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(Circulation. 2008;118:1433-1441.)
© 2008 American Heart Association, Inc.

Heart Failure

Transition From Chronic Compensated to Acute Decompensated Heart Failure

Pathophysiological Insights Obtained From Continuous Monitoring of Intracardiac Pressures

Michael R. Zile, MD; Tom D. Bennett, PhD; Martin St. John Sutton, MD; Yong K. Cho, PhD; Philip B. Adamson, MD; Mark F. Aaron, MD; Juan M. Aranda, Jr, MD; William T. Abraham, MD; Frank W. Smart, MD; Lynne Warner Stevenson, MD; Fred J. Kueffer, MS, MD; Robert C. Bourge, MD

From the Medical University of South Carolina and RHJ Department of Veterans Affairs Medical Center, Charleston (M.R.Z.); Medtronic, Inc, Minneapolis, Minn (T.D.B., Y.K.C., F.J.K.); University of Pennsylvania, Philadelphia (M.S.J.S.); University of Oklahoma Health Sciences Center, Oklahoma City (P.B.A.); St Thomas Hospital, Nashville, Tenn (M.F.A.); University of Florida, Gainesville (J.M.A.); Ohio State University, Columbus (W.T.A.); Texas Heart Institute, Houston (F.W.S.); Brigham and Woman’s Hospital, Harvard University, Boston, Mass (L.W.-S.); and University of Alabama at Birmingham (R.C.B.).

Correspondence to Michael R. Zile, MD, Division of Cardiology, Department of Medicine, Medical University of South Carolina, 135 Rutledge Ave, Suite 1201, PO Box 250592, Charleston, SC 29425. E-mail zilem{at}musc.edu

Received January 22, 2008; accepted July 10, 2008.

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 <50% (SHF) and 70 had EF 50% (DHF). DHF patients had EF of 58±8%, end-diastolic dimension of 50±10 mm, estimated resting pulmonary artery diastolic pressure (ePAD) of 16±9 mm Hg, and diastolic distensibility index (ratio of ePAD to end-diastolic volume) of 0.11±0.06 mm Hg/mL. In contrast, SHF patients had EF of 24±10%, end-diastolic dimension of 68±11 mm, ePAD of 18±7 mm Hg, and diastolic distensibility index of 0.06±0.04 mm Hg/mL (P<0.05 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 17±7 to 22±7 mm Hg (P<0.05) in DHF and from 21±9 to 24±8 mm Hg (P<0.05) 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 decompensated HF in both SHF and DHF.

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