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Load dependent diastolic dysfunction in heart failure
T C Gillebert1, A F Leite-Moreira, S G De Hert
1Division of Cardiology, University of Antwerp, Belgium. gillebe@uia.ua.ac.be
Insights
Load-dependent diastolic dysfunction, a cause of congestive heart failure (CHF), occurs when heart muscle relaxation is impaired by increased pressure or venous return. Treatment involves reducing systolic pressures and venous return.
Area of Science:
- Cardiology
- Physiology
Background:
- Congestive heart failure (CHF) can stem from systolic or diastolic dysfunction.
- Diastolic dysfunction involves impaired left ventricular filling due to structural or functional causes.
- Slow and incomplete myocardial relaxation is a key functional cause of diastolic dysfunction.
Purpose of the Study:
- To analyze slow and incomplete myocardial relaxation in response to changes in systolic pressure and venous return.
- To investigate the concept of load-dependent diastolic dysfunction.
Main Methods:
- Analysis of myocardial relaxation dynamics in response to varying systolic pressure and venous return.
- Examination of the transition point from myocardial contraction to relaxation.
Main Results:
- Myocardial relaxation becomes slow and incomplete when load exceeds a critical transition point (0.82 of peak isovolumetric pressure).
- This load-dependent diastolic dysfunction occurs in normal hearts with high afterload and in diseased hearts.
- This dysfunction contributes to elevated filling pressures in severe CHF.
Conclusions:
- Load-dependent diastolic dysfunction is a significant factor in CHF pathophysiology.
- Decreasing systolic pressures or venous return can reverse this dysfunction.
- Aggressive treatment of CHF patients with diuretics and vasodilators is supported by these findings.
Abstract:
Congestive heart failure may result from cardiovascular overload, from systolic or from diastolic dysfunction. Diastolic left ventricular dysfunction may result from structural resistance to filling such as induced by pericardial constraint, right ventricular compression, increased chamber stiffness (hypertrophy) and increased myocardial stiffness (fibrosis). A distinct and functional etiology of diastolic dysfunction is slow and incomplete myocardial relaxation. Relaxation may be slowed by pathological processes such as hypertrophy, ischemia and by asynchronous left ventricular function. The present contribution analyses the occurrence of slow and incomplete myocardial relaxation in response to changes in systolic pressure and in response to changes in venous return. The regulation of myocardial relaxation by load is critically dependent on the transition from myocardial contraction to relaxation, which occurs in dogs when 82% of peak isovolumetric pressure has developed or at a relative load of 0.82. This corresponds to early ejection in normal hearts, but is situated even before aortic valve opening in severely diseased hearts. When load is developed beyond this transition, relaxation becomes slow and even incomplete. This is load dependent diastolic dysfunction. Load dependent diastolic dysfunction occurs in normal hearts facing heavy afterload and in severely diseased hearts even with normal hemodynamic parameters. This dysfunction should contribute to elevating filling pressures in most patients with severe congestive heart failure. This dysfunction can be reverted by decreasing systolic pressures or by decreasing venous return. Load dependent diastolic dysfunction gives us an additional reason to aggressively treat CHF patients with diuretics and vasodilators.