Relaxation–Systolic Pressure Relation

Abstract

This contribution reviews the regulation of left ventricular pressure (LVP) fall by load and relates this regulation to left ventricular contractility. Load regulation of LVP fall has to be distinguished from neurohumoral regulation, from effects induced by arterial reflected waves and from long-term load effects on contractility. The response of LVP fall to a moderate elevation of systolic LVP is highly variable. It depends on the ratio between the actual systolic pressure and peak isovolumetric pressure, defined as "relative load". Up to a relative load of 81% to 84%, LVP fall accelerates. Above this relative load, LVP fall decelerates. Depending on the level of relative load there is a wide variety of effects ranging from moderate acceleration of LVP fall to marked deceleration of LVP fall. Acceleration of LVP fall in response to a load elevation is associated with normal cardiac function, while slowing of LVP fall is associated with impaired cardiac function. Similar but opposite effects are observed with reductions of systolic LVP. Effects of changes in systolic LVP on time constant tau reveal a fair correlation with systolic elastance (Ees), peak dP/dtmax and regional fractional shortening (or ejection fraction). There is an excellent correlation with measured isovolumetric LVP, indicating that contraction-relaxation coupling is close when contractility is expressed in terms of peak isovolumetric pressure. Assessment of contractility with systolic LVP-relaxation relation is precise and load independent and can be performed with the sole use of a high-fidelity pressure gauge positioned in the left ventricular cavity.

Time course and mechanisms of left ventricular systolic and diastolic dysfunction in monocrotaline-induced pulmonary hypertension

“…While in healthy hearts small afterload elevations accelerate LV pressure fall and only marked afterload increases slow it, in failing hearts even slight increases in afterload may induce slower relaxation. At a similar systolic LV pressure, in failing hearts the relative load, defined as the ratio of systolic LV pressure to isovolumetric LV pressure, is higher, the afterload reserve is surpassed and afterload mismatch yields a pronounced slowing of LV pressure fall, compared with healthy hearts [10,31].…”

“…In the present study, we analyzed biventricular hemodynamics, LV myosin heavy chain (MHC) protein isoforms, LV myocardial expression of genes involved in neurohumoral activation (angiotensin-converting enzyme and endothelin-1), extracellular matrix remodelling (tenascin-C gene expression and interstitial fibrosis) and apoptosis (TUNEL assay), 4 and 6 weeks after MCT injection. Hemodynamics were studied at baseline and in response to single-beat afterload elevations, which allow the detection of diastolic dysfunction that may not be evident during evaluation at rest, but is revealed during exercise or hemodynamic stress [9,10,19,20,26,48].…”

Distinct load dependence of relaxation rate and diastolic function in Oryctolagus cuniculus and Ratus norvegicus

“…The preceding beat is control and the following beat is test heartbeat. The analysed intervention, therefore, was a selective alteration of afterload without changes in preload or long-term load history (Gillebert et al 1997). Systolic LVP of the first heartbeat following the intervention varied as a function of the extent of aortic constrictions.…”

Left Ventricular Relaxation Abnormality Is Detectable by Analysis of the Relaxation Time Constant in Patients With Atrial Fibrillation

“…13 Both the horizontal and vertical positions of the J-shaped curve are dependent on the magnitude of the peak isovolumetric LV pressure and could be manipulated by inotropic interventions. 13,17 Moreover, Eichhorn et al demonstrated that relaxation became highly afterloaddependent with systolic dysfunction. 16 They demonstrated that R (the slope of the -to-end-systolic pressure relation) was flat when contractility was normal.…”

“…16,17 Moreover, this method of analysis of LV relaxation was successfully applied to a tachycardia-induced heart failure model in dogs. 18 Therefore, in the present study we analyzed on a beat-to-beat basis in patients with both AF and impaired LV systolic function by means of the force (relaxation) -interval relationships, as well as afterload-dependence.…”