Each sound signal of the first and the second heart sounds of humans was divided into three equal segments. The frequency spectrum of each segment was analyzed using the fast-Fourier-transform technique. Theory predicts that if the first and second heart sounds are caused principally by the respective vibrations of the atrioventricular and semilunar valves, then the frequency of these sounds should increase with an increase in the pressure difference across these valves. In other words, the frequency of the heart sounds should increase with time, as the pressure difference across these valves increases with time for most of the duration of the sounds. Our frequency analysis, however, showed that there is no systematic relation between the predominant frequency of successive segments of the sound signals. This therefore appears to indicate that it is quite unlikely that the vibrations of the heart valves are the principal contributor to the origin of the first and second heart sounds.

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Two-dimensional echocardiography (2DE) was utilized in 49 patients with a first transmural myocardial infarction, within 6 hours (±3SD) after admission and again at 48 hours, in order to correlate initial left ventricular wall motion (LVWM) abnormalities with subsequent in-hospital cardiac complications. Analysis of systolic endocardial motion was made in 15 left ventricular segments in each patient and a total wall motion (WM) score was derived as a measure of the extent of myocardial involvement. LVWM abnormalities in relation to Killip class, peak total serum creatine kinase (CK) and serum glutamic oxaloacetic transaminase (SGOT) enzyme levels were also studied.
Adequate echocardiograms for LVWM analysis were obtained in 43 patients. Thirteen patients had no infarct-related complications (group I) and 30 had complications (group II). The mean initial WM score in group I patients was 5.7±2.6 which was significantly lower than the 13.5±3.9 in group II (p<0.0001). A WM score of ≥10 correlated with the occurrence of complications in 93% of patients. The WM score was significantly higher in admission Killip class 1 and 2 patients in group II compared with group I patients in class 1. However, no difference was noticed between the mean WM score of patients assigned to these 2 classes in group II. Peak CK and SGOT levels showed a poor correlation with the WM score in group I patients. In group II patients, only the peak SGOT levels correlated significantly with this score.
We conclude that in patients with acute infarction, 2DE soon after admission can identify those likely to have in-hospital cardiac complications.

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QRST isointegral maps were made from 87 body surface ECGs in 41 patients with prior myocardial infarction. To evaluate the abnormalities of QRST isointegral maps, a deviation map was constructed from a deviation index, which expressed the deviation of the QRST time-integral value from the normal value at each lead point. Patients were divided into 3 groups according to the asynergic site on left ventriculograms: patients with anterior wall asynergy (n=13), those with inferior wall asynergy (n=13) and those with both anterior and inferior asynergies (n=15). A consistent deviation map pattern was obtained in each group regardless of the QRS duration. Consequently, the deviation map was considered to be a practical method of identifying the asynergic site in patients with myocardial infarction, especially in those with intraventricular conduction disturbances. It is suggested that the deviation map can reveal abnormally altered intrinsic ventricular recovery properties resulting from a loss of the electromotive force of the infarcted myocardium.

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A noninvasive method for real time blood-flow imaging using ultrasound has long been required in the fields of cardiology, and cardiovascular surgery. Recently, we developed a method of two-dimensional Doppler echocardiography (hereafter abbreviated as "2-D Doppler") for clinical use which allows us to obtain noninvasively, intracardiac blood-flow images in real time. The main purpose of this paper is to describe the newly developed blood-flow imaging system "2-D Doppler" and to demonstrate its clinical usefulness in acquired valvular diseases, particularly in the evaluation of valvular regurgitation.
The device, in principle, combines a conventional pulsed-Doppler system and a newly developed auto-correlator, in which blood-flow images within a given cross section of a beating heart are noninvasively displayed in real time, simultaneously with conventional two-dimensional echocardiograms. The system can provide three kinds of information, direction, velocity and turbulence of blood flow.
The 2-D Doppler examinations were carried out on 72 patients with acquired valvular diseases whose diagnoses were confirmed by angiography and/or surgery. Studies were performed comparing the findings of the 2-D Doppler and those of angiography (for aortic and mitral lesions) or with operative findings (for tricuspid lesions) in the quantitative evaluation of valvular regurgitation. Aortic, mitral and tricuspid valvular regurgitation have been quantitatively demonstrated with 2-D Doppler, and, for each value, the severity of the regurgitation showed a high correlation between the findings of 2-D Doppler and of angiography or surgery. In conclusion, we have found that (1) 2-D Doppler is very useful in detecting and estimating the severity of valvular regurgitation, and that (2) 2-D Doppler may replace conventional angiography in some situations.

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It is believed that the prognosis of patients with surgically induced right bundle branch block (RBBB) related to correction of congenital heart diseases varies according to the site of block. Thus, it is necessary to differentiate the proximal type from the distal type of RBBB. The main purpose of this study was to develop a practical and precise method for the determination of the site of block. The right ventricular papillary muscle activation time (V-PM) was measured 1 or 2 weeks after surgery by means of a temporary pacing electrode placed on the epicardial surface of the right ventricular anterior papillary muscle. This technique is referred to as "right ventricular papillary muscle electrography (PME)". The presence of a proximal RBBB is diagnosed by the finding of a prolongation of V-PM.
The unique characteristics of this newly developed PME are as follows: 1) the appropriate site of electrode placement is selected anatomically during surgery by observations of local systolic concavity, and 2) with a unipolar lead, the local activation time can be measured with sufficient accuracy.
The average V-PM was 21.0±6.3msec (±S.D.) in 64 patients without RBBB and 51.1±7.5msec in 13 patients with confirmed proximal RBBB in whom distal RBBB had been excluded in view of the surgical procedures that had been performed. As a result, the criterion for the diagnosis of proximal RBBB was established as a V-PM of longer than or equal to 35msec.
According to this criterion, the incidence of proximal RBBB found in surgically repaired tetralogy of Fallot (TF), membranous ventricular septal defect (VSD (2)) and supracristal ventricular septal defect (VSD (1)) were 46% (11/24), 33% (15/45) and 11% (2/18), respectively. Distal RBBB was observed only in TF, where the incidence was 17% (4/24).

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1. In a well-controlled study the clinical efficacy of a single intravenous injection of mexiletine (3mg/Kg) on ventricular premature contractions was compared with that of procainamide (10mg/Kg) using continuous electrocardiographic recordings.
2. Of the 56 subjects studied, 55 were analyzed. These consisted of 28 cases in the mexiletine group and 27 in the procainamide group. The backgrounds of both groups were considered to be equivalent.
3. Effectiveness on VPC ("marked and moderate improvement", as judged by the subcommittee) was seen in 88% of the mexiletine group and 84.6% of the procainamide group. This difference was not significant. The duration of efficacy was almost the same in the 2 groups.
4. Overall improvement was the same as improvement in VPC.
5. No significant difference was observed in the incidence of side effects. Five patients in the mexiletine group and 3 in the procainamide group reported side effects. The main side effect was light-headedness in the mexiletine group and a decrease in blood pressure in the procainamide group. A decrease in blood pressure was observed in 1 case in the mexiletine group but this was restored by an intravenous infusion of noradrenaline.
6. Mexiletine had little effect on blood pressure, while procainamide induced a drop in the systolic pressure. This difference was significant.
7. Overall utility ("markedly and moderately useful", as judged by the subcommittee) was seen in 84.0% of the mexiletine group and 84.6% of the procainamide group. There was no significant difference between the 2 groups.
8. From the above results, it is concluded that mexiletine (3mg/Kg) is as efficacious as procainamide (10mg/Kg) in the treatment of VPC but that, unlike procainamide, mexiletine has little effect on blood pressure.

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In low-renin hypertensive patients, the acute effect of the angiotensin I-converting enzyme inhibitor, captopril, was evaluated in relation to the response of plasma bradykinin (PBK) levels as a parameter of its inhibitory effect on kininase II. Captopril significantly lowered the blood pressure and increased PBK levels. While there was no significant relationship between the reduction of blood pressure and pretreatment plasma renin activity, a significant correlation was observed between the antihypertensive effect of captopril and changes in PBK (r=-0.834, p<0.01, n=10). Furthermore, in a patient with primary aldosteronism and, also, in a patient with glucocorticoid responsive hyperaldosteronism, captopril increased plasma PBK with reduction of the blood pressure. It is likely, therefore, that in low-renin hypertension, the vasodepressor effect of acute converting enzyme inhibition is due mainly to kinin accumulation rather than inhibition of angiotensin II formation.

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The angiotensin I-converting enzyme of rat aorta was solubilized with Triton X-100 and partially purified by chromatography with DEAE-cellulose and Sephadex G-200. The specific activity of the purified enzyme was 4.01 units/mg of protein. The enzyme was separated into 6 isozymes with different molecular weights of 460, 000, 440, 000, 260, 000, 220, 000, 217, 000 and 119, 000 by Sephadex G-200 gel filtration. All the isozymes migrated as a single band with a molecular weight of 112, 000 on SDS/polyacrylamide gel electrophoresis. These isozymes showed the same optimal pH (8.3) and temperature (30°C). Converting-enzyme, which might be produced in the arterial wall, may play a role in the local control of vascular tone through the conversion of angiotensin I into II in vascular tissue.

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Intracerebroventricular (ICV) injections of carbachol produced biphasic blood pressure responses consisting of initial vasodepression of short duration followed by a sustained pressor phase, which were accompanied by corresponding changes in sympathetic nerve activity in normotensive outbred-Wistar rats (NT) under urethaneanesthesia. In both normotensive Kyoto Wistar rats (WKY) and spontaneously hypertensive rats (SHR), on the other hand, carbachol elicited purely pressor responses, and accompanying sympathetic nerve activity was little affected. The magnitude of the pressor responses was larger in SHR than in WKY or NT rats. Spinal sectioning did not affect the magnitude of the pressor responses. Vasopressor responses to intravenous injections of arginine-vasopressin were not significantly different between WKY and SHR.
These results indicate that carbachol injected intracerebroventricularly produces vasopressor effects mainly by releasing pituitary hormones, probably vasopressin, and that augmented pressor responses in SHR may be due to excessive release of vasopressin.
When central noradrenergic neurons had been destroyed with ICV injections of 6-hydroxydopamine in both NT and WKY rats, carbachol-induced vasopressor responses were markedly augmented and resulted in responses similar to those of SHR. These findings indicate that central noradrenergic vasodepressive neurons are deficient and that the augmented vasopressor responses to carbachol resulted from deranged central noradrenergic mechanisms in SHR.

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The authors studied the number of myocardial β-adrenergic receptors and the cyclic nucleotide concentration in both male spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY) at 4 to 5, 10 to 15, 20 to 25 and 35 to 55 weeks of age. A potent β-adrenergic antagonist, (¹²⁵I) iodohydroxybenzylpindolol was used to estimate the number and affinity of β-adrenergic receptors. β-adrenergic receptors in cardiac membranes from SHR of 4 to 5 weeks and 10 to 15 weeks numbered 63.1±4.6 and 51.6±4.6 f mol/mg protein, respectively. These were significantly (p<0.02) greater than the number in WKY at 4 to 5 weeks and 10 to 15 weeks (42.2±5.1 and 31.5±5.4 f mol/mg protein, respectively). The dissociation constant in the membranes was the same in WKY and SHR, and no significant differences were found in the number of receptors and affinity of SHR and WKY at 20 to 25 weeks or 35 to 55 weeks of age. Also, there was no difference in the concentration of myocardial cyclic nucleotides at the various ages. Since cardiac hypertrophy in SHR had appeared before the onset of hypertension at about 7 weeks, the present results suggest that the SHR heart is hypersensitive to catecholamines and hemodynamically hyperkinetic due to the increased numbers of β-receptors in the pre- and early stages of hypertension.

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Postsynaptic α₂-adrenoceptors have been reported to exist in various tissues, including vascular smooth muscle. In order to investigate the possibility of their mediating a positive inotropic change and clarify the influence of the thyroid on their responsiveness, we examined the effects of clonidine, a known α₂-agonist, on the isolated left atria and femoral vascular beds of rats which were made hypo-, hyper- or euthyroid. Clonidine caused a dose-dependent positive inotropic change in the hypothyroid rat atrium, which was thought to be due to its α₁-stimulating action because of the antagonistic effect exerted by either phentolamine (10^-6M) or prazosin (10^-7M), but not by yohimbine (10^-7M) or cimetidine (10^-5M). In the hyperthyroid rat atrium, clonidine exerted a negative inotropic effect at high concentrations, which was thought to be due to its direct action on the cardiac muscle. Clonidine did not cause any inotropic change in the euthyroid rat atrium. Thus, an inotropic change mediated by the postsynaptic α₂ adrenoceptors could not be demonstrated in the rat heart. In the experi-ment involving hindlimb perfusion, clonidine caused vasoconstriction which was antagonized by yohimbine (10μg/min). This effect was significantly augmented in the hypothyroid rats but not changed in the hyperthyroid ones. The vasoconstrictive effect of phenylephrine was found to be reduced in both hypo- and hyperthyroid rats. These results suggest that, in the peripheral vascular system, thyroid function also influences the postsynaptic α₂-adrenoceptors, but not in the same way as it affects the α₁-adrenoceptors.

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The cardiotonic effect of AR-L 115 BS was assessed in 5 dog heart-lung preparations in which cardiac function had been severely depressed by pentobarbital. AR-L 115 BS in doses of 1-60mg improved cardiac function in a dose-dependent manner and at 30 and 60mg improved it beyond control values. These doses of AR-L 115 BS, however, produced neither a significant increase in heart rate nor arrhythmias. The results indicate that the drug would be of use in the treatment of heart failure.

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Cardiac and coronary vasodilator effects of AR-L 115 BS and theophylline were compared in isolated, blood-perfused papillary muscle, sino-atrial (SA) node, and atrioventricular (AV) node preparations of dogs. Furthermore, the inhibitory effects of both drugs on crude cyclic AMP phosphodiesterase (PDE) prepared from the dog heart ventricle were examined. In the blood-perfused dogheart preparations, AR-L 115 BS (3μg-1mg) and theophylline (3μg-1mg) were injected intra-arterially. Both drugs increased sinus rate and force of contraction and rate of automaticity of the papillary muscle, and decreased AV nodal conduction time in the respective preparations. The 2 drugs both increased blood flow. However, AR-L 115 BS was far more selective for inotropy than for chronotropy as compared with theophylline. AR-L 115 BS was also more selective for inotropy than for coronary blood flow as compared with theophylline, whereas the latter had the opposite selectivity. Both drugs were less effective on ventricular automaticity. Both drugs (0.3-3mM) inhibited PDE activity; however, AR-L 115 BS was less effective than theophylline in this respect, although the former was about 3 times as potent as the latter in producing a positive inotropic effect. The present results suggest that unknown mechanisms other than PDE-inhibition greatly contribute to the positive inotropic effect of AR-L 115 BS.

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A decrease in cardiac function and intracellular calcium, and an increase in cardiac sarcolemmal ATPase have been reported in experimentally induced aortic stenosis of 6 to 9 months duration. Prazosin has been used in the treatment of heart failure due to mechanical ventricular overload. It is, however, not known whether prazosin treatment gives only hemodynamic benefit with accompanying subjective improvement or if it also improves the condition of the myocardium in terms of contractility and biochemical changes. The present investigation deals with the effects of 3 months of prazosin treatment on cardiac function, electrolytes, and ATPase in dogs with aortic stenosis of 3 months duration. Although there were no significant changes in most of the left and right ventricular hemodynamic parameters, the left ventricular enddiastolic pressure increased significantly after 3 months of aortic stenosis. Prazosin prevented further deterioration of cardiac function. All the dogs developed left ventricular hypertrophy and all chest X-rays showed cardiomegaly. Concomitant with these changes, there was a tendency towards a decrease in total tissue Ca⁺⁺ and intracellular Ca⁺⁺ and K⁺ and a tendency towards an increase in sarcolemmal Na⁺-K⁺-ATPase. Prazosin treatment, although it markedly reduced left ventricular end-diastolic pressure, did not reduce the cardiomegaly. There were no significant changes in any of the other hemodynamic parameters. Prazosin treatment decreased sarcolemmal ATPase and tended to increase intracellular Ca⁺⁺. It appears therefore that prazosin not only tends to bring the cardiac function towards control values but also tends to correct the ATPase and intracellular Ca⁺⁺ levels of the failing heart.

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