The hemodynamic manifestation of normal myocardial relaxation. A framework for experimental and clinical evaluation.
Myocardial relaxation clinically manifests itself as left ventricular pressure (LVP) fall. The transition from contraction to relaxation is the precise moment at which 81-84% of peak isometric force has developed or the equivalent timing early during ejection. Defining the completion of relaxation and distinguishing relaxation from diastole appears merely semantic. Diastole is not a passive phase of the cardiac cycle. During diastole mechanical left ventricular properties still change due to incomplete relaxation, due to creep and stress relaxation, and due to autoregulation by preload and by nitric oxide. Description of timing and rate of LVP fall may provide useful information on underlying cardiac diseases such as ischaemia and hypertrophy. This information will however only be reliable if systolic cardiac function and systolic load are normal, and in the absence of a significant degree of nonuniformity, such as induced by conduction disturbances or by regional myocardial ischemia. The various effects of load and of nonuniformity on myocardial relaxation in the normal heart are reviewed. Coupling of timing and rate of LVP fall are explained in terms of cross-bridge mechanics. Specific effects of systolic pressure on LVP fall and their relation to systolic cardiac function are emphasized. These data constitute a conceptual framework for the analysis of myocardial relaxation in cardiovascular research and in the cardiac patient. Comparison of clinical and experimental data during manipulation of afterload should lead to an improved understanding of clinical relaxation disturbances and to a therapeutic approach, which is relevant from the physiopathological point of view. LVP fall may provide useful and quantitative information on systolic LV function if measurements are performed under different conditions of systolic load. This information is similar to systolic pressure-volume relations, but can be performed with the sole use of a micromanometer in the LV cavity.
Gillebert
T C
TC
Division of Experimental Surgery, Cardiology, University of Antwerp, Belgium.
Leite-Moreira
A F
AF
De Hert
S G
SG
D000818:Animals; D004285:Dogs; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D009200:Myocardial Contraction / Q000502:physiology*; D016277:Ventricular Function, Left / Q000502:physiology; D017725:Ventricular Pressure / Q000502:physiology