Determinants of ejection performance in aortic stenosis.

Abstract

SUMMARY The cause of reduced ejection performance in patients with aortic stenosis is controversial. The relative contribution of afterload and contractility was evaluated in 76 patients with pure or predominant valvular aortic stenosis studied by left ventricular micromanometry and quantitative cineangiography. Thirteen patients without detectable heart disease served as controls. The ejection performance was assessed in terms of the mean normalized systolic ejection rate (MNSER, normal 2 2.0 end-diastolic volumes (EDV)/sec), contractility by total pressure Vmax (normal 2 1.47 muscle lengths/sec) and/or peak measured velocity of shortening (normal 1.14 muscle lengths/sec) and afterload by peak systolic circumferential wall stress (normal < 460 dyn . 10'/cm2).The patients were divided into four groups according to the level of isovolumic contractility and peak systolic wall stress. In group 1, contractility and wall stress were normal. In group 2, contractility was normal and wall stress was increased. Wall THE NATURE of depressed left ventricular ejection performance in chronic pressure-overload hypertrophy due to aortic stenosis is controversial. Whereas excess afterload accompanied by inadequate hypertrophy of normally functioning cardiac muscle has been suggested as the cause of impaired left ventricular shortening,' intrinsic depression of contractility of the hypertrophied myocardium has also been considered, at least in part, to be the cause of altered ejection performance.2 We studied 76 patients with aortic stenosis using high-fidelity micromanometry and quantitative cineangiocardiography and found evidence that both altered contractility and increased afterload are operative in depressing left ventricular ejection performance. Depression of contractile state occurred not only in a subset of patients with inadequate hypertrophy,f' 7 but also in a subset of patients with adequate hypertrophy, suggesting a nonuniform quality of the myocardium in pressure-overload hypertrophy. Material and Methods PatientsSeventy-six patients (17 females and 59 males) with pure or predominant aortic stenosis were studied by right-and left-heart catheterization and cineangiocardiography.

Influence of aortic valve disease on systolic stiffness of the human left ventricular myocardium.

“…18 A depression in both the velocity-load and shortening-load relationship have been observed in experimental models of pressure overload. 19 By the latter relationship, shortening deficits have identified patients with either aortic stenosis or aortic insufficiency.9 20 However, the ejection fraction-afterload relationship is limited as a measure of inotropic state by the extent to which ejection fraction is dependent on resting length ("preload"). In FIGURE 1.…”

“…The finding that depressed ejection performance was accompanied by elevated systolic stress led Gunther and Grossman22 to conclude that afterload mismatch, and not contractile impairment, was responsible for depressed performance. However, Huber et al 20 derived subnormal values of maximum shortening velocity (Vmax) in subsets of patients with aortic stenosis in whom hypertrophy was severe. This result was corroborated by Wisenbaugh et al' with ejection fraction-afterload relationships indicating that shortening deficits could not be attributed solely to afterload mismatch.…”

“…Thus one could speculate that differences in results among previous studies of aortic stenosis lie in the different methods of estimating contractile state: those based on force, which demonstrated normal function,21 and those based on shortening potential, which demonstrated abnormal function. 20 There is precedent for the concept that some pathologic processes may produce a disparity between systolic stiffness and shortening potential. Sunagawa et al ' ESPVR data previously published by others, increased normalized chamber stiffness was found in patients with decompensated congestive heart failure.…”

Evaluation and Management of Patients With Aortic Stenosis

“…Depressed ejection fraction in aortic stenosis has two basic causes: afterload mismatch and contractile dysfunction. 18 Huber and colleagues 19 have demonstrated that afterload mismatch is at least partially responsible for left ventricular dysfunction in approximately three quarters of the patients who have it. The greater the role of afterload mismatch for reduced ejection fraction, the better the response to surgery.…”

mRNA cargo no longer on time

“…Here there was an attempt to gain insight into the causes of hypertrophic growth cessation that occurs well before the biological limits of cardiocyte hypertrophy have been reached (3,6). This work is based on the recent experimental observation by Cooper's group (17) that during the progression of pressure overload in canine hearts the dogs broke into two groups: one group developed extensive hypertrophy while retaining normal left ventricle (LV) stress and contractile function; the LVs of the second group initially developed hypertrophy but then stopped growing and developed high LV wall stress and very depressed contractile function.…”