Pre- and postoperative left ventricular contractile function in patients with aortic valve disease.

Krayenbuehl, H. P.; Turina, Marko; Hess, Otto M.; Rothlin, M; Senning, Å

doi:10.1136/hrt.41.2.204

Cited by 50 publications

(17 citation statements)

References 22 publications

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“…The present results combined with the clinical studies of Krayenbuehl et al (1979), and their unpublished studies with Mirsky, may provide a clue as to the appropriate timing of surgical/medical intervention in patients with pressure-overloaded ventricles. Krayenbuehl et al (1979) have shown in a number of pre-and postoperative studies in patients with valvular heart disease that prognosis is poor in those patients whose ventricles have overcompensated for wall mass, since their wall masses and volumes were not markedly reduced postoperatively.…”

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confidence: 60%

Time course of changes in the mechanical properties of the canine right and left ventricles during hypertrophy caused by pressure overload.

Mirsky¹,

Laks²

1980

Circulation Research

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We developed a mathematical model of the right and left ventricles to determine whether there is a change in the mechanical properties of muscle during the hypertrophy process resulting from pulmonary arterial banding. Pressure-volume data were obtained from 10 normal dog hearts and 8 dog hearts in which the pulmonary artery was banded for periods of 2--40 weeks. These data were applied to the model, and the time course of wall stress and muscle stiffness was quantified for both ventricles. The results demonstrate that (1) myocardial stiffness is increased in pressure-overload hypertrophy (2) normal right and left ventricular muscle exhibits similar mechanical properties and (3) the relationships between wall stresses and the volume/mass ratios to the period of banding are biphasic. We concluded that (1) increase in muscle stiffness is due to several factors. In the early stages of hypertrophy, it may be predominantly due to fibrosis and, in the later stages, to substantial increases in muscle mass. (2) The progressive increase in muscle stiffness concomitant with the increase in muscle mass may be due to the presence of myocardial cellular projections and fibrosis. (3) The appropriate timing for surgical/medical intervention should take place before low volume:mass ratios and, hence, low wall stresses are attained.

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confidence: 60%

Time course of changes in the mechanical properties of the canine right and left ventricles during hypertrophy caused by pressure overload.

Mirsky¹,

Laks²

1980

Circulation Research

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“…Patients with aortic valve disease who had residual left ventricular dysfunction after aortic valve replacement showed a significantly higher preoperative muscle mass than those with a normal or nearly normal postoperative left ventricular function. 23 In conclusion, we present evidence that in chronic pressure overload from aortic stenosis, ejection performance is not solely determined by the extent of afterload, but is also influenced by the actual inotropic state. Thus, there is no unique inverse relationship between systolic stress and ejection performance; rather, this relationship is shifted to a lower level when contractility is depressed.…”

Section: Discussionmentioning

confidence: 83%

Determinants of ejection performance in aortic stenosis.

Huber¹,

Grimm²,

Koch³

et al. 1981

Circulation

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155

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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.

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“…15 16 The effect of aortic valve replacement on myocardial structure is, however, not yet established, and it is not known whether there is a regression of hypertrophy at the cellular level parallel to the decrease in angiographically measured muscle mass, or whether interstitial fibrosis remains unchanged after aortic valve replacement. Since myocardial structure is the major determinant of diastolic myocardial function,4 14 we determined diastolic chamber and myocardial stiffness from viscoelastic pressure-circumference and stress-strain relationships in 21 patients with aortic valve disease before and after successful valve replacement and compared these data to structural findings obtained from left ventricular endomyocardial biopsies taken during cardiac catheterization.…”

Section: Discussionmentioning

confidence: 99%

Diastolic stiffness and myocardial structure in aortic valve disease before and after valve replacement.

Hess¹,

Ritter²,

Schneider³

et al. 1984

Circulation

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225

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Passive diastolic properties were determined in 10 control patients and 21 patients with aortic valve disease before and 17.5 months after successful valve replacement. Ten patients had severe aortic stenoses (AS), five had combined aortic valve lesions (AS + aortic insufficiency [AI]), and six patients had severe Al. Left ventricular endomyocardial biopsies were obtained before and after surgery in patients with AS, AS + AI, and AI. Simultaneous echocardiographic and high-fidelity pressure measurements were made in all patients, and left ventricular chamber stiffness was calculated from a viscoelastic pressure-circumference relationship and left ventricular myocardial stiffness from a viscoelastic stress-strain relationship. The constant of chamber stiffness, ,B', was slightly although not significantly increased in patients with AS (0. 27 before and 0.24 after surgery), but was normal in those with AS + AI (0.22 before and 0. 17 after surgery) and slightly decreased in those with AI (0. 18 before and 0.16 after surgery) when compared with in control subjects (0.21). The constant of myocardial stiffness P3 was normal in patients with AS (13.2), AS + AI (11.5), and AI (11.7) before surgery compared with in the control group (12.5). increased, however, significantly in those with AS (25.2; p < .02), but not in those with AS + AI (16.3; NS) and AI (12.8; NS) after surgery. Myocardial morphologic characteristics showed a significant decrease in muscle fiber diameter in patients with AS, AS + AI, and AI, as well as a significant increase in interstitial fibrosis from 15% to 26% (p < .05) in those with AS and a slight increase from 15% to 22% (NS) in those with AS + AI and from 19% to 24% (NS) in those with AI. Left ventricular fibrous content (left ventricular muscle mass index multiplied by interstitial fibrosis) remained, however, unchanged in all three groups after aortic valve replacement. In conclusion, left ventricular chamber stiffness is increased in AS but decreased in AI, whereas LV myocardial stiffness is normal in patients with aortic valve disease before surgery. After surgery, left ventricular myocardial stiffness increased significantly in AS patients but remained unchanged in those with AI. Postoperative changes in myocardial structure were characterized by a decrease in muscle fiber diameter and a relative increase in interstitial fibrosis, whereas fibrous content remained unchanged. Thus, regression of myocardial hypertrophy in aortic valve disease is accompanied by an increase of myocardial stiffness in concentric hypertrophy that is not seen in eccentric hypertrophy. Circulation 69, No. 5, 855-865, 1984. MYOCARDIAL HYPERTROPHY is a basic adaptive mechanism of the heart to compensate for an increased mechanical load. An (group 2) with a mean regurgitant fraction of 0.59 and no or only a mild systolic pressure gradient <20 mm Hg (mean systolic pressure gradient 2 mm Hg). A coronary arteriographic examination was carried out in each patient, and in only one patient was a 50% stenosis o...

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Pre- and postoperative left ventricular contractile function in patients with aortic valve disease.

Cited by 50 publications

References 22 publications

Time course of changes in the mechanical properties of the canine right and left ventricles during hypertrophy caused by pressure overload.

Time course of changes in the mechanical properties of the canine right and left ventricles during hypertrophy caused by pressure overload.

Determinants of ejection performance in aortic stenosis.

Diastolic stiffness and myocardial structure in aortic valve disease before and after valve replacement.

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