© 2004 by European Society of Cardiology
Copyright © 2004, European Society of Cardiology
Mechanisms of heart failure with well preserved ejection fraction in dogs following limited coronary microembolization
aDepartment of Cardio-Nephrology, Chinese PLA General Hospital, 28 Fuxing Road, Beijing 100853, China
bDivision of Anesthesiology, College of Physicians and Surgeons of Columbia University, New York City, NY 10032, USA
cDivision of Cardiovascular Medicine, Henry Ford Heart and Vascular Institute, Henry Ford Health System, Detroit, MI 48202, USA
dDivision of Circulatory Physiology, College of Physicians and Surgeons of Columbia University, New York City, NY 10032, USA
eDepartment of Surgery, University of Maryland School of Medicine, Baltimore, MD 21201, USA
* Corresponding author. Tel.: +86-10-68152720; fax: +86-10-67089714. E-mail address: hekunlun2002{at}yahoo.com
Objective: It has been suggested that in some settings, heart failure (HF) may occur with normal ejection fraction (EF) as a consequence of undetected systolic dysfunction. However, others have argued that this can only occur in the presence of diastolic dysfunction. We therefore sought to determine the contribution of diastolic dysfunction in an animal model of HF with normal EF. Methods and results: Limited myocardial injury was induced in 21 dogs chronically instrumented to measure hemodynamics and LV properties by daily coronary microembolization (
115 µm beads) until LV end diastolic pressure (LVEDP) was 
16 mm Hg. Nine dogs developed HF within 16±6 days (LVEDP 12±2 vs. 21±2 mm Hg, p<0.001) with no significant change in dP/dtmax (2999±97 vs. 2846±189 mm Hg/s), mean arterial pressure (103±4 vs. 100±4 mm Hg), EF (57±5% vs. 53±4%) or Ees (end-systolic elastance, 3.1±0.9 vs. 2.9±0.8 mm Hg/ml) but with an 10 ml increase in Vo (14±12 vs. 25±16 ml; p<0.01). The EDPVR and time constant of relaxation (
, 25±3 vs. 28±3 ms) did not change significantly. These animals were hemodynamically stable out to 3 1/2 months. Neurohormonal activation occurred (elevations of NE, AngII, BNP) and there was intravascular volume expansion by 16% (p<0.05). Conclusions: A small amount of myocardial injury can lead to neurohormonal activation with intravascular volume expansion and elevation of LVEDP in the absence of reductions in dP/dtmax or EF and without diastolic dysfunction. Thus, HF with preserved EF does not a priori equate with diastolic heart failure.
KEYWORDS Heart failure; Diastole; Autonomic nervous system; Pressure–volume relationships
Time for primary review 19 days
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