Background-Approximately half of all patients with chronic heart failure (HF) have a decreased ejection fraction (EF) (systolic HF [SHF]); the other half have HF with a normal EF (diastolic HF [DHF]). However, the underlying pathophysiological differences between DHF and SHF patients are incompletely defined. The purpose of this study was to use echocardiographic and implantable hemodynamic monitor data to examine the pathophysiology of chronic compensated and acute decompensated HF in SHF versus DHF patients. Methods and Results-Patients were divided into 2 subgroups: 204 had EF Ͻ50% (SHF) and 70 had EF Ն50% (DHF).DHF patients had EF of 58Ϯ8%, end-diastolic dimension of 50Ϯ10 mm, estimated resting pulmonary artery diastolic pressure (ePAD) of 16Ϯ9 mm Hg, and diastolic distensibility index (ratio of ePAD to end-diastolic volume) of 0.11Ϯ0.06 mm Hg/mL. In contrast, SHF patients had EF of 24Ϯ10%, end-diastolic dimension of 68Ϯ11 mm, ePAD of 18Ϯ7 mm Hg, and diastolic distensibility index of 0.06Ϯ0.04 mm Hg/mL (PϽ0.05 versus DHF for all variables except ePAD). In SHF and DHF patients who developed acute decompensated HF, these events were associated with a significant increase in ePAD, from 17Ϯ7 to 22Ϯ7 mm Hg (PϽ0.05) in DHF and from 21Ϯ9 to 24Ϯ8 mm Hg (PϽ0.05) in SHF. As a group, patients who did not have acute decompensated HF events had no significant changes in ePAD. Conclusions-Significant structural and functional differences were found between patients with SHF and those with DHF; however, elevated diastolic pressures play a pivotal role in the underlying pathophysiology of chronic compensated and acute

Background-Postinfarction left ventricular remodeling (LVR) is associated with reductions in myocardial high-energy phosphate (HEP) levels, which are more severe in animals that develop overt congestive heart failure (CHF). During high work states, further HEP loss occurs, which suggests demand-induced ischemia. This study tested the hypothesis that inadequate myocyte oxygen availability is the basis for these HEP abnormalities. Methods and Results-Myocardial infarction was produced by left circumflex coronary artery ligation in swine. Studies were performed in 20 normal animals, 14 animals with compensated LVR, and 9 animals with CHF. Phosphocreatine (PCr)/ATP was determined with 31 P NMR and deoxymyoglobin (Mb-␦) with 1 H NMR in myocardium remote from the infarct. Basal PCr/ATP tended to be decreased in postinfarct hearts, and this was significant in animals with CHF. Infusion of dobutamine (20 g ⅐ kg Ϫ1 ⅐ min Ϫ1 IV) caused doubling of the rate-pressure product in both normal and LVR hearts and resulted in comparable significant decreases of PCr/ATP in both groups. This decrease in PCr/ATP was not associated with detectable Mb-␦. In CHF hearts, rate-pressure product increased only 40% in response to dobutamine; this attenuated response also was not associated with detectable Mb-␦. Conclusions-Thus, the decrease of PCr/ATP during dobutamine infusion is not the result of insufficient myocardial oxygen availability. Furthermore, in CHF hearts, the low basal PCr/ATP and the attenuated response to dobutamine occurred in the absence of myocardial hypoxia, indicating that the HEP and contractile abnormalities were not the result of insufficient oxygen availability. (Circulation. 1999;99:942-948.)

Bioenergetic abnormalities in remodeled myocardium are related to the severity of LV dysfunction, which, in turn, is dependent on the severity of the initiating myocardial infarction.