Diastolic pressure and volume (P-V) curves were approximately exponential and fitted the equation, dP/dV = aP + b, where a was left ventricular volume elastic constant. Stress and strain (σ-ε) curves were expressed by the equation, dσ/dε = kσ + c, where k was wall stiffness constant. These exponential curves have been fitted over the whole diastole, but theoretically, the mid-diastole should reflect diastolic elastic properties best. In the present study, therefore, special attention was paid to the mid-diastole in each patient, and both P-V and σ-ε relationships were analyzed by fitting the data to the above mentioned curves during this period of time. This analysis was made in two separate groups of patients. One was the control group consisting of 2 patients with normal hearts, 2 patients with mild pulmonary stenosis, and 25 patients with post mucocutaneous lymphnode syndrome. The other group consisted of patients with postoperative congenital heart disease, that is, 8 patients with atrial septal defect and 5 patients with tetralogy of Fallot. The elastic constant (a) could not be compared if the size of the hearts differed. The results of the present study, however, demonstrated that the size of the heart was closely related to the constant, a. In the control group, the constant (a) was exponentially related to the size of the heart, and expressed as follows: a = 0.30e^-0.037EDV + 0.045 (r = 0.94, p < 0.01) In contrast, the wall stiffness constant (k) was not related to the size of the heart. After surgical repair of congenital heart disease, the stiffness constant in the left ventricle was normal in patients with postoperative atrial septal defect, while it was significantly increased in patients with postoperative tetralogy of Fallot.

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QRS deflection area vector (A^^→qrs), T deflection area vector (A^^→t) and ventricular gradient (G^^→) in right ventricular hypetrophy were studied in 53 subjects divided on the basis of cardiac catheterization data into four subgroups; normal controls, mild MS group, right ventricular pressure overload group and right ventricular volume overload group. A^^→qrs, A^^→t and G^^→ of the four subgroups were calculated using a microcomputer and compared. A^^→qrs in right ventricular pressure overload group and volume overload group was shifted to the right and slightly anteriorly from that in normal control group. A^^→t in right ventricular pressure overload group and volume overload group was shifted slightly upwards and significantly posteriorly from that in the normal control and mild MS groups. G^^→ in right ventricular pressure overload group and volume overload group was shifted to the right and significantly posteriorly from that in normal control and mild MS groups. Using multivariative analysis, we developed criteria for diagnosing right ventricular hypertrophy with A^^→t: 0.059At(Z) - 0.0145|A^^→t| - 0.2608 &les; 0. Application of this criteria achieved 82.4% (28 of 34) sensitivity in the patients with right ventricular hypertrophy and 90.9% (10 of 11) specificity in the normal control subjects.

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Wall thickness, the extent of disarray, the number and the size of myocytes and the amount of interstitial space were measured in the ventricular septum (VS) and left ventricular (LV) free wall in hearts of 6 patients with chronic systemic hypertension and asymmetric septal hypertrophy (ASH). Twenty-five subjects (15 with no cardiac disease, and 10 with systemic hypertension) without ASH served as the controls. In the six patients with ASH, the degree of ASH ranged from 1.3 to 1.6. The extent of disarray in VS was 20% in one heart and within normal limits (mean ± SD = 3 ± 3%) in the other 5. The size of myocytes increased both in the VS and LV free wall and the VS/LV ratio ranged from 0.9 to 1.0. There was no significant difference in the % area of interstitial space between hearts with ASH and controls, and the VS/LV ratio ranged from 0.9 to 1.1. The number of transmural muscle layers (number of myocytes) was 680 ± 90 in the VS and 440 ± 40 in the LV free wall of these with ASH, and 500 ± 60 in the VS and 490 ± 60 in the LV free wall of control subjects. The VS/LV ratio of the number of myocytes ranged from 1.3 to 1.7 and was correlated with the VS/LV ratio of wall thickness. Although the sample is small, our findings suggest that most hearts from patients with chronic systemic hypertension and ASH have no diffuse disarray in the VS and that ASH probably occurs secondary to pressure overload. An increase of number of myocytes in the VS is a pathogenetic factor of ASH, regardless of the extent of disarray or the presence of HCM.

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Twelve patients with uncomplicated systemic hypertension were treated with nifedipine (30 mg/day) and diltiazem (180 mg/day) for 1 month each, and performed two stage (50 watt and 100 watt) of bicycle ergometer exercise before and after each period of administration. Both drugs produced significant reduction in systolic and diastolic blood pressure at rest and during exercise, while the mean values of systolic blood pressure tended to be less with nifedipine than with diltiazem. Nifedipine caused a nonsignificant increase in heart rate at rest and during exercise, but diltiazem significantly decreased it at rest and during exercise. Cardiac output was significantly increased at rest and during mild exercise (50 watt), but not during more strenuous exercise (100 watt) with both drugs. Thus, different actions in arterial vasodilation and chronotropism between nifedipine and diltiazem in usual clinical doses were noted. However, nifedipine and diltiazem may be effective in hypertensive patients, probably with left ventricular dysfunction, because both drugs reduced systemic blood pressure even during exercise with simultaneous increase in cardiac output at rest and during mild exercise.

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Coronary vasospasms are usually indicated by ST elevation or depression in the electrocardiogram (ECG). To test the hypothesis that ST elevation represents more severe myocardial ischemia than does ST depression, we determined the coronary sinus blood flow (CSBF) and the transcardiac lactate extraction ratio (LER) in 19 selected patients who had focal vasospasms in the left anterior descending artery. In 10 patients, ergonovine (0.11 ± 0.02 mg, mean ± SEM) provoked severe (total or subtotal) coronary vasospasm with ST elevation. Under these conditions, CSBF significantly decreased (from 97 ± 8 ml/min to 79 ± 5 ml/min, p < 0.01) with a marked reduction in LER (from 29 ± 5% to -14 ± 6%, p < 0.01). In contrast, 10 vasospastic events with ST depression after ergonovine (0.15 ± 0.04 mg, NS) were recognized as mild spastic narrowing or severe spasms with well developed collateral circulation. Alteration of CSBF was significant in only a few patients and the overall CSBF response was non-significant (from 106 ± 12 ml/min to 103 ± 13 ml/min). The reduction in LER in this group was less pronounced than those in patients with ST elevation (p < 0.05). These results indicate that coronary vasospasm with ST elevation may be related to the more pronounced reduction in coronary blood flow accompanied by more severe myocardial ischemia. Such observations may support the contention that some ischemic events associated with ST elevation or depression can be interpreted as a continuous spectrum of vasospastic disorders.

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We assessed the histochemical, ultrastructural and cytochemical effects of reperfusion on ischemic myocardial cells during the early and late reperfusion phases in two groups of dogs. Group A were 8 dogs undergoing 1 hour occlusion of LAD, and Group B were 14 dogs undergoing 1 hour occlusion of LAD followed by 2 hour reperfusion period. The results of the histochemical study (PAS stain) demonstrated that in Group A, a patchy distribution of glycogen occurred primarily in the subepicardial region. Three-dimensional analysis of this distribution revealed peninsulas of glycogen running parallel with a vessel. The cells in Group B, mainly subepicardium, showed a moderate glycogen content which was more extensive than those in Group A. The ultrastructural changes were assessed after a 60-minute ischemia and subsequent recovery (after 5 minutes and 120 minutes of reflow) using transmural biopsy specimens. Each myocardial cell was graded from 0-4 according to the degree of ischemic injury and recovery. The degree of ischemic damage varied in intensity from slight to severe, in both the subepicardium and the subendocardium. Ca⁺⁺-ATPase activity was examined cytochemically in myocardial cells of Group B. After 60-minute occlusion, the moderately ischemic cells (especially in the subepicardium) that were without amorphous dense bodies or marked sarcolemmal lifting-off made significantly greater ultrastructural recovery (p < 0.05) with restoration of Ca⁺⁺-ATPase activity on sarcoplasmic reticulum and mitochondria after 120 minutes of reflow. This occurred even though after 5 minutes of reflow the cell showed temporary deterioration such as contraction bands, vacuoles and severe destruction of some mitochondria.

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The changes of hemodynamics were measured in spontaneously hypertensive rats (SHR) of increasing ages. Male SHR and Wistar rats of the Kyoto strain (WKY) at 4, 12, 24 and 48 weeks of age were used. The right jugular vein and the left femoral artery were cannulated and a thermister was placed in the ascending aorta. After 24-hour rest, heart rate (HR), mean arterial pressure (MAP) and cardiac output (CO) were measured .The ratio of left ventricular weight (LVMI) of 4 week-old SHR had already increased significantly when compared to WKY. The HR in 4-week-old SHR was significantly higher than WKY. The increased HR in young SHR indicates the hypersensitivity of the sympathetic nervous system. Increased CO in 4 week-old SHR was due to high HR. The ratio of heart work to left ventricular mass (HW/LVM) of SHR at all age groups was not different from that of WKY, although the ratio of heart work to body weight (HWI) had a tendency to rise in SHR as compared to that in WKY. Our conclusion is that the development of LVM adapts to HW.

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A case of acute aortic valve endocarditis is reported, in which the complications of pericarditis and myocardial abscess were diagnosed clinically. Two dimensional and M-mode echocardiography showed large echo-free spaces and a marked thickening of the interventricular septum which had not been detected previously, suggesting pericardial effusion and myocardial abscess. This is the first case in Japan to our knowledge, in which the pericarditis and myocardial abscess were detected preoperatively and successfully treated surgically.

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We reported the case of a 67-year-old man with Ebstein's anomaly, the oldest patient with this disease in Japan as far as we know. His condition was often accompanied by ectopic junctional tachycardia with isorhythmic AV dissociation, which made him complain of palpitation by elevating right intra-atrial pressure. Although enhanced automaticity was the most likely mechanism of this tachycardia, it was abruptly initiated and terminated by a single premature contraction. Because this interesting character can not be explained solely by the usual ideas of automaticity, we suggest that ectopic junctional tachycardia in the present case may somewhat resemble the phenomenon of triggered automaticity.

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