Analysis of beat to changes in left ventricular (LV) ejection time during cardiac pacing was utilized to assess the atrial contribution to ventricular filling in coronary artery disease. The recordings of aortic pressure were made during atrial and ventricular pacing at a rate of 5 to 10 beats/min above sinus rhythm. During ventricular pacing, LV ejection time became maximum when an atrial contraction preceded a ventricular contraction by a physiologic interval and was similar to that obtained during atrial pacing (max ET). When the atrial systole occurred with or followed the paced ventricular contraction, LV ejection time became minimum (min ET). The atrial contribution was calculated as (max ET - min ET)/max ET × 100 (%). Patients with coronary artery disease had a significantly large atrial contribution. In patients without myocardial infarction, the atrial contribution was increased to compensate for impaired early diastolic filling. In patients with myocardial infarction, the atrial contribution was reduced when LV end-diastolic pressure was markedly high. The atrial contribution generally plays an important role in increasing stroke volume, but it had less effect despite the forceful atrial contraction as LV filling pressure became more elevated.

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In order to evaluate the etiology of so-called idiopathic ventricular tachycardia, endomyocardial biopsies were performed in four patients with electrocardiographically documented recurrent and sustained ventricular tachycardia. During the episodes of ventricular tachycardia, standard ECG showed a QRS pattern of right bundle branch block with left axis deviation in two patients and left bundle branch block in two patients. The episodes were associated with palpitation, dyspnea and hypotension in all cases. No organic heart disease was detected by physical examination, chest X-ray films, echo-cardiograms, left ventriculograms or coronary cineangiograms. His bundle electrograms showed blocks at various sites in the atrioventricular conduction system. The biopsy specimens revealed nonspecific myocardial degeneration in the right and left ventricles. These findings suggest mild but wide-spread myocardial damage in both the working myocardium and the conduction system. The clinical course of these patients appeared benign according to follow-up data of one to nine years' duration. None developed overt clinical signs of dilated, hypertrophic or restrictive cardiomyopathy.

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In order to evaluate the magnitude of pulmonary "systolic runoff" we studied the pulmonary vein blood flow velocity waveform by positioning a catheter-tip velocity-pressure transducer into the extraparenchymal pulmonary vein just distal to the left atrium. We recorded blood flow velocity and pressure simultaneously, and subsequently identified the zero blood flow velocity with blood flow velocity level of the pulmonary artery in diastole. Patients with atrial septal defect were used as subjects because of the technical ease although the altered hemodynamics were present. Two kinds of flow velocity waveforms were consistently demonstrated. One was a waveform of two peaks with the first peak in late systole and the second peak in early diastole (n=9). The other was a waveform of one peak with a summit near the end of systole (n=5). On the assumption that the blood flow velocity waveform obtained with this method is roughly equivalent to the flow volume waveform, we initiated the second study. The area encompassed between the actual flow velocity waveform and the line of zero flow velocity was divided into two compartments, i.e., ventricular systole (S) and diastole (D). The ratios of the area in systole to the sum of the areas in systole and diastole, i.e., (S)/((S)+(D)), which are analogous to the pulmonary "systolic runoff", were 0.45 ± 0.07 (mean ± SD, n=13). This suggests that about 40% of the right ventricular stroke volume flows into the pulmonary veins, the left atrium and a portion of the right atrium through the atrial septal defect during ventricular systole.

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In order to evaluate the role of adrenergic receptor-mediated vasomotions of large epicardial coronary arteries in changing coronary blood flow (CBF), the effects of intracoronary norepinephrine (NE), 1.0 μg/min, were examined in dogs with coronary stenosis which preserved stenosis vasomobility. In untreated dogs, NE caused no significant changes in CBF and stenosis resistance (SR). In dogs treated with propranolol, NE decreased CBF by 65 ± 7.0% (mean ± SE) and produced 12-fold intensification of SR followed by LV dP/dt reduction. Similar detrimental responses to NE were observed in dogs treated with atenolol. In dogs treated with phentolamine, NE increased CBF by 33 ± 5.6% and decreased SR by 65 ± 7.1%. When NE was administrated directly distal to the stenosis to exclude responses of the stenosed coronary segment, NE failed to affect CBF and SR. These results indicated that α receptor stimulation intensified stenosis severity, profoundly decreased CBF and evoked myocardial ischemia, whereas β stimulation dilated coronary stenosis and increased CBF. The net effects of NE were due to balanced α and β stimulation. Thus, disproportionate activation of α and β (probably β₁) adrenergic receptors in large coronary arteries with pliable stenosis could modulate their tone and plays an important role in the regulation of CBF.

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Diastolic property of left ventricle (LV) was estimated by the passage of time using an experimental model of volume overload. Volume overload was surgically induced in dogs by means of bradycardia (complete A-V block). LV dimension and LV pressure were simultaneously recorded and pressure-volume curve (P-V curve) was obtained at the three stages, i.e., just after the creation of bradycardia; 8∼14 days after the operation; and 2∼4 months after the operation. The rightward shift of P-V curve was confirmed as being associated with the development of eccentric hypertrophy; but this study showed no significant changes in indices of LV chamber elasticity. Indices of muscle elasticity derived from myocardial stress-strain (σ-ε) relationship also remained constant in the three stages. It was demonstrated that the shift of the P-V curve resulted neither from the changes of LV chamber elasticity, nor myocardial elasticity.

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The time course of pulmonary congestion and pulmonary edema was examined using a gravimetric method in 19 open-chest anesthetized dogs. Balloon catheters in the left atrium (LA) were inflated to elevate LA pressure more than 25 mmHg. The dogs were divided into 4 groups (G) according to the duration of the elevated LA pressure: G.1 (n=6) as control; G.2 (n=4) for 15 minutes; G.3 n=4 for 30 minutes; and G.4 (n=5) for 60 minutes. Although no significant increase of extravascular lung water content (an indicator of pulmonary edema) was observed in G.2 (4.97 ± 0.85 g/kg) and G.3 (4.46 ± 0.96) compared with G.1 (4.02 ± 0.88), a significant increase was observed in G.4 (6.81 ± 1.21, p < 0.05). Residual pulmonary blood content (an indicator of pulmonary congestion) was significantly increased in G.2, 3 and 4 compared with G.1. By light and electron microscopes, pulmonary congestion was revealed in G.2, whereas interstitial pulmonary edema was demonstrated only in G.4. Thus, it was concluded that pulmonary congestion occurred within 15 minutes, but pulmonary edema occurred 30 to 60 minutes after left atrial pressure was elevated more than 25 mmHg. This time lag may be an important factor in explaining the discrepancy between the elevated left atrial pressure and the clinical manifestation of pulmonary edema.

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To analyze the conflicting data on the relationship between sodium intake and sympathetic activity, the effects of a chronically excessive intake of sodium on renal sympathetic activity and blood pressure were investigated in normotensive rats. Renal sympathetic activity was estimated by urinary excretion of free norepinephrine (NE) and the turnover of NE in the kidneys. Blood pressure increased in rats receiving a high sodium diet when compared with that of the basal sodium diet. Urinary-free NE, epinephrine (E) and dopamine (DA) excretions in rats receiving a high sodium diet were enhanced significantly from those in the basal sodium diet. The turnover of NE in the kidneys was more enhaced in the high sodium group than in the basal sodium group. By blocking the sympathetic tone with ganglionic blockade, hexamethonium, enhanced excretion of urinary NE and elevation of blood pressure in response to salt loading were blocked to the levels of the basal sodium diet. These results suggest that a chronically exessive intake of sodium enhances the renal sympathetic and adreno-medullary activities, leading to a rise in blood pressure in normotensive rats.

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Arteriolar dimensions were determined during vasodilated states of natural vasomotion in unanesthetized rabbits using the ear chamber technique. Analysis of 383 arteriolar segments were made in 16 New Zealand white rabbits, 8-9 weeks after implantation of the ear chamber under the conditions of 25.5 ± 0.5°C (room temperature), 33.6 ± 1.4°C (ear surface temperature), 38.3 ± 0.5°C (rectal temperature), 66.5 ± 3.2 mmHg (aortic mean blood pressure) and 238.6 ± 33.0 beats/min (heart rate). Inside diameter (ID) and outside diameter were measured by closed circuit television microscopy using a Vista model 308 video image splitter. Wall thickness (WT) vs. ID, wall-to-lumen ratio (W/L) vs. ID and cross-sectional wall area (CSWA) vs. ID were fitted to the formulae: WT=0.14×ID+3.8 (r=0.76, p<0.001), W/L=4.23÷ID+0.12 (r=0.84, p<0.001) and CSWA=0.57×ID²+11.0×ID+93.7 (r=0.93, p<0.001), respectively. W/L increased rapidly in precapillary arterioles, especially below 30 μm ID, since WT has a finite size while ID does not. This structural property of resistance vessels is important in regulating peripheral resistance, blood flow, and downstream capillary density.

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Duplication of the mitral valve is a rare congenital cardiac anomaly .We encountered a case of duplication of the mitral valve associated with a partial form of endocardial cushion defect in a 6-year-old girl. The mitral orifice was separated by a fibrous tissue and each orifice provided papillary muscle and complete subvalvular mechanisms except for the cleft region. The fibrous tissue also provided a subvalvular apparatus. The cleft region. The fibrous tissue also provided a subvalvular apparatus. The cleft was repaired without complication. The short axis view of the two-dimmensional echocardiogram demonstrated two separate holes in the mitral valve, which constituted the most obvious diagnostic sign prior to surgery.

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