Quantification and Prediction of Myocardial Failure

Siegel, John H.; Sonnenblick, Edmund H.

doi:10.1001/archsurg.1964.01320060094019

Cited by 31 publications

(7 citation statements)

References 15 publications

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“…[10][11][12][13][14][15][16][17][18] However, since in the ejecting ventricle isovolumic dp/dt usually reaches a peak at the opening of the semilunar valves,19 this ratio, as well as peak dp/dt itself, are influenced profoundly by the level of arterial diastolic pressure, and, therefore, the value of these measurements as indices of myocardial contractility are seriously limited. 8 In the present investigation, the possibility was considered that the relation between dp/dt and the simultaneously developed pressure throughout the course of isovolumic contraction, or the dp/dt at a given level of intraventricular pressure during isovolumic systole, might provide an accurate and practical measure of ventricular contractility independent of changes in preload and afterload.…”

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confidence: 99%

Assessment of Cardiac Contractility

et al. 1971

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SUMMARYIt was considered that the relationship between dp/dt and simultaneously developed pressure during the course of isovolumic contraction might afford a more accurate measure of contractility than the maximum rate of intraventricular pressure rise (peak dp/dt). In six cat papillary muscles contracting isometrically from any given preload, the ratio of the rate of tension development (dT/dt) to simultaneously occurring isometric tension always varied directly with the contractile state. This ratio rose slightly as preload was increased, but it was not affected by changes in afterload. In 17 experiments in an intact canine heart preparation in which left ventricular end-diastolic pressure was constant, dp/dt at any given pressure during isovolumetric contraction again was observed to be a function of the contractile state when the latter was enhanced by norepinephrine and acetylstrophanthidin. High-fidelity left ventricular pressures and dp/dt were recorded throughout isovolumic contraction in eight patients. Isoproterenol and exercise raised the level of dp/dt at any given pressure prior to ejection. Interventions known to alter ventricular loading but not to influence the contractile state, such as elevation of ventricular end-diastolic pressure by leg raising and increases in aortic pressure induced by methoxamine, did not influence this relation significantly. In conclusion, the determination of dp/dt and intraventricular pressure throughout isovolumic contraction in the presence of variable arterial pressure and small changes of preload provides a useful, simple, and experimentally verified approach to the assessment of alterations of the contractile state of the heart in intact man.

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confidence: 99%

Assessment of Cardiac Contractility

et al. 1971

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“…In experimental heart failure in the intact dog (19) and in heart failure in man (20) a smaller stroke volume may be associated with an increased diastolic volume, and geometrical considerations therefore imply that delivery of a smaller stroke volume from the same or a larger spherical volume must be associated with a reduction in the extent of shortening of the circumference; further, geometrical factors necessitate that maintenance of systolic ventricular pressure in the face of an enlarged chamber volume results in increased wall tension (21). Finally, several studies have indicated that in the failing ventricle the rate of pressure development during the isometric phase of contraction may be reduced (22,23) and that the time to maximal rate of pressure development may be increased (24).…”

Section: Discussionmentioning

confidence: 99%

The Mechanics of Left Ventricular Contraction in Acute Experimental Cardiac Failure*

Ross¹,

Covell²,

Sonnenblick³

1967

J. Clin. Invest.

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Summary. The effects of acute cardiac failure induced by pentobarbital or pronethalol on the basic mechanical properties of the intact left ventricle were examined in the dog, and the influence on auxotonic and isovolumic contractions of the increase in end-diastolic volume that usually accompanies cardiac failure was assessed. The right heart bypass preparation was employed, and isovolumic beats were induced by sudden balloon occlusion of the aortic root. The ventricular pressure-volume curve was determined directly, and the mechanical responses of the myocardial fibers and contractile elements were calculated.When end-diastolic pressure was held constant, failure reduced the extent of circumferential fiber shortening, and the tension-velocity relation calculated during isovolumic beats was always shifted, with reductions in both maximal velocity (average decrease 30%) and maximal developed tension (average 23%); in addition, during failure achievement of maximal contractile element velocity and maximal tension was delayed, whereas the total duration of contraction was always prolonged. Acetylstrophanthidin tended to reverse all of these changes. When end-diastolic volume was augmented during failure at a constant stroke volume, the extent of circumferential fiber shortening was reduced (3.82 cm to 2.02 cm), and during ejection the fiber and contractile element velocities were diminished at wall tensions comparable to control; maximal velocity and velocity at peak tension were also decreased. The tension-velocity relation during isovolumic beats was shifted by failure with consistent reductions in maximal shortening velocity, but changes in maximal tension were small. Maximal instantaneous power was always reduced by failure, and a striking alteration occurred in the relation between work expended in stretching the series elastic component and the external work; the former, "internal work," increased by an average of 90%, the latter diminished by 11%, and the total contractile element work remained essentially unchanged. These findings are discussed within the framework of a three dimensional model that included fiber length, wall tension, and contractile element velocity. The experimental techniques employed appear to permit a more complete definition of the abnormalities of the ventricular myocardium in experimental failure. They are potentially applicable in the closed-chest animal and allow quantitative determinations of the contractile properties of the left ventricle. Introductionanalysis in terms analogous to those which describe The pattern of left ventricular contraction in the mechanical properties of isolated muscle.

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“…'-5 In the clinical setting, ejection fraction has been shown to be one of the most useful.6'-For example, it is related to prognosis as well as operative risk in patients with coronary artery disease and in those with other forms of heart disease.' [1][2][3][4][5] The angiographic technique for determination of left ventricular ejection fraction is based on the actual calculation of end-diastolic and end-systolic volumes, using the area-length method of Dodge and associates. '6' 17 These calculations require precise measurements of the distances between the left ventricle, the x-ray tube and image intensifier, and then filming a calibration grid at the level of the left ventricle.…”

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Left ventricular ejection fraction calculated from volumes and areas: underestimation by area method.

Wisneski¹,

Pfeil²,

Wyse³

et al. 1981

Circulation

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SUMMARY The ejection fraction is one of the most widely used measurements of left ventricular systolic function. Angiographic measurement of ejection fraction is based on determination of roentgenographic magnification and calculation of end-diastolic and end-systolic volumes, assuming a prolated ellipse. Because it is simple and radiographic magnification may not have been determined, some laboratories have obtained an "ejection fraction" by comparison of end-diastolic and end-systolic areas. A comparison of the two methods was made using ventriculograms of 538 patients from three cardiac catheterization laboratories. The area method of ejection fraction calculation consistently underestimates ejection fraction from left ventricular volumes. A regression equation was derived that allows adjustment of the ejection fraction obtained from areas to that from volumes.LEFT VENTRICULAR FUNCTION has been assessed by many methods. '-5 In the clinical setting, ejection fraction has been shown to be one of the most useful.6'-For example, it is related to prognosis as well as operative risk in patients with coronary artery disease and in those with other forms of heart disease.' [1][2][3][4][5] The angiographic technique for determination of left ventricular ejection fraction is based on the actual calculation of end-diastolic and end-systolic volumes, using the area-length method of Dodge and associates.'6' 17 These calculations require precise measurements of the distances between the left ventricle, the x-ray tube and image intensifier, and then filming a calibration grid at the level of the left ventricle.'8 Some laboratories omit this measurement of the roentgenographic magnification and report an "ejection fraction" based solely on comparison of enddiastolic and end-systolic silhouette areas. Studies have appeared without a description of the method for the determination of ejection fraction.'121 We compared the two techniques of calculating ejection fraction and present a regression curve that allows an accurate and simple determination of ejection fraction without having to take roentgenographic magnification and volume calculation into account. From MethodsThirty-degree right anterior oblique (RAO) left ventriculograms of 538 cases from three cardiac catheterization laboratories were reviewed. Patients with coronary artery disease, valvular disease, cardiomyopathies and congenital heart disease were included. The end-diastolic and end-systolic silhouettes were hand-traced. Volume MethodAssuming the ventricle to be ellipsoid, the volume of each silhouette was derived using the formulas of Dodge and associates.'6-8 Long-axis length (L) was measured from the mid-aortic root to the apex. Area (A) was measured by planimetry and minor axis (D) was calculated as 4A irLThe volumes (V) were then calculated by The areas of the end-diastolic and end-systolic silhouettes measured by planimetry were used to calculate an ejection fraction as

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Quantification and Prediction of Myocardial Failure

Cited by 31 publications

References 15 publications

Assessment of Cardiac Contractility

Assessment of Cardiac Contractility

The Mechanics of Left Ventricular Contraction in Acute Experimental Cardiac Failure*

Left ventricular ejection fraction calculated from volumes and areas: underestimation by area method.

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