Japanese Heart Journal
Online ISSN : 1348-673X
Print ISSN : 0021-4868
ISSN-L : 0021-4868
Volume 18, Issue 6
Displaying 1-14 of 14 articles from this issue
  • Tadashi KAMBE, Norio HIBI, Kinya NISHIMURA, Toshinori SAKAKIBARA, Tada ...
    1977 Volume 18 Issue 6 Pages 743-750
    Published: 1977
    Released on J-STAGE: December 09, 2008
    JOURNAL FREE ACCESS
    The present study was undertaken to discuss the echo source of systolic hump in hypertrophic obstructive cardiomyopathy (HOCM) from a viewpoint of B-mode echocardiography. Cross-sectional images were obtained from 4 patients with HOCM using a Sonolayergraph of Toshiba, SSL-51H. This equipment is characterized by its high speed mechanical sector scanning and wider angle.
    Recordings were made with ordinary 35mm camera or Polaroid in conjunction with 8mm cinecamera.
    Our data showed that systolic hump in this lesion was not caused by anterior systolic movement of anterior mitral leaflet, but was emanated from the chordae tendineae attached to the anterior or posterior mitral leaflet. In systole, the anterior mitral leaflet moved backward for closure, while the chordae tendineae approached the bulged interventricular septum resulting in the formation of systolic hump.
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  • Toshihide SHU, Tsuneko KASAHARA, Masao KABASAWA, Shigeo KAMATA, Hirono ...
    1977 Volume 18 Issue 6 Pages 751-764
    Published: 1977
    Released on J-STAGE: December 09, 2008
    JOURNAL FREE ACCESS
    1) Diastolic descent rate (DDR) of the anterior mitral leaflet improved after the surgery. However, this improvement was not modified with a) atrial fibrillation b) damages of the subvalvular supporting tissue c) valvular calcification d) the method of the operation, namely the open or closed commissurotomy.
    2) DDR was fairly well correlated with the mitral orifice area, the cardiac output and the pressure gradient across the mitral valve.
    Therefore, the echocardiographic diagnosis and the follow up evaluation of the mitral stenosis after the surgery were thought to be very reliable, considering the accuracy of this diagnosis as disclosed in this study. The contributory effect to DDR was discussed.
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  • Zainul ABEDIN, P.S. BIDWAI, H.N. KHATTRI
    1977 Volume 18 Issue 6 Pages 765-776
    Published: 1977
    Released on J-STAGE: December 09, 2008
    JOURNAL FREE ACCESS
    Fifty-one patients with dominant rheumatic mitral stenosis were studied by clinical, electrocardiographic, and radiological criteria for evaluation of pulmonary hypertension. Predicted pulmonary artery pressure from these criteria were then compared with the pulmonary artery pressure measured during cardiac catheterization.
    In the first 31 patients, the assessment of pulmonary hypertension using combined clinical, electrocardiographic, and radiological methods gave better results than any one single method alone.
    On the basis of these observations, a composite criterion was arrived at. This new criterion was then prospectively applied to the next 20 consecutive patients with dominant mitral stenosis. In 14 of the 20 patients, the predicted pulmonary artery mean pressures were in the same range as the measured mean pulmonary artery pressures when the new composite criterion was used.
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  • Michio OKADA
    1977 Volume 18 Issue 6 Pages 777-788
    Published: 1977
    Released on J-STAGE: December 09, 2008
    JOURNAL FREE ACCESS
    Seventy-six atrial pacing induced Wenckebach periods in 20 patients were analyzed. They were divided into 5 types according to the manner of increment change of P'V prolongation. Fifty-four % of the periods were atypical (Types II-V). There was a significant increase in the incidence of atypical periods as the length of the periods increased. The recovery curve of the A-V node was obtained by plotting P'V against preceding VP'. The curve was convex and the slope became greater than 45 degrees near the absolute refractory period in the majority of the cases, although there was 1 case in which the slope was less than 45 degrees throughout the curve. The P'V interval was found to be determined mainly by the preceding VP' interval. The mechanism by which these different types of Wenckebach periods develop can be explained by the relationship between the shape of the recovery curve and the pacing rate. The types II, III, and IV periods which have been dealt with as atypical periods were understood to develop by the same mechanism as type I (typical) periods.
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  • Tadashi KAMBE, Hisao TADA, Arata MIWA, Kinya NISHIMURA, Takemi ARAKAWA ...
    1977 Volume 18 Issue 6 Pages 789-797
    Published: 1977
    Released on J-STAGE: December 09, 2008
    JOURNAL FREE ACCESS
    In order to study the intracardiac murmurs in coronary venous system, right heart catheterization was carried out on 35 patients with or without mitral regurgitation. The double-lumen phonocatheter of A.E.L. was used for 33 cases but for 2 the microtip phonocatheter of Millar was employed. As a rule, simultaneous recording of intracardiac and external phonocardiograms was made with the pressure tracing in the majority of cases.
    The examined subjects were divided into 3 groups; 9 cases with mitral regurgitation confirmed by left ventriculography (Group I), 20 without mitral regurgitation (Group II), and 6 with functional systolic murmur (Group III). In Group I, a loud systolic murmur was recorded in 7 cases (MR 5, MR+AR 1, ECD 1), but in none of IHSS in the coronary sinus or great coronary vein. In Group II, no systolic bruit was noted in VSD and other lesions except ASR in the coronary venous system. The same was true in patients with functional systolic murmur (Group III).
    Intracardiac phonocardiography is thought to be useful to record mitral regurgitant murmurs in the coronary venous system, since the latter is in the close proximity to the mitral posterior commissure or mitral annulus.
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  • Keiji UEDA, Koei KITANO, Junichiro MIFUNE, Shinichiro OHKAWA, Masaya S ...
    1977 Volume 18 Issue 6 Pages 798-811
    Published: 1977
    Released on J-STAGE: December 09, 2008
    JOURNAL FREE ACCESS
    Clinical and electrophysiologic studies were performed in 10 aged cases (50-82 years of age) with WPW syndrome and following results were obtained: 1) Episodes of paroxysm of supraventricular tachyarrhythmias were observed in 7 and complication of sinus node dysfunction was noted in 3. 2) P-delta intervals on electrocardiogram exceeding 0.12 sec were observed in 4 cases. 3) Patterns of normalization of QRS complex in 4 cases were characterized by tachycardia-dependent in 2 and bradycardia-dependent in 2. 4) Effective refractory period of the accessory pathway (AP) in antegrade direction exceeded that of A-V node in 5 cases and the former exceeding 500 msec was observed in 2 cases. The relations between the changes of the electrophysiologic properties of the AP and altered clinical manifestations of the WPW syndrome in aged cases were discussed.
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  • Fibrosis of Papillary Muscles and Focal Cardiac Myocytolysis
    Arthur STEER, Teruyuki NAKASHIMA, Taketsugu KAWASHIMA, Kelvin K. LEE, ...
    1977 Volume 18 Issue 6 Pages 812-822
    Published: 1977
    Released on J-STAGE: December 09, 2008
    JOURNAL FREE ACCESS
    Three types of small cardiac lesions were described and illustrated: (1) focal type of papillary muscle fibrosis, evidently a healed infarct of the papillary muscle present in 13% of the autopsies, is a histologically characteristic lesion associated with coronary artery disease and healed myocardial infarction, (2) diffuse type of papillary muscle fibrosis, prob-ably an aging change present in almost half of the autopsies, is associated with sclerosis of the arteries in the papillary muscle, is identifiable histologically, and apparently is not associated with any cardiac abnormality, and (3) focal cardiac myocytolysis, a unique histologic lesion, usually multifocal without predilection for any area of the heart, is associated with ischemic heart disease, death due to cancer complicated by nonbacterial thrombotic endocarditis and microthrombi in small cardiac arteries as well as with other diseases. Differentiation of the 2 types of papillary muscle fibrosis is important in the study of papillary muscle and mitral valve dysfunction. Focal cardiac myocytolysis may contribute to the fatal extension of myocardial infarcts.
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  • Kailash PRASAD, Jagdish C. KHATTER, Baikunth BHARADWAJ
    1977 Volume 18 Issue 6 Pages 823-840
    Published: 1977
    Released on J-STAGE: December 09, 2008
    JOURNAL FREE ACCESS
    Various cardiovascular parameters (blood pressure, pressures in the 4 chambers of the heart, cardiac output, cardiac index, dp/dt and (dp/dt)/IIP of left and right ventricular pressures, heart rate, total peripheral resistance, left ventricular work index, roentgenogram, electrocardiogram) were assessed before and after various intervals of mitral insufficiency in 45 dogs produced by detaching 2 or 3 chordae tendineae from one papillary muscle through left atrial route to raise the left atrial pressure up to 2.5 to 3 times the normal. Fourteen of 45 dogs that died within 2 weeks had left atrial pressure more than 60mmHg. The present method of production of mitral insufficiency was compatible with prolonged survival (11 months). Systolic thrills, cine-angiocardiography, and left atrial expansion during systole prior to sacrifice documented the presence of mitral insufficiency. Roentgenograms, hemodynamic measurements and necropsy data documented the presence of left ventricular hypertrophy and failure. Hemodynamic measurements performed just prior to sacrifice showed that there was an increase in the left ventricular function during the early stage of ventricular adjustments to a chronically increased volume overload. Later on as hypertrophy progressed, cardiac function became depressed and left ventricular failure subsequently developed. The hemodynamic and autopsy data indicated that the right ventricle and right atrium were not affected initially. Later on because of the back pressure, the right side of the heart also began to show the effect of back pressure. There was an increase in the blood pressure and total peripheral resistance. The present results provide an experimental model of chronic cardiac hypertrophy and failure to study the pathophysiology of heart failure due to mitral insufficiency.
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  • Hitonobu TOMOIKE, Motoomi NAKAMURA, Yoshiaki NOSE, Akio KUROIWA
    1977 Volume 18 Issue 6 Pages 841-850
    Published: 1977
    Released on J-STAGE: December 09, 2008
    JOURNAL FREE ACCESS
    This study is designed to investigate whether a selective hypotension of the left circumflex coronary artery (LCCA) causes selectively increased ischemia in the posterior papillary muscle (PPM-L) of the dog. Regional myocardial flow was measured by Rb86 clearance technique. In control animals, the distribution of blood flow between subendocardium and subepicardium, between the left and right ventricles and the septum, and between the free wall and the papillary muscle was studied. In normal situation, the subendocardial to subepicardial flow ratio of the left and right ventricle was approximately unity, however, in the papillary muscle the subendocardial perfusion was less than that of the central core. In selective LCCA hypotension by partial obstruction, the subendo/central core flow ratio of the PPM-L increased in contrast to a marked decrease of subendo/subepi flow ratio of the left ventricular free wall. The ratio of blood flow in the ischemic PPM-L and/or posterior wall of the left ventricle to that in the normally perfused anterior wall of the left ventricle dropped profoundly when LCCA is sufficiently narrowed to cause a pressure drop in the distal portion of the vessel. The flow drop in the PPM-L was greater than that in the other part of the subendocardium. These results demonstrated a selective impairment of blood flow to the posterior papillary muscle after partial obstruction of the left circumflex artery which may have direct clinical relevance.
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  • Masayasu HIRAOKA
    1977 Volume 18 Issue 6 Pages 851-859
    Published: 1977
    Released on J-STAGE: December 09, 2008
    JOURNAL FREE ACCESS
    Voltage clamp experiments were carried out with short Purkinje fibers exposed to acetylstrophanthidin. A consistent change in membrane current was an appearance of a transient inward current on repolarization to the resting potential from the preceding depolarization, when preparations were treated with sufficient concentration of acetylstrophanthidin to cause the transient depolarization. This transient inward current displayed voltage- and time-dependence on the preceding depolarization, of which kinetics were different from the pacemaker K+ current. The transient inward current was easily blocked by manganese ions. The results indicated that acetylstrophanthidin induced the transient inward current which was the basis of the transient depolarization and the current might represent an abnormal state of the slow inward current possibly related to the altered internal Na+ and Ca++ concentrations.
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  • Takashi AKASU, Yhukou OHTA, Kyozo KOKETSU
    1977 Volume 18 Issue 6 Pages 860-866
    Published: 1977
    Released on J-STAGE: December 09, 2008
    JOURNAL FREE ACCESS
    The effects of epinephrine (1×10-6-1×10-5M) on the resting membrane potential and the K+-activated hyperpolarization of bullfrog atrial heart muscles were studied by the single sucrose-gap method or by intracellular microelectrode filled with 3M KCl. Epinephrine-induced hyperpolarization (Ep-hyperpolarization) was completely eliminated by the effect of ouabain or by removal of extracellular K+. The amplitude of K+-activated hyperpolarization, which was produced when the extracellular K+ concentration was raised from zero to 2mM, was markedly increased in the presence of epinephrine. The membrane depolarizations, due to high extracellular K+ concentration in the presence of ouabain (5×10-6M) which completely and reversibly eliminated the K+-activated hyperpolarization, were not altered under the effect of epinephrine.
    These results suggested that Ep-hyperpolarization of bullfrog atrial heart muscles was due to the acceleration of electrogenic Na+ pump which produced the K+-activated hyperpolarization.
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  • Katsuo OZAWA
    1977 Volume 18 Issue 6 Pages 867-877
    Published: 1977
    Released on J-STAGE: December 09, 2008
    JOURNAL FREE ACCESS
    This experimental study was performed to evaluate the possibility that the site per se of infarction or ventricular aneurysm after acute myocardial infarction had a unique important role in left ventricular function.
    Acute myocardial infarction and ventricular aneurysm were made in either the anterior or the inferior wall of the left ventricle using 24 dogs. Infarction was made by the multiple ligation method. The weight of the infarcted area was 23.1±3.9% of the left ventricular free wall in the anterior wall group (12 dogs), and was 23.8±4.8% in the inferior wall group (12 dogs). Ventricular aneurysm was made of right atrial homograft. The capacity of ventricular aneurysm, measured by casts, was 37.8±7.7% of the left ventricular cavity in the anterior wall group and was 38.3±7.3% in the inferior wall group. There was no significant difference in either the size of infarction or the capacity of ventricular aneurysm between 2 groups (p=0.05).
    Ventricular function curves were obtained before infarction (control), after infarction, and after the creation of ventricular aneurysm, plotting left ventricular stroke work (LVSW) per body weight against left atrial mean pressure (LAMP). The change in ventricular function curves after infarction and the creation of ventricular aneurysm was not different significantly between 2 groups.
    In the anterior wall group, LVSW/LAMP decreased to 47.8±9.8% of the control after infarction, and further to 27.1±6.9% after the creation of ventricular aneurysm. In the inferior wall group, it lowered to 47.6±12.5% and again to 26.5±6.4%, respectively. There was no difference in these values between 2 groups statistically (p=0.05).
    From the result of this experiment, it was concluded that the impairment of left ventricular function was equal between these 2 groups not only after infarction but also after the creation of ventricular aneurysm and that the anterior wall would not have more important contribution to the pumping ability of the left ventricle as compared with the inferior wall.
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  • F.J. Ten CATE, W.B. VLETTER, van de BRAND, J. ROELANDT
    1977 Volume 18 Issue 6 Pages 878-882
    Published: 1977
    Released on J-STAGE: December 09, 2008
    JOURNAL FREE ACCESS
    This case report describes the disparity between the findings of the plain chest film and the echocardiogram in a patient with severe coronary artery disease. Whereas the plain chest film shows a normal cardiothoracic ratio of 50% indicating normal LV size, the echocardiogram shows features characteristic of a dilated cardiomyopathic left ventricle with low amplitude of wall motion and consequently low ejection fractoin. These echocardiographic findings were confirmed at cardiac catheterization and angiography. We propose the use of echo instead of the plain chest film in the evaluation of LV size in the cardiac patient.
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  • Respiration Dependent Cyclic Changes in Mitral and Aortic Valve Motion : A Case Report
    Tsuguya SAKAMOTO, Chuwa TEI, Terumi HAYASHI, Hirofumi ICHIYASU, Keiko ...
    1977 Volume 18 Issue 6 Pages 883-895
    Published: 1977
    Released on J-STAGE: December 09, 2008
    JOURNAL FREE ACCESS
    The mechanism of production of pulsus paradoxus was echocardiographically studied in a 74-year-old male with subacute effusive-constrictive pericarditis which developed to constrictive pericarditis under the observation. Echocardiography disclosed the following phenomena during inspiration: 1) mitral valve did not open until the atrial systole, probably because of the lack of antegrade mitral flow during rapid filling phase (the E wave was not observed), 2) concomitantly, aortic valve opening decreased markedly in its grade, and 3) left ventricular ejection time (LVET) decreased and pre-ejection period (PEP) increased, resulting in a higher PEP/LVET ratio (up to 1.32). The opposite was true during expiration (PEP/LVET ratio was 0.40).
    This is probably the first case, in which the mechanism of pulsus paradoxus was investigated by aortic and mitral valve echograms.
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