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To examine the mechanism of myocardial ischemia in hypertrophic cardiomyopathy (HCM), coronary flow velocity was measured in the left anterior descending coronary artery (LAD) using a Doppler guide wire in 11 patients with HCM and in 8 normal controls. The average peak velocity (APV), percent increase of APV (%APV), and APV during systole (Vs) and diastole (Vd) were calculated at rest and during rapid atrial pacing. The APV in HCM reached a peak value at a heart rate of 90 beats/min, while in the controls the APV increased continuously until the heart rate reached 130 beats/min [%APV (130 beats/min); 103+/-30% in HCM vs 139+/-23% in controls, p<0.04]. During rapid atrial pacing, Vs in the controls increased, whereas Vs in HCM decreased further. During high-rate pacing, Vd in HCM reached a peak value at a heart rate of 90 beats/min, whereas in the controls, Vd increased continuously until the heart rate reached 130 beats/min. The acceleration rate of early diastolic flow was significantly lower in HCM than in the controls (1.85+/-0.66 vs 3.18+/-1.62 m/s2, p<0.03). This abnormal response might be due to an increase in the reverse systolic flow and a decrease in the diastolic flow, probably caused by a slow acceleration of early diastolic flow velocity in the LAD.

This study was undertaken to investigate the effect of chronic right ventricular (RV) volume overload on left ventricular (LV) diastolic function. Twelve patients with atrial septal defect and 7 age-matched normal controls were examined. Patients with atrial septal defect were divided into 2 groups based on their Qp/Qs values (ASD1:Qp/Qs < or = 3, n = 7; ASD2:Qp/Qs > 3, n = 5). The LV volume curve and its first derivative were derived by a frame-by-frame analysis of the left ventriculogram. The peak filling rate was defined by the peak positive first derivative of the LV volume curve. We measured the time constant, isovolumetric relaxation time, stiffness constant and compliance at LV end-diastole. The time constant was significantly prolonged in the ASD2 group compared with the controls, and the isovolumetric relaxation time in both atrial septal defect groups was also prolonged compared with the controls. The peak filling rate, which was normalized by end-diastolic volume, was lower in the ASD2 group than in the controls. Although the stiffness constant and the compliance at LV end-diastole in the controls were not significantly different from those in the atrial septal defect group, an upward and leftward displacement of the left ventricular pressure-volume curve was observed in patients with atrial septal defect. Moreover, a significant correlation (r = 0.78, p < 0.01) was observed between the time constant and RV end-diastolic pressure. Thus, these results suggest that chronic RV volume overload affects left ventricular diastolic function.

The total stroke volume of the left ventricle (LV) is equal to the sum of the regional cavity shrinkage. Since nonuniformity of regional wall motion in LV has been well documented even in normal subjects, the extent of the contribution of each region to total stroke volume cannot be easily determined. To assess the left ventricular regional contributions to total stroke volume under normal conditions and in compensated chronic mitral or aortic regurgitation, LV cineangiograms were analyzed in 14 normal subjects (N), 8 patients with mitral regurgitation (MR) and 10 patients with aortic regurgitation (AR). We assumed that the LV cavity could be viewed as a stack of 30 half-cylindrical discs, 15 in the anterior and 15 in the inferior wall regions. LV chamber shape was more spherical in MR than in N, but was more conical in AR. Percent regional hemichordal shortening was significantly decreased in the anterobasal and anteroapical walls in AR, but was similar between N and MR. The regional contribution to total stroke volume showed a significant quadratic correlation with the end-diastolic regional shape index (N, r = 0.87; MR, r = 0.79; AR, r = 0.90), which was defined as the regional hemiaxial length divided by the LV long-axis length, but was not correlated with percent regional hemichordal shortening. Therefore, stroke volume is generated mainly in the mid-ventricular portion in N and MR, but in the basal portion in AR due to the characteristic change in cavity shape.

The effect of nifedipine on ventriculoarterial coupling was examined in 8 patients with old myocardial infarction who showed a depressed ejection fraction (37 +/- 7%). Left ventricular (LV) pressure and LV volume were determined simultaneously by micromanometer and conductance catheter, respectively. We measured the slope (Ees) of the end-systolic pressure-volume relation during transient inferior vena caval occlusion, the slope (Ea) of the end-systolic pressure-stroke volume relation, the ratio of Ea to Ees (Ea/Ees), and the work efficiency (the ratio of external work to the systolic pressure-volume area) at baseline and after the sublingual administration of nifedipine (10 mg). Nifedipine slightly increased the heart rate from 71 +/- 14 to 78 +/- 17 beats/min. Although nifedipine had little effect on Ees (2.54 +/- 0.68 vs 2.47 +/- 0.62 mmHg/ml/m2, ns), it significantly decreased Ea from 3.47 +/- 1.16 to 2.37 +/- 0.54 mmHg/ml/m2. Consequently, Ea/Ees decreased from 1.42 +/- 0.47 to 0.97 +/- 0.31 and work efficiency increased from 48 +/- 12 to 59 +/- 13% after nifedipine administration. These data suggest that nifedipine reduces afterload (Ea) and improves left ventriculoarterial coupling without depressing left ventricular contractility in patients with failing hearts due to old myocardial infarction.

The effect of the left ventricular (LV) regional wall motion during isovolumetric relaxation period (IRP) were studied in 9 patients with old anteroseptal myocardial infarction (OMI) and 8 normal subjects (NOR). There were no significant differences in heart rate, peak LV systolic pressure and peak (+) dP/dt between the groups. LV cavity was divided into the anterior and inferior sides by a long axis, which was equally divided with 3 perpendicular lines, creating 4 areas in each side. The sums of the 2 middle areas in each side were defined as Aa and Ab, respectively. During IRP the pattern of (-) dP/dt at the upstroke phase was convex-downward in OMI, but convex-upward in NOR. Time constant (T) was significantly prolonged in OMI compared with NOR (50 +/- 9 vs 37 +/- 6 msec; p less than 0.01). On NOR, Aa increased significantly after 33.4 msec from peak (-) dP/dt, while Ab remained unchanged. In OMI, Ab increased after 50.1 msec from peak (-) dP/dt, associated with decrease in Aa, suggesting the passive shortening of the anterior wall by the active expansion of the inferior. Such asynchronous LV wall motions during IRP might impair LV relaxation and influence the upstroke pattern of (-) dP/dt.

Our recent clinical studies on the negative dP/dt upstroke pattern suggested that the left ventricular pressure (LVP) deviated from the exponential curve during isovolumic relaxation period (IRP) in diseased hearts. To examine this further two types of monoexponential curve fitting were done in various heart diseases (normal (N): 8, angina pectoris (AP): 8, myocardial infarction (MI): 13, hypertrophic cardiomyopathy (HCM): 10, dilated cardiomyopathy (DCM): 8). LVP was measured by a Millar's catheter-tip transducer, and four types of time constant (T1-T4) were derived: T1 was calculated by an exponential curve fitting e-t/T1 + B (B is constant), T2 by the ratio Pm/peak (-) dP/dt (Pm is LVP at peak (-) dP/dt), T3 by the best exponential curve fit e-t/T3 + B + C (C is constant), and T4 by the ratio (Pm-C)/peak (-) dP/dt. If the exponential curve fitting was reasonable, the relation between T1 and T2, or T3 and T4, should be on the line of identity. The result was as follows: T2 = 1.4 T1 - 6.1 (r = 0.84) and T4 = 1.1 T3 - 10.7 (r = 0.94). Additionally, C (mmHg) in MI (-26 +/- 15), HCM (-36 +/- 19) and DCM (-32 +/- 20) were lower (p less than 0.05) than in N (-13 +/- 7). These findings suggest that the LVP during IRP could deviate from the monoexponential curve and that careful attention should be given to calculate the time constant in diseased hearts.

A 54-year-old man presented with continual angina pectoris at rest, associated with an anomalous coronary artery. He also had an aneurysm at the submitral region of the left ventricular postero-lateral wall, without evidence or prior myocardial infarction, which showed hypokinetic inward motion during systole. We assume that this was a rare case of left ventricular aneurysm without prior myocardial infarction, the etiology which might related to the anomalous coronary artery.