VENTRICULAR PERFORMANCE 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 suprastemal 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 < .001). In patients with ejection fractions of 40% or less, peak acceleration (8 ± 2 mlsec/sec) was markedly lower than in patients with ejection fractions greater than 60% (p <. 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. Circulation 74, No. 2, 323-329, 1986. IN 1964 Rushmer suggested that the left ventricle acts as an impulse generator and that the "initial ventricular impulse" is a descriptive term for the dynamic properties of ventricular ejection.1 Ventricular impulse was defined as the product of force and time, where the net force (mass x acceleration) acts over time from the beginning of ejection to the attainment of peak flow. Because the peak acceleration of blood out of the ventricle occurs in early systole, it is thought to represent a manifestation of the initial ventricular impulse.' Studies by Noble et al.2 suggested that peak acceleration was closely related to the maximum force exerted by the ventricle in early systole, and they believed that peak acceleration was also related, in some way, to the maximum initial velocity of shortening of left ventricular muscle. Studies by Stein and Sabbah3 showed that blood acceleration was intrinsic to the rate of change in power developed by the left ventricle and related closely to it. Peak blood acceleration was also shown to be a function of both the rate and acceleration of shortening of the radius of the left ventricle.4 Studies in anesthetized dogs showed that peak acceleration of aortic blood flow was sensitive to alterations in the inotropic state but was less affected by an augmentation of preload and afterload.3 Peak acceleration of aortic blood flow was also found to be sensitive to alterations in the contractile state induced by temporary regional myocardial ischemia in conscious dogs.2 Studies by Stein and Sabbah5 using catheter-tip velocity sensors during cardiac catheterization in patients showed that peak acceleration was capable of differentiating patients with normal from those with abnormal left ventricular performance. In 12 patients undergoing diagnostic cardiac catheterization, Bennett et al. ,6 using catheter-tip velocity transducers, demonstrated a close relationship between peak acceleration and left ventricular ejection fraction calculated angiographically.6 The above investigations establish peak blood acceleration as a good index of global left ventricular perVol. 74, No. 2, August 1986 From Henry Ford Heart and Vascular Institute, Detroit. Address for correspondence: Paul D. Stein, M.D., Henry Ford Hospital, 2799 West Grand Blvd., Detroit, MI 48202. Received Dec. 2, 1985; revision accepted May 8, 1986. 323 by gest on Jauary 5, 2018 http://ciajournals.org/ D ow nladed from