NONINVASIVE ASSESSMENT OF INTRINSIC VENTRICULAR LOAD DYNAMICS IN DILATED CARDIOMYOPATHY

On the basis of hemodynamic theory, a new noninvasive method is developed to provide improved insights into the significance of depressed Doppler left ventricular ejection variables in patients with dilated cardiomyopathy. The net force (F) associated with intraventricular flow throughout ejection can be written as: F = A.dv/dt + B.v2, where v is the ejection velocity and A and B are variables related to the geometry of the ventricle and its outflow tract. Instantaneous levels of this force were calculated in 9 normal subjects and 10 patients with dilated cardiomyopathy using Doppler, M-mode and two-dimensional echocardiography. The maximal ejection force (Fmax) was 47.5 +/- 8.5 kdyn in normal subjects and 25.5 +/- 6.2 kdyn in those with dilated cardiomyopathy (p = 0.0001). Peak local acceleration and outflow velocity were severely depressed in those with cardiomyopathy compared with normal subjects (1,260 +/- 129 versus 2,671 +/- 430 cm/s2 and 71 +/- 14 versus 109 +/- 7 cm/s, respectively; p = 0.0001). Maximal ejection force was attained very early in ejection. A significant linear correlation was found between peak outflow acceleration and maximal ejection force (n = 19; r = 0.91, p = 0.0001). At the time of peak ejection velocity, the net force had decreased to 64% of its peak value in those with cardiomyopathy, whereas in normal subjects, it had decreased to only 84% of its peak value (p = 0.008). In normal subjects, the ejection force was positive during the first 75% of ejection, but in those with cardiomyopathy, it was positive only during the first 54% (p = 0.0003). Once its peak value was attained, total left ventricular systolic wall stress declined rapidly during ejection in normal subjects (to 33% of its peak value by end-ejection), whereas it remained elevated throughout ejection in patients with cardiomyopathy (at 60% of its peak value by end-ejection, p = 0.0001 versus normal). The maximal ejection force corresponded to a calculated intraventricular peak pressure gradient of 9.8 +/- 1.6 mm Hg in normal subjects and 6 +/- 1.2 mm Hg in those with cardiomyopathy (p = 0.0001). The average contribution of the intrinsic component of the left ventricular systolic load (that is, wall stress associated with the ventricular to aortic pressure gradient) to the total myocardial load was 9.1% (range 7.3% to 11.2%) in normal subjects and 6.2% (range 3.9% to 7.5%) in those with cardiomyopathy (p = 0.0001). Normal flow velocity and acceleration levels in cardiomyopathy would result in large augmentations of the intrinsic load component and myocardial metabolic requirements. In view of the inverse force-velocity relation of the myocardium and the time course of the ejection load, it is concluded that decreased outflow acceleration and velocity in patients with dilated cardiomyopathy result from augmented feedback loading functions in addition to an impaired contractile state.