Published online before print April 2, 2007, doi: 10.1161/CIRCULATIONAHA.106.659763
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(Circulation. 2007;115:1982-1990.)
© 2007 American Heart Association, Inc.
Heart Failure |
Cardiac Structure and Ventricular–Vascular Function in Persons With Heart Failure and Preserved Ejection Fraction From Olmsted County, Minnesota
From the Division of Cardiovascular Diseases, Mayo Clinic and Foundation, Rochester, Minn (C.S.P.L., V.L.R., R.J.R., B.A.B., S.R.O., M.M.R.); Yong Loo Lin School of Medicine, National University of Singapore, Singapore (C.S.P.L.); Department of Cardiology, University Policlinico Hospital, Modena, Italy (F.B.); and Division of Cardiology, Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, Md (D.A.K.).
Correspondence to Margaret M. Redfield, MD, Mayo Clinic and Foundation, 200 First St SW, Rochester, MN 55905. E-mail redfield.margaret{at}mayo.edu
Received August 21, 2006; accepted February 16, 2007.
Background— Mechanisms purported to contribute to the pathophysiology of heart failure with normal ejection fraction (HFnlEF) include diastolic dysfunction, vascular and left ventricular systolic stiffening, and volume expansion. We characterized left ventricular volume, effective arterial elastance, left ventricular end-systolic elastance, and left ventricular diastolic elastance and relaxation noninvasively in consecutive HFnlEF patients and appropriate controls in the community.
Methods and Results— Olmsted County (Minn) residents without cardiovascular disease (n=617), with hypertension but no heart failure (n=719), or with HFnlEF (n=244) were prospectively enrolled. End-diastolic volume index was determined by echo Doppler. End-systolic elastance was determined using blood pressure, stroke volume, ejection fraction, timing intervals, and estimated normalized ventricular elastance at end diastole. Tissue Doppler e' velocity was used to estimate the time constant of relaxation. End-diastolic volume (EDV) and Doppler-derived end-diastolic pressure (EDP) were used to derive the diastolic curve fitting (
) and stiffness (ß) constants (EDP=EDVß). Comparisons were adjusted for age, sex, and body size. HFnlEF patients had more severe renal dysfunction, yet smaller end-diastolic volume index and cardiac output and increased EDP compared with both hypertensive and healthy controls. Arterial elastance and ventricular end-systolic elastance were similarly increased in hypertensive controls and HFnlEF patients compared with healthy controls. In contrast, HFnlEF patients had more impaired relaxation and increased diastolic stiffness compared with either control group.
Conclusions— From these cross-sectional observations, we speculate that the progression of diastolic dysfunction plays a key role in the development of heart failure symptoms in persons with hypertensive heart disease.
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