© 1999 by European Society of Cardiology
Copyright © 1999, European Society of Cardiology
Afterload induced changes in myocardial relaxation
A mechanism for diastolic dysfunction
Department of Physiology, Faculty of Medicine, University of Porto, Porto, Portugal
* Corresponding author. Tel.: +351-2-5508-452; fax: +351-2-5519-194 amoreira{at}med.up.pt
Background: Diastolic left ventricular (LV) dysfunction manifests as an upward shift of the diastolic pressure–volume relation. One of the possible causes of diastolic LV dysfunction is incomplete myocardial relaxation. It is well known that high afterload slows myocardial relaxation. This contribution investigated to what extent afterload elevation could also affect LV filling pressures including end-diastolic LV pressure (LVP). Methods: Selective, beat-to-beat elevations of afterload were induced in anaesthetised open-chest rabbits (n=9) by abrupt narrowing of the ascending aorta during the diastole of the preceding heartbeat. This was performed with physiological heart rate and blood pressure. Results: These interventions increased systolic LVP from 90±3 mm Hg at baseline to 103±4, 123±5, 139±5 and 154±6 mm Hg. The last intervention was a total aortic occlusion inducing a first beat isovolumetric contraction. Smaller afterload elevations decreased 
(accelerated LVP fall) and did not elevate diastolic pressure-internal diameter relation (P-ID). Larger afterload elevations increased (decelerated LVP fall), induced an upward shift of the diastolic P-ID and increased end-diastolic LVP. Effects of afterload on end-diastolic LVP were correlated with effects on (r=0.89; P<0.01). Incomplete relaxation or load-dependent residual active state appeared to be the mechanism for this diastolic dysfunction. Similar findings were made retrospectively in dogs instrumented with circumferential segment length gauges (n=16). Conclusions: Diastolic LV dysfunction was induced by elevated afterload in healthy hearts of rabbits and dogs. If this mechanism could be shown to be operative in the failing heart, reversal of diastolic dysfunction should contribute to the beneficial effects of vasodilating and inotropic therapy on pulmonary congestion.
KEYWORDS ID, Anterior–posterior left ventricular internal diameter; LV, Left ventricle or left ventricular; LVP, Left ventricular pressure; Relative load, ‘systolic LVP/isovolumetric LVP (%)’; ED(pre), End-diastole at the beginning of the cardiac cycle; ED(post); End-diastole at the end of the cardiac cycle
1 T.C. Gillebert is from the Department of Cardiology, University of Antwerp, Belgium.
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