We developed a method for estimating the instantaneous viscoelastic properties of the left ventricle (LV). This impedance-curve method is based on the instantaneous impedance-frequency curve of the left ventricle generated by a rapidly oscillating mechanical impulse applied to the epicardial surface of the heart. The theoretical basis of the method and experimentally obtained instantaneous impedance-frequency curves were examined to evaluate the validity of our basic assumptions. Using these impedance-curve data, we calculated the instantaneous viscoelastic properties of the LV during the cardiac cycle. The impedance curve shows a configuration that is almost the same as the theoretical curve based on the assumption that an RCL (R, resistor; C, capacitor; L, inductor) parallel circuit is the electrical analog for the LV. The impedance curve varied moment by moment during the development of instantaneous LV pressure. The elastic and viscous coefficients, calculated from the impedance curve, increased with increase of LV pressure. We concluded that the impedance-curve method can delineate the instantaneous viscoelastic properties of the ventricle (especially of the ventricular myocardium).

To obtain the instantaneous left ventricular transfer function curve (instantaneous TFC) under conditions of regional ischemia, sinusoidal accelerations ranging from 30 to 150 Hz were applied to a small area of the epicardium of cross-circulated isovolumic canine left ventricle, and the contralateral acceleration was measured under control and during regional coronary occlusion (n = 11). The TFC is the ratio of the output to input acceleration amplitudes. The instantaneous TFC was characterized as a single-peaked configuration under control coronary perfusion. However, TFCs progressively changed from a single-peaked to a double-peaked configuration during regional ischemia. To quantify this change in instantaneous TFC, we defined an index D as the mean squared difference of TFC during ischemia from TFC during control. Index D was linearly related to the percent mass of the ischemic region at 40 minutes after onset of ischemia. We conclude that 1) transfer function curves are sensitive measures of myocardial heterogeneity and 2) the fractional ischemic weight of the ventricle is a major factor in determination of the deformation in instantaneous TFC at the later stages of regional ischemia.

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In experimental studies, minute sinusoidal vibration has been reported to induce functional depression of the left ventricle and to be an index for evaluation of myocardial crossbridge kinetics. Therefore, to examine whether or not this vibration-induced functional depression could also be observed in the human ventricle, motion of the left ventricular (LV) wall or LV pressure was measured by echocardiography (n= 16) or by left heart catheterization (n=4), in which 100 Hz, 2.07 mm-amplitude sinusoidal vibration was applied to the subject's precordium. In the echocardiographic study, left ventricular wall shortening did not change by vibration in nine healthy volunteers, but was depressed in two patients with aortic regurgitation (AR) and in one patient with ischemic heart disease (IHD). In measurement of LV pressure, the decrease in LV systolic pressure caused by vibration was obviously observed in two patients (AR and IHD) but was not observed in two patients with hypertrophic cardiomyopathy. These results suggest that we might be able to extend previously proposed experimental idea on early detection of the abnormality in myocardial crossbridge kinetics to the clinical setting.crossbridge kinetics ; crossbridge detachment ; echocardiography ; left heart catheterization In applying minute sinusoidal vibration to the left ventricular (LV) epicardium, inotropy dependent LV functional depression has been observed in canine open chest preparations. That is, the magnitude of depression in LV systolic pressure ranged from 0 to approximately 15% in accordance with the basic inotropic state of myocardium (Koiwa et al. 1989). However, we cannot find any reports referring that vibration-induced functional depression (VID) does occur in clinical setting. Therefore, to determine whether or not we could induce human LV functional depression by mechanical vibration, 100 Hz sinusoidal vibration (2.07 mm magnitude) of approximately 5 sec duration was applied by attaching a vibrator onto the human anterior chest wall (n=20). We measured the response of the ventricle by echocardiography or LV pressure during routine cardiac

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