Preload dependence of fiber shortening rate in conscious dogs with left verntricular hypertrophy

Abstract

Employing the new concept of systolic myocardial stiffness, this study addresses the questions of linearity of the end-systolic stress-strain relations in left ventricular hypertrophy and the preload dependence of fiber shortening rate. Pressure overload hypertrophy was induced in six puppies by banding the ascending aorta. Ultrasonic crystals were implanted for measurement of short axis and wall thickness in the six dogs with hypertrophy and in five control dogs. A pressure catheter was inserted through the apex for left ventricular pressure measurement. Load was altered by graded infusions of phenylephrine in the setting of beta-adrenergic blockade. Linearity of the end-systolic stress-strain relations was observed in all cases, and preload-corrected shortening rate-afterload relations were derived from these stress-strain relations. Without preload correction, mid wall and endocardial shortening rate were depressed (p less than 0.05 and p less than 0.005, respectively) in the hypertrophy group. However, with preload correction at 35 g/cm2, there was no significant difference in shortening rate between the control and hypertrophy groups at afterloads of 150, 200 and 250 g/cm2. Endocardial shortening rate at a preload of 25 versus 35 g/cm2 demonstrated a preload dependence in both the control (p less than 0.04) and the hypertrophy group (p less than 0.01). Mid wall shortening rate displayed a preload dependence only in the hypertrophy group (p less than 0.05). It is concluded that end-systolic stress-strain relations are linear in control conditions and in hypertrophy, fiber shortening rate is preload-dependent and, thus, shortening rate-afterload relations currently used to assess myocardial contractility need to be modified to account for these preload effects.

Wall thickness referenced to myocardial volume: a new noninvasive framework for cardiac mechanics

“…Results comparable with the present study are theoretically obtainable when midwall measurements are normalized or referenced to calculated values at zeroluminal volume rather than end-diastolic dimensions, as have been used previously (12,13,20,27,30). The mathematical relationship between wall-thickness ratios and midwall-diameter ratios is not linear, however (see the APPENDIX); therefore, the shapes of the relationships with stress, work, and power may also be different.…”

“…Other noninvasive methods of ventricular performance assessment, such as FS (7), velocity of circumferential fiber shortening (VCF) (5), and corrected VCF (VCF c ) (8), use end diastole as a reference state. This is also true for some invasive methods (20). However, natural variation in end-diastolic distension from beat to beat would be expected to result in additional random scatter not accounted for by an underlying Fig.…”

Echocardiographic assessment of left ventricular midwall mechanics in spontaneously hypertensive rats

“…Supernormal LV performance has been recognized in subsets of humans 12,13 and animals with experimental hypertension, 14 due to an increased contractility and/or the use of preload reserve, especially in the absence of adequate LV hypertrophy. 15,16 As shown in human studies, 17,18 in rats with renovascular hypertension 19 and in Dahl salt-sensitive animals, 20 the assessment of LV function by measuring the extent of fiber shortening at the endocardium level is less appropriate than using the value calculated at the midwall. This region represents both the anatomical site of circumferential myocardial fibers and the approximate level where mean transmural wall stress is applied.…”

Impaired Left Ventricular Circumferential Midwall Systolic Performance Appears Linked to Depressed Preload, but Not Intrinsic Contractile Dysfunction or Excessive Afterload, in Paradoxical Low-Flow/Low-Gradient Severe Aortic Stenosis

“…Thirty years ago, in an experimental model of pressure-overload LV hypertrophy, Mirsky et al [ 26 ] demonstrated that the correction for preload, considerably lower in animals with versus without pressure overload-induced concentric LV hypertrophy for any given afterload, entirely eliminated an artifactual depression of LV contractility derived from end-systolic stress–shortening relations when preload was not accounted for. In brief, depressed LV systolic performance might result not from an apparent impairment of the intrinsic LV contractile state, but from a smaller LVd according to the Frank–Starling law.…”

“…In particular, circumferential LV strain [ 30 , 31 , 32 , 33 ] and meridional ESS [ 34 ] were comparable in P-LFLG-AS and NFHG-AS, in contrast to early impairment of longitudinal LV systolic function in P-LFLG-AS [ 1 , 30 , 31 , 32 ] which was linked to elevated Zva and diminished systemic arterial compliance [ 30 , 31 , 32 , 34 ]. Importantly, mwFS is largely controlled by circumferentially oriented fibers which predominate in the myocardial midwall, while subendocardial fibers are mainly oriented in the meridional direction [ 14 , 15 , 16 , 17 , 26 ].…”