This article briefly reviews recent experimental studies which show that beta-adrenergic receptor stimulation produces an important enhancement of the force-frequency relation on myocardial contractility. The basic property of the force-frequency effect to progressively enhance myocardial contractility as heart rate increases is augmented at each level of increasing adrenergic stimulation. This newly described intrinsic mechanism for the control of cardiac inotropic state, graded beta-adrenergic amplification of the force-frequency relation, is strongly manifested during normal exercise and infusion of a beta-adrenergic agonist at rest, and it influences both systolic and diastolic ventricular function. Significant impairment of adrenergic amplification of the force-frequency relation is observed in experimental heart failure and could contribute to impaired cardiac function during stress or exercise in this setting.

These findings indicate that force-frequency effects on the inotropic state of the intact LV are markedly enhanced by exercise.

Descending intervention induced greater prolongation of T than ascending intervention. Prolongation of T was closely related to an increase in AoESP in the descending intervention but a decrease in AoESP in the ascending intervention. These data suggest that not only the loading sequence but also the pressure level at the onset of isovolumic relaxation determines LV relaxation.

Left ventriculography with simultaneous pressure micromanometry was performed in 11 normal control subjects and 17 patients with dilated cardiomyopathy (DCM). Left ventricular silhouettes in the right anterior oblique projection were divided into eight areas, and regional wall stress was computed by Janz's method in each area excluding the two most basal areas. Wall stress was higher in DCM patients than in control subjects (p<0.01). The percent area changes from end diastole to end systole in each area were lower in DCM patients than in control subjects (mean for six areas, 22+14% versus 54±9%o, respectively, p <0.01), but the coefficient of variation for the percent area changes in the six areas of the left ventricle in DCM patients was greater than that in control subjects (32±17% versus 15±4%, respectively, p<0.01), indicating regional differences in hypokinesis. There was a significant negative correlation between end-systolic regional wall stress and percent area change (r=-0.60 to -0.86, p<0.05) in each area. Thus, excessive regional afterload may play an important role in causing regional hypokinesis in DCM. (Circulation 1990;82:2075-2083 iffuse hypokinesis of the left ventricular wall D motion has been reported in patients with dilated cardiomyopathy (DCM).' However, recent studies on DCM with the use of left ventricular cineangiography2-5or radionuclide ventriculography6,7 suggest that left ventricular wall motion is not always diffusely hypokinetic and that regional differences in the degree of hypokinesis are frequently present. In clinical settings, patients with segmental wall motion abnormality may have better global left ventricular function and better prognosis than patients with diffuse wall motion abnormality.6 Thus, the importance of estimating left ventricular regional wall dynamics in patients with DCM has been emphasized.3-7

No abstract