Abstract 4369: Reduced Exercise Capacity Is Associated With Impaired Cardiac Energetics In Patients With Heart Failure With Preserved Ejection Fraction (HFpEF) In The Absence Of Coronary Artery Disease Or Diabetes: A Study Using 3 Tesla 31P Magnetic Resonance Spectroscopy
BACKGROUND: Pressure-volume loop studies have shown that patients with heart failure with a preserved ejection fraction (HfpEF) exhibits impaired cardiac active relaxation during handgrip exercise. In the canine rapid pacing heart failure model a reduction in high energy phosphate status precedes objective evidence of impairment of LV systolic function. We hypothesize that this abnormality in cardiac active relaxation is related to a reduction in cardiac energetic and that this plays an important part in the patho-physiology of patients with HfpEF in the absence of diabetes and coronary artery disease.
METHODS: We used 31P cardiac Magnetic Resonance Spectroscopy (MRS) at 3 Tesla to measure the myocardial energetic status. All subjects also underwent echocardiography, metabolic exercise test (VO2 max) and full pulmonary function testing. HFpEF patients had normal ejection fraction (EF), reduced VO2 max, in sinus rhythm, absence of coronary artery disease and diabetes. Twenty-Three HfpEF patients and Thirteen age-gender matched healthy controls were studied.
RESULTS: HfpEF patients were 68.5 ± 1.4 years old with a Left ventricular Ejection Fraction (LVEF) of 65.2 % ± 2.0 and a VO2 max of 19.1 ml/kg/min ± 0.8 (61% of predicted). HV were 65.5 ± 2.1 years old (p=0.22) with a LVEF of 64.8% ± 2.2 (p=0.86) and a VO 2 max of 34.4 ml/kg/min ± 2.0 (101% of predicted) (p<0.0001). Patients with HfpEF had significantly lower PCr/γ ATP ratio compared to healthy volunteers, 1.52 ±0.10 and 2.10 ±0.15, respectively, P = 0.005. Importantly, PCr/γ ATP ratio correlated significantly with VO2 max with a Pearson correlation 0.34 (P = 0.023). (Mean ± SEM)
CONCLUSION: We have shown that patients with HfpEF, in the abscence of diabetes or coronary artery disease, have abnormal cardiac energetics which may lead to a reduction in active relaxation at maximal exercise, resulting in symptoms and a reduction in VO2 max.