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Afterload induced changes in myocardial relaxation: a mechanism for diastolic dysfunction
A F Leite-Moreira1, J Correia-Pinto, T C Gillebert
1Department of Physiology, Faculty of Medicine, University of Porto, Portugal. amoreira@med.up.pt
Cardiovascular Research
|October 28, 1999
Summary
Elevated afterload can cause diastolic dysfunction by slowing myocardial relaxation, leading to increased left ventricular filling pressures. This study demonstrates this effect in healthy animal hearts.
Area of Science:
- Cardiology
- Physiology
- Heart Mechanics
Background:
- Diastolic left ventricular (LV) dysfunction is characterized by an elevated diastolic pressure-volume relationship.
- Incomplete myocardial relaxation is a potential cause of diastolic LV dysfunction.
- High afterload is known to impede myocardial relaxation.
Purpose of the Study:
- To investigate the impact of afterload elevation on LV filling pressures, specifically end-diastolic LV pressure (LVP).
- To determine the extent to which increased afterload affects diastolic function.
Main Methods:
- Selective, beat-to-beat afterload increases were induced in anesthetized open-chest rabbits by aortic narrowing.
- Physiological heart rate and blood pressure were maintained during interventions.
- Retrospective analysis was performed on data from instrumented dogs.
Main Results:
- Larger afterload elevations decelerated LVP fall (increased tau) and shifted the diastolic pressure-internal diameter relation upward.
- Increased end-diastolic LVP was observed with significant afterload elevation.
- The effects of afterload on end-diastolic LVP correlated strongly with effects on tau (r = 0.89).
Conclusions:
- Elevated afterload can induce diastolic LV dysfunction in healthy rabbit and dog hearts.
- The mechanism involves incomplete relaxation or a load-dependent residual active state.
- Reversing diastolic dysfunction may contribute to the benefits of certain therapies in failing hearts.