In view of the fact that stable echocardiograms are easily obtained during atrial pacing, pacing echocardiography was performed to evaluate the usefulness for detecting regional wall motion abnormalities during pacing-induced ischemia and to investigate the relationship between changes in the R wave and left ventricular dimension. The patients were 12 cases of angina pectoris (10 of coronary artery disease; CAD, and 2 of coronary patent aortic valvular disease; AVD) and 6 control cases. Simultaneous recording of two-dimensional and M-mode echocardiograms and electrocardiograms was done before, during and after the atrial pacing at increasing heart rate until angina appeared or the heart rate of at least 140/min was reached. In 12 angina cases, angina and ST depression were induced in 10 and 11, respectively. Excursion of the interventricular septum (IVS) decreased during pacing-induced ischemia in 6 of 7 CAD cases, in which the left anterior descending coronary artery was significantly stenosed (more than 75%). Excursion of the left ventricular posterior wall (LVPW) decreased during pacing-induced ischemia in 4 of 7 CAD cases, in which the vessels giving rise to posterior descending coronary artery were significantly stenosed (more than 75%). In 2 AVD cases, excursion of both IVS and LVPW decreased during ischemia. Left ventricular end-diastolic dimension (LVEDD) increased in only 2 angina cases, although R wave amplitude increased in 6 angina cases.
In conclusion, echocardiography was of use in detecting decrease in the wall motion during pacing-induced ischemia. In atrial pacing, changes in the R wave amplitude were neither sensitive for detecting pacing-induced ischemia nor reflect the left ventricular dimensional change during ischemia.

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This study compared a new method to estimate sinoatrial conduction time (SACT) using continuous atrial pacing proposed by Narula et al with the widely used method using premature atrial stimulation originally proposed by Strauss et al. The estimated SACTs by the two methods were obtained in 19 patients with normal sinus node (SN) function (Group A) and 8 patients with abnormal SN function (Group B).
Estimate of the SACT by the Narula method was taken as the difference between the first atrial return cycle after pacing and the basic sinus cycle length (BSCL). The Narula method was performed for a train of 8 consecutive beats at three different pacing cycle length (PCL); PCL (1)_??_BSCL-50, PCL (2)_??_BSCL-100 and PCL (3)_??_BSCL-150 msec.
In group A, the estimated SACTs by the Strauss method was 185±49.3 msec, meanwhile the SACTs by the Narula method were 148±80.7 at PCL (1), 181±58.7 at PCL (2) and 212±84.5 msec at PCL (3) (mean±SD); the coefficient of correlation between the Strauss method and the Narula method were 0.58, 0.84, and 0.67, respectively.
On the other hand, in group B, atrial return cycles by the Narula method were abnormally prolonged (over 215 msec) in 5 of 8 cases (63%) even at PCL (2) and in all of the cases (100%) at PCL (3). By the Strauss method, SACTs in 6 of 8 cases could not be defined; however it was possible to assess the type of SN dysfunction by the pattern of the atrial return cycles.
In conclusion, the estimated SACT by the Narula method at PCL (2) corresponded well with the SACT by the Strauss method in patients with normal SN function. However, it was difficult to determine SACT in patients with Sick Sinus Syndrome by both methods.

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Vectorcardiograms in 163 clinical subjects of normal and various abnormal conditions obtained by Frank lead system and in 17 dogs of experimental myocardial injury or intra-ventricular conduction disturbances by McFee-Parungao method were transformed by exchange of axes of co-ordinates by the method of McFee et al. The non-planarity index, from the axes of the transformed frontal plane, was significantly higher during myocardial injury and bundle branch blocks as well as from diffuse intra-myocardial conduction disturbances than during normal clinical cases and the control records in animal experiments. The non-planarity index was not increased in localized block of the conduction system in dogs. Therefore, results suggest that this index might be a useful parameter to assess these conditions.

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The left ventricular function and severity of LV volume overload were assessed in 30 patients with aortic regurgitation by a combined use of echocardiography and indicator dilution method.
With decreasing functional capacity of patients, there tended to be greater increase in EDV, and decreases in CO, EF, Vcf, and BAP(DN)/ESV, and shift of LV function curve downward and to the right, reflecting LV myocardial dysfunction.
There was a substantial correlation between functional capacity and the severity of regurgitation as well as LV myocardial function, suggesting the possibility that clinical symptoms may depend upon both the myocardial function and severity of aortic regurgitation. In contrast with many patients with AR of functional class I or II, who had relatively normal LV function, the patients of class III consistently showed substantial LV myocardial dysfunction.
After sublingual administration of ISDN, BAP lowered, EDV and RF decreased. Lowering of BAP and RF were more prominent in class III than in class I.
It has been proved that a combined use of echocardiography and indicator dilution method is of value in assessing the left ventricular function and regurgitant fraction in patients with aortic regurgitation, allowing a better understanding of the disease process and the potential for recognizing patients who may require early valve replacement.

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The hemodynamic differences between chronic mitral (MR: n=30) and chronic aortic regurgitation (AR: n=37) at various functional stages were investigated by echocardiography and compared with the findings in healthy subjects (n=20). The ordinary statistical analysis revealed that in MR myocardial contractility and afterload to the left ventricle (LV) well preserved even at the stage of decompensation, while in AR the contractility deteriorated and the afterload was elevated even at the asymptomatic stage. By the multivariate statistical analysis, the functional differences and characteristics of the 2 diseases were clarified with 2 statistic factors derived from 6 hemodynamic parameters (LV end-diastolic and end-systolic dimensions, mean velocity of circumferential fiber shortening, LV mid-systolic stress, LV mass, and left atrial dimension). In the differentiation between the 2 diseases by the multivariate analysis, left ventricular size tended to be smaller, contractility was preserved and loading of the left atrium was increased in MR more than in AR. Furthermore, a quantitative system which could explain the functional state by these echocardiographic parameters was derived from this multivariate analysis. The functional states was found to be strongly affected by LV end-systolic dimension and left atrial dimension. This quantitative method of determining the functional state, along with an accurate assessment of cardiac symptoms, provides a useful guideline for the clinical evaluation of the 2 diseases.

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This study was undertaken to assess the conditions necessary to cause the "coronary steal" phenomenon in human subjects. We studied 42 patients (36 males, 6 females, ages 27-70 years) with known or suspected coronary artery diseases using continuous monitoring of the changes in blood pressure and electrocardiogram, thallium-201 myocardial imaging and selective coronary arteriography. Dipyridamole in a dose of 0.4mg/Kg was given as an intravenous infusion for 4min and thallium-201 was injected at the 4th minute after completion of the dipyridamole infusion. None of the 20 patients without significant coronary artery disease complained of anginal chest pain or showed ischemic S-T segment depression. Dipyridamole images showed no perfusion abnormalities in 17 of the 20 patients. On the other hand, in 4 of the 22 patients with significant coronary artery disease, anginal chest pain accompanied with S-T segment depression occurred after the dipyridamole infusion. Dipyridamole images showed perfusion abnormalities in 18 of the 22 patients. The 4 patients who experienced an anginal attack had 3 vessel disease on the coronary arteriogram and showed regional perfusion defects on scintigrams corresponding to the regions receiving collaterals. Before the onset of pain, the double product (heart rate × systolic arterial pressure) was unchanged significantly but there was a reduction in the systemic blood pressure. The overall data exhibit the following conditions under which attacks of angina pectoris are induced by dipyridamole: 1) the presence of multiple vessel disease, 2) a fall in systemic blood pressure, and 3) regional malperfusion caused by dipyridamole.

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We have studied the effects of chronic oral verapamil therapy on exercise performance in 26 patients with arteriographically proven coronary disease and positive exercise stress tests. Maximal, multistage treadmill exercise tests were performed before and after 2, 4, and 8 weeks therapy with verapamil 120mg t. i. d. The time to angina and the distance walked increased from 279 to 452sec and from 255 to 443 meters respectively. The frequency of anginal attacks decreased from 24 to 9 per week after 8 week treatment while the nitroglycerin consumption decreased from 20 to 8 tablets per week. Functional aerobic impairment improved from 42.7% to 29.3% whilst there was no change in pressure-rate product, cumulative ST segment depression or EEV₁/FVC ratios.

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The extents of superprecipitation and contractile protein contents of myosin B in the myocardium and conduction system were compared. The extents of superprecipitation of myosin B of the two types of cardiac muscle were similar, but the onset of the superprecipitation reaction of myosin B from the conduction system was delayed and the clearing phase of the reaction was prolonged. On sodium dodecyl sulfate (SDS)-polyacrylamide gel (6%) electrophoresis of myosin B, myosin, actin, and tropomyosin were clearly separated. The amounts of protein present in stained bands of polyacrylamide gels were estimated. The weight ratios of myosin: actin, tropomyosin: myosin, and actin: tropomyosin in myosin B were not significantly different in the two types of cardiac muscle. However, the compositions of myosin light chains in the two types of cardiac muscle were quite different. It was suggested that this difference of myosin subunits might contribute to the difference in superprecipitation of myosin B.

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In the present study an attempt has been made to characterize the β-adrenoceptors of coronary vasculature in dog. Blockade of β₁-adrenoceptors with ICI 50172 or β₂-adrenoceptors with RB₂ showed only partial antagonism of isoprenaline-induced decrease in coronary resistance. However, combined treatment with ICI 50172 and RB₂ completely blocked the isoprenaline-induced fall in coronary resistance. Essentially similar results were observed in controlled heart rate experiments where the drugs were administered locally into the coronary circulation. These results demonstrate the involvement of both β₁ and β₂ adrenoccptors in isoprenalineinduced coronary vasodilatation.

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Although the end of ejection of the left ventricle has been generally accepted as almost synonymous with the end of mechanical systole of the ventricle, recent experimental studies showed the cases in which end ejection lagged markedly behind end systole as identified by the time at which the ventricular pressure-volume data point reached the peak isovolumic pressure-volume relation curve. To obtain a better insight into cardiovascular conditions of the delayed end ejection, a computer simulation study was carried out in which the performance of a time-varying elastance model of the ventricle connected with a modified Windkessel model of the arterial load was analyzed. Any change in the Windkessel parameters, ventricular contractility and heart rate sensitively shifted end ejection relative to end systole. Although end ejection coincided with end systole under limited circumstances, end ejection variably lagged behind end systole under most circumstances. These results suggest that the interval between end systole and end ejection of the left ventricle in vivo is also variable depending on changes in the arterial loading conditions, ventricular contractility and heart rate.

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In a case with the Wolff-Parkinson-White syndrome, the phenomenon "entrainment without interruption" was observed during spontaneous tachycardia. Electrophysiologic study revealed that the tachycardia was due to reentry with the antegrade limb being the AV node-His axis and the retrograde limb being the accessory pathway. This report is the second report showing "entrainment" phenomenon which is consistent with macro reentry as the mechanism of tachycardia as shown in atrial flutter.

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A patient with markedly elevated diaphragm due to massive ascites secondary to nephrotic syndrome demonstrated an intense early diastolic sound with low- and medium-pitch. This abnormal sound coincided closely with the "D" point of the anterior mitral valve echogram. This sound remarkably diminished in intensity during inspiration with lowering of diaphragm, and after removing ascites it completely disappeared. Noninvasive study with phonoechocardiograms showed neither constrictive pericarditis nor large pericardial effusion. These findings lead us to believe that the sound may be related to an abnormal ventricular recoil striking the extracardiac structures at the end of the isovolumetric relaxation time. To our knowledge, the fact that the elevated diaphragm itself can produce an early diastolic sound ("pseudo-knock sound") has not been previously reported.

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