H. N. Sabbah

Noninvasive evaluation of left ventricular performance based on peak aortic blood acceleration measured with a continuous-wave Doppler velocity meter.

Peak aortic blood acceleration is recognized to be a sensitive index of global left ventricular performance. In the present study peak acceleration was assessed noninvasively in patients with a continuous-wave Doppler velocity meter. Peak aortic blood velocity and peak blood acceleration were measured by placing the ultrasonic transducer at the suprasternal notch. Measurements were obtained in 36 patients undergoing diagnostic cardiac catheterization. Peak velocity and acceleration were measured at rest just before left ventriculography. In patients with ejection fractions greater than 60%, peak acceleration was 19 +/- 5 m/sec/sec. In patients with ejection fractions of 41% to 60%, peak acceleration was lower, at 12 +/- 2 m/sec/sec (p less than .001). In patients with ejection fractions of 40% or less, peak acceleration (8 +/- 2 m/sec/sec) was markedly lower than in patients with ejection fractions greater than 60% (p less than .001). Peak acceleration showed a good linear correlation with ejection fraction (r = .90), and a better power fit (r = .93). These results indicate that peak acceleration, measured noninvasively with a continuous-wave Doppler velocity meter, is a useful indicator of global left ventricular performance.

Modulating effect of regional myocardial performance on local myocardial perfusion in the dog.

We studied the effect of regional contractile performance on regional coronary blood flow and flow distribution in 10 dogs. The left anterior descending (LAD) coronary artery was cannulated and perfused. Maximal vasodilation was obtained with adenosine. Consequently, variations of LAD flow reflected changes of extravascular resistance, lidocaine injected in the LAD caused a localized reduction of contractile performance as shown by the absence of systolic wall thickening. Global left ventricular performance and pressure were unchanged. Coronary extravascular resistance diminished and LAD flow increased from 4.8 ± 0.5 to 6.2 ± 0.6 ml/min per g (P< 0.02). The endocardia!: epicardial ratio increased from 1.02 ± 0.07 to 1.28 ± 0.07 (P < 0.001). Isoproterenol in the LAD augmented systolic wall thickening. Regional coronary flow diminished from 5.1 ± 0.5 to 3.3 ± 0.4 ml/ min per g (P < 0.001), and the endocardia!:epicardial ratio diminished from 1.08 ± 0.07 to 0.75 ± 0.07 (P < 0.01). These data indicate that myocardial contractility is a major component of extravascular coronary resistance and is a mechanical determinant of coronary blood flow and its transmural distribution. Circ Res 45: 634-841, 1979

Comparison of the distribution of intramyocardial pressure across the canine left ventricular wall in the beating heart during diastole and in the arrested heart. Evidence of epicardial muscle tone during diastole.

Computations of compliance of the left ventricle (LV) during diastole assume passive tissue characteristics. To evaluate this assumption, we measured diastolic LV intramyocardial pressure simultaneously in the subepicardium and subendocardium in 18 open-chest dogs, using 1-mm in diameter micromanometers. Subepicardial pressure, 26 ± 1 mm Hg (mean ± SKM) exceeded subendo-cardial pressure, 14 ± 1 mm Hg (P < 0.001), and it exceeded left ventricular end-diastolic pressure (LVEDP) (9 ± 1 mm Hg) (P < 0.001). After an infusion of dextran-40 (10 dogs), subepicardial diastolic pressure increased to 42 ± 4 mm Hg which was higher than diastolic subendocardial pressure, 26 ± 2 mm Hg (P < 0.001) and LVEDP, 24 ± 2 mm Hg (P < 0.001). Following cardiac arrest (12 dogs) with the intramyocardial probes unchanged in position, LV intracavitary pressure, 9 ± 1 mm Hg, and suben-docardial pressure, 13 ± 3 mm Hg, did not differ significantly from the pressures in the beating heart. Subepicardial pressure, 9 ± 1 mm Hg, was lower than in the beating heart (P < 0.001). Following distension of the arrested LV (12 dogs), subepicardial pressure, 31 ± 7 mm Hg, was lower than both subendocardial pressure, 58 ± 12 mm Hg (P < 0.001) and LV intracavitary pressure, 54 ± 11 mm Hg (P < 0.001). These observations indicate that tone is maintained by the subepicardium during diastole. Furthermore, the LV wall does not appear to behave as a passive shell during ventricular filling. Circ Res 47: 258-267, 1980

Exploration of the cause of the low intensity aortic component of the second sound in nonhypotensive patients with poor ventricular performance.

SUMMARYThis investigation was undertaken to explore the cause of the diminished second sound (S2) that may occur in normotensive patients with poorly performing ventricles. Intraaortic sound and pressure were measured in 16 patients with angina; eight had normal ventricular performance (ejection fraction .60%) and eight had poor performance (ejection fraction < 50%). The amplitude of S, was lower in patients with poor ventricular performance as was negative dp/dt. Aortic pressure was com- parable in both groups. The ampitude of S2 was linearly related to the rate of change of the pressure gradient that developed across the aortic valve during diastole (r = 0.82). The latter also correlated with negative dp/dt (r = 0.82). These observations indicate that in patients with poor ventricular performance, isovolumic relaxation may be compromised. This would cause a reduction of the rate of development of the diastolic pressure gradient, which would result in a diminished S2.

The aortic closure sound in pure aortic insufficiency.

The second sound in aortic insufficiency has been described as accentuated, normal, or moderately diminished. A study of intracardiac phonocardiograms was performed to evaluate its intensity and to eliminate extracardiac factors. Pressure and intracardiac sound measurements were made in 28 patients undergoing diagnostic cardiac catheterization. Recordings were obtained above the aortic valve and within the left ventricle in 14 patients with normal aortic valves and 11 patients with aortic insufficiency uncomplicated by aortic stenosis. The amplitude of the aortic closure sound in the patients with pure aortic insufficiency, 1000 ± 100 dynes/cm, was significantly lower than in those patients with normal aortic valves, 3100 ± 200 dynes/cm2 (P < 0.001). The results indicate, therefore, that the presence of aortic insufficiency causes a diminished amplitude of the aortic closure sound. These results are supportive of the theory that the second heart sound is caused by diastolic vibrations of the closed aortic cusps. Diminished valvular vibrations and sound would occur in pure aortic insufficiency if the valve is unable to properly tense during diastole, or if the rate of development of the driving pressure is diminished.

Intramyocardial pressure and coronary extravascular resistance

Intramyocardial pressure is an indicator of coronary extravascular resistance. During systole, pressure in the subendocardium exceeds left ventricular intracavitary pressure; whereas pressure in the subepicardium is lower than left ventricular intracavitary pressure. Conversely, during diastole, subepicardial pressure exceeds both subendocardial pressure and left ventricular pressure. These observations suggest that coronary flow during systole is possible only in the subepicardial layers. During diastolic, however, a greater driving pressure is available for perfusion of the subendocardial layers relative to the subepicardial layers. On this basis, measurements of intramyocardial pressure contribute to an understanding of the mechanisms of regulation of the phasic and transmural distribution of coronary blow flow.

Assessment of papillary muscle function in the intact heart.

A technique is described to localize the anterolateral papillary muscle and to assess its performance in vivo. Using this technique, we measured sequentially the pressure generated within the anterolateral papillary muscle and its changes in length during the cardiac cycle in eight open-chest anesthetized dogs. Pressure within the anterolateral papillary muscle was measured with a 1.6 mm diameter micromanometer probe. Its dimensional changes were measured with ultrasonic crystals. Pressure within the anterolateral papillary muscle exceeded left ventricular pressure throughout the entire cardiac cycle. A difference of 200 +/- 23 mm Hg was present between systolic pressure in the anterolateral papillary muscle and left ventricular systolic pressure (348 +/- 25 vs 149 +/- 6 mm Hg) (p less than .001). Shortening of the anterolateral papillary muscle began 25 +/- 2 msec after the upstroke of the aortic pressure, continued throughout isovolumic relaxation, and was maximal 68 +/- 5 msec after the apex of the aortic incisura. The extent and velocity of shortening of the anterolateral papillary muscle were maximal when pressure within the muscle was lowest. This temporal dissociation between pressure and dimensional changes of the anterolateral papillary muscle appeared to result from cyclic changes of loading imposed on the muscle.