The forces underlying left ventricular ejection were investigated by applying a wavefront analysis to blood pressure (P) and velocity (U) waveforms measured in the ascending aorta of anesthetized dogs (n = 13). Wavefronts travel forward (to the periphery) and/or backward (to the heart) after peripheral reflection. They are characterized by the rate of pressure change they cause, i.e., the time derivative of pressure (dP/dt): compression wavefronts have dP/dt > 0: expansion wavefronts have dP/dt < 0. Wave intensity is defined as (dP/dt)(dU/dt), where dU/dt is the time derivative of U. Forward wavefronts contribute positively to wave intensity and backward wavefronts contribute negatively. Therefore, wave intensity indicates whether the effects of forward wavefronts are predominant or whether those of backward wavefronts predominate in the formation of pressure and velocity waveforms. Under control conditions, wave intensity was positive in early and late systole, indicating that forward compression and expansion wavefronts dominate aortic acceleration and deceleration, respectively. Compression wave intensity was increased during inotropic stimulation by dobutamine (10-15 microg/kg per min i.v. infusion; +161% +/- 31% mean change in peak value +/- SEM (%), P < 0.05), and was reduced during beta-blockade by propranolol (1 mg/kg i.v. injection; -58% +/- 7%, P < 0.05). Expansion wave intensity was unchanged by dobutamine and propranolol (n = 6). In a separate group of animals (n = 7), expansion wave intensity was reduced during vasodilatation by nitroglycerin (0.5mg i.v. injection and 0.02 microg/kg per min infusion; -32% +/- 12%, P < 0.05), but was unchanged during vasoconstriction by methoxamine (2 mg i.v. injection). However, methoxamine reduced compression wave intensity (-46% +/- 14%, P < 0.05). These results indicate that (1) compression and expansion wavefronts generated by the left ventricle dominate acceleration and deceleration in the ascending aorta, (2) compression wave intensity is related to the inotropic state of the left ventricle, but is reduced during vasoconstriction, and (3) expansion wave intensity is reduced during vasodilatation. This time domain analysis of traveling wavefronts readily provides information concerning the dynamics of the ventriculoarterial interaction.

The inertia force of late systolic aortic flow contributed to ventricular relaxation in the normal heart.

To evaluate the effect of coronary artery bypass grafting (CABG) on regional diastolic function of the left ventricular wall, we applied the concept of the stiffness constant to the diastolic sigma-ln (1/H) relation, where sigma is the mean wall stress, and H is the wall thickness of the region of concern, and ln (1/H) is the natural logarithm of the reciprocal of wall thickness. We assessed 12 cardiac regions in six patients with coronary artery disease who underwent CABG at the Cardiovascular Hospital of Central Japan between May 1994 and January 1995. Left ventricular pressure and regional wall thickness were measured simultaneously, with a micromanometer-tipped catheter and by two-dimensional echocardiography, respectively, before and after CABG. The stiffness constant (K) was obtained by fitting the diastolic sigma-ln (1/H) data points to an exponential curve with zero asymptote: sigma = Cexp[Kln (1/H)]. Preoperatively, the stiffness constant in the affected region (CABG region) was greater than that in the unaffected region (non-CABG region) (4.79 +/- 2.56 vs 2.95 +/- 0.72). Postoperatively, the stiffness constant in the CABG region was significantly decreased, to 3.21 +/- 1.22. The stiffness constant, which is derived from the sigma-ln (1/H) relation, is useful for the assessment of LV regional diastolic function.

We evaluated the effects of disopyramide in terms of the balance between myocardial oxygen supply and demand in patients with hypertrophic obstructive cardiomyopathy (HOCM). The myocardial oxygen supply was evaluated by measuring coronary flow velocity and the myocardial oxygen demand was assessed by the pressure-volume area (PVA). The time velocity integral of coronary flow did not change significantly (20 +/- 6 to 21 +/- 8 cm), but the peak left ventricular pressure and left ventricular external work decreased significantly (206 +/- 44 to 157 +/- 37 mmHg, P < 0.001; 1.09 +/- 0.33 to 0.80 +/- 0.23 J/beat, P < 0.001) after disopyramide administration. From theoretical analysis using these data, we concluded that disopyramide improves the myocardial oxygen supply-demand balance in patients with HOCM.

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