDVi, LVESVi, SVi, LVEF, the presence and extent of perfusion defects, and perfusion reversibility. Peak oxygen consumption (VO2), the oxygen uptake efficiency slope (OUES), oxygen (O2) pulse, ventilatory efficiency (VE/VCO2 slope), ventilatory anaerobic threshold, respiratory exchange ratio, exercise time, and maximum heart rate were obtained from CPX. Data are expressed as mean (±standard deviation). Univariate and multivariate linear regression was performed.

Results: We identified 23 subjects who had completed both an exercise SPECT-MPI and a CPX. Patients were more commonly women (83%), black (65%), middle age (50 [±7.3] years), and obese (Body Mass Index [BMI] 39.7 [±6.0] kg/m). Greater LVEDVi and LVESVi correlated positively with peak VO2 (R=+0.648, P=0.001; R=+0.601, P=0.002), O2 pulse (R=+0.686, P<0.001; R=+0.625, P=0.001) and OUES (R=+0.882, P<0.001; R=+0.779, P<0.001). The LVEF correlated inversely with peak VO2 and OUES (R=-0.450, P=0.031; R=-0.485, P=0.035). Perfusion defect area, grade of severity, and presence of reversibility were not associated with CRF variables.

Conclusions: Postexercise reduced LV volumes correlate with measures of impaired CRF in patients with HFpEF, thus supporting a pathophysiologic role of concentric remodeling in impaired CRF in HFpEF.