Copyright © 1990 by the European Society of Cardiology.
© 1990 The European Society of Cardiology
Regulation of left ventricular pressure fall
Department of Physiology and Department of Cardiology, University of Antwerp Belgium
Address of Correspondence: Dirk L Brutsaert, MD, PhD, Department of Physiology, RUCA, University of Antwerp, Groenerborgerlaan, 171, 2020 Antwerpen, Belgium
Left ventricular pressure (LVP) fall is a manifestation of relaxation and is therefore regulated by non-uniformity and load, besides regulation by muscle inactivation.
Non-uniformity and load are important and independent regulators of LVP fall. Non-un formity induces a premature onset and decreased rate of LVP fall. With regard to load, the effects of preload, systolic LVP levels and systolic LVP waveform are distinct. In order to assess underlying muscle inactivation with indexes of LVP fall, it is critical to control non-uniformity and various aspects of load. This control should be inherent in experiments designed to evaluate interventions. If careful control of non-uniformity and load cannot be achieved, at least the effects of non-unformity and load on timing and rate of LVP falls should be appreciated.
Isovolumetric left ventricular pressure fall is a complex event including a rapid early andslower late phase. As a consequence, LVP fall cannot be described by a single index. Peak – dP/dt is measured at the transition between early and late LVP fall. Its value can be affected by changes of both phases. Interpretation of peak – dP/dt should therefore be cautious. LVP fall at and after mitral valve opening might be regulated differently from late LVP fall, as evaluated by the time constant
. Loading effects of LVP fall after mitral valve opening can therefore not always bepredictedfrom changes in
.
Load dependence is a concept based on experimental observations in isolated cardiac muscle, which describes the separation in time between shorter isotonic and longer isometric twitches. Temporal separation is illustrated by the response of cardiac muscle to late systolic load. The latter induces premature onset of relaxation, followed by accelerated isotonic, or decelerated isometric relaxation. LVP fall is regulated by load dependence. When LVP increases, LVP fall is delayed. Late LVP fall seems to be predominantly regulated by isometric load dependence, and decelerates with increased late systolic LVP. Early LVP fall can accelerate with late systolic LVP. The relation of this phenomenon to isotonic load dependence is as yet unclear.
Key Words: Relaxation diastolic function pressure fall
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