The serious arrhythmias have been regarded as one of the important complications in patients with acute myocardial infarction. clinical and experimental observations were made of the arrhythmogenecity in acute myocardial infarction in special reference to the high free fatty acidemia (HFFA). The results obtained were as follows: (1) The incidence of arrhythmia in 35 patients with acute myocardial infarction, in whom the serum free fatty acid (FFA) value was measured, was 34.0%. (2) The serum FFA values of arrhythmic patients were significantly higher than those of patients without arrhythmia (P<0.001). (3) It was also revealed that the serum FFA values of patients with ventricular premature contraction (VPC) were significantly higher than those of non-arrhythmic patients (P<0.001). (4) Each of the rate of incidence of VPC in total arrhythmic patients and the serum FFA value on the day of attack was significantly higher than that on the following days, respectively. (5) HFFA was experimentally produced in infarcted dog with the coronary ligation by the infusion of Intralipid and heparin and its effect on the ventricular fibrillation threshold (VFT) was observed. The VFT was markedly decreased promptly after the coronary ligation and a trend of natural recovery of the VFT was seen in a period later than 60 minutes after the coronary ligation. The recovery phase was significantly suppressed by the treatment producing HFFA (P<0.01). The deleterious effect of HFFA on the VFT was prevented by the treatment with glucose and insulin solution (GI solution) (P<0.02). From these results, it is postulated that HFFA in patients with acute myocardial infarction acts as an arrhythmogenic factor by lowering the VFT and GI solution prevents the occurrence of arrhythmia by lowering the serum FFA value.

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On 55 patients with acute myocardial infarction blood gas changes and A-aDO₂ while breathing room air were observed for a period of 5 weeks. PaO₂ during the 35% O₂ inhalation was measured on admission and 5 weeks later for comparisons with the PaO₂ while breathing room air. Pulmonary circulatory hemodynamics was measured in 290 cases on admission using Swan-Ganz's right heart flow directed catheter 7F, and the catheter was kept inn the pulmonary artery in 13 cases for a ;maximum of 9 days. The mean PaO₂ while breathing room air on admission was 66.7 mmHg in the 55 cases. It was 52.3 mmHg in the heart failure group and 74.9 mmHg in the non-heart failure group, showing prominent hypoxemia in the heart failure group. The mean PaO₂ recovered to normal (84.1 mmHg and 87.0 mmHg) 5 weeks later. Inhalation of 35% O₂ was performed for 20 minutes on admission and 5 weeks later. The elevation of PaO₂ during the oxygen inhalation on admission was smaller than that 5 weeks later, significantly smaller in the heart failure group (P<0.001). The mean A-aDO₂ on admission was higher in the heart failure group (58.1 mmHg) than in the non-heart failure group (34.8 mmHg). PaO₂ showed significant correlations with cardiac index and Sv^^-O₂. Although it was significantly correlated with PA diast. and TPR, no correlation with CVP was observed. Hypoxemia in acute myocardial infarction is caused by the following process: the onset of myocardial infarction causes low output, leading to left ventricular failure. As the result of elevated left atrial pressure and pulmonary venous pressure, interstitial pulmonary edema develops provoking ventilation-perfusion inequality, intra-pulmonary shunting, and diffusing defect.

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In 20 limbs of 10 healthy subjects and 55 limbs of 41 patients with occlusive arterial diseases of the legs, muscle blood flow was measured in the flexor hallucis brevis muscle by ¹³³ Xe clearance technique. The clearance curves after the ischemic exercise differenciated limbs with intermittent claudication of the foot from normals and limbs without claudication. An attempt was also made with arteriographic findings in 102 limbs of 84 patients with occlusions of the leg and/or foot arteries only. From results obtained, it is concluded that ¹³³Xe clearance technique applied in the flexor hallucis brevis muscle can be used for diagnosis of foot pain during walking of uncertain origin and intermittent claudication of the foot is caused by severe circulatory insufficiencies of the plantar muscles during walking in the patients with involvements of the posterior tibial and/or plantar arteries.

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1. The effects of clonidine on blood pressure, cerebral norepinephrine content and vascular structures of the kidneys were investigated in 21 SHR. although the body weight was not affected by long term clonidine treatment up to 36 weeks, the systolic blood pressure was significantly reduced. The reduction of the blood pressure was already obvious after 1 week administration of clonidine, but the effect was more prominent after long term treatment of 30 weeks or longer. 2. The cerebral norepinephrine content was significantly lower in SHR, regardless of with or without clonidine treatment, than in the control Wistar rats. Although the cerebral norepinephrine content was slightly increased following clonidine treatment in SHR, the increase was not statistically significant. 3. Angiographic study of the kidneys revealed a poor opacification of the blood vessels and glomeruli in SHR compared with the control Wistar rats. There was no difference in the sizes of the arcuate and interlobular arteries in SHR and the control Wistar rats, although the medial muscular hypertrophy of the arteries was slightly more prominent in the SHR histologically. The angiographic and histologic findings of the renal arteries were not altered following long term clonidine treatment. A possibility was considered that the renal arterioles are mainly functionally affected in SHR.

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In the isolated rabbit heart, verapamil reduced the rate of rise and the slope of diastolic slow depolarization, the maximum, diastolic potential (Ed) and the membrane potential at the peak of depolarization (Ea) of the SA node without preventing regenerative responses in ventricular and Purkinje fibers. This effect of verapamil on SA node was counteracted by raising the extra-cellular calcium ion concentration. On the other hand, tetrodotoxin (TTX) had almost no effect on these parameters of the SA node, but it reduced the maximum rate of rise of the ventricular and Purkinje fibers markedly and eventually rendered these tissues non-excitable. The difference in the actions of verapamil and TTX on the SA node suggests that the SA nodal action potential comes from a different ionic channel (slow channel) from that of the Purkinje fibers or the working myocardium, and the effect of calcium ion suggests that this ion plays an important role in the generation of the SA nodal action potential. The difference in the effect of verapamil on the repolarization phase between ventricular and Purkinje fibers was pointed out and the possible participation of calcium ion in the repolarization phase of these two tissues was discussed.

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Ten patients with angina pectoris underwent multistage maximal treadmill exercise with hemodynamic measurements before, and again 6 months following coronary artery surgery. Subjectively, 9 patients experienced total, and one patient partial relief from angina, and all patients noted improved exercise tolerance following surgery. Objectively, significant improvement was found in duration of exercise, maximal oxygen intake maximal cardiac output, maximal heart rate, and maximal pressure-rate product. Surgery did not significantly affect systemic or pulmonary arterial pressures during exercise. Despite these improvements, maximal cardiac output did not return to normal levels following surgery, due to an unexpected but significant reduction in stroke volume.

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Clinical pictures of 107 cases of familial heart diseases belonging to 30 families were studied. 1. Initial manifestations frequently observed were palpitation, chest pain, becoming aware of irregular heart beats, dyspnea and a syncopal attack. The initial manifestation was most frequently observed in the second or the third decade. In familial idiopathic cardiomyopathy a systolic murmur was the most common auscultatory finding followed by the third and fourth hear sounds. 2. the cardiothoracic ratio was not necessarily increased. 3. In the ECG of familial idiopathic cardiomyopathy, arrhythmia was frequently observed. A-V block was rare but a premature ventricular contraction was frequent. During a syncopal attack, the ECG showed ventricular tachycardia. an abnormal Q-wave, ST segment depression and a negative T-wave were also observed but their incidence did not differ from one lead to the other. Some cases of familial heart diseases showed QT_c-prolongation but QT_c was not over 0.47 seconds and was not as markedly prolonged as in familial QT-prolongation syndrome. 4. A similarity of clinical findings was observed among cases belonging to the same family. There was a striking similarity among the patients belonging to the same family initial symptoms, characters of a systolic murmur, morphology of the cardiac silhouette, morphology of an abnormal Q-wave or ST segment depression and in the leads which showed these abnormalities. 5. The most frequent mode of death was sudden death. A cardiothoracic ratio of 0.6 or more, an abnormal R-wave in V₁ suggesting high dorsal wall damage, left axis deviation, and the low voltage of S_V1+ R_V5 of 1.5 mV or less suggested a poor prognosis.

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Observations are presented about the effects of four kinds of coronary vasodilators (dipyridamole, oxyfedrine, prenylamine and trimetazidine) on coronary circulation in the heart with coronary sclerosis which has been induced by intravenous injection of allylamine in the dog. Following results are obtained: 1) All of the drugs examined increase coronary blood flow and decrease coronary vascular resistance in the dogs with coronary sclerosis as well as in the normal dogs. 2) An amplitude of response of coronary circulation to the coronary vasodilators is significantly less in the dogs with coronary sclerosis than in the normal dogs. 3) The clinical value of coronary vasodilator has been discussed.

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It was reported for a long that break was found in the intima under coronary thrombus. Some authors^14-17 reported recently that the rupture of the intima would be important as the cause of coronary thrombosis. The present study was undertaken to investigate the incidence of coronary thrombus with ruptured intima, morphogenesis of the thrombus and causes of the rupture of the intima. Materials and Methods After fixation in 10% formalin, coronary arteries were sectioned transversely at 2-5 mm intervals. When thrombus or severe intramural hemorrhage was found, transverse sections were made at longer intervals and as parallel as possible. Calcified arteries were removed and decalcified before the sectioning. Serial blocks were removed so that the thrombus or the intramural hemorrhage would be included as a whole. The blocks were processed through alcohol, xylol and paraffin, and sectioned serially at 5μ with AO Spencer No. 820 rotary microtome. Incomplete sections at the beginning were stained with hematoxylin and eosin, and all of the other sections were numbered. Sections numbered 1, 6, ... were stained with hematoxylin and eosin. Those numbered 2, 7, ... were stained with elastica Van Gieson and those numbered 3, 8, ... were stained with Mallory azan method. Other sections were preserved. Thus, 22 thrombosed coronary segments were obtained from 17 cases (12 of whom were male), aged 29 to 90 years. Results In all of the 22 specimens, marked atherosclerotic thickening of the intima was found. Stenosis rate of 12 specimens were 76% or over and that of the rests were 51 to 75%. Nine specimens had breaks of the intima under the thrombus. Five of them had two or more rents (Table I).

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Recently, it has become clear that the body surface isopotential maps (referred to below as map, for short) contain important diagnostic information which is not available in a conventional electrocardiogram or a vectorcardiogram. This report will investigate whether or not the diagnostic accuracy can be achieved from the maps in differentiating the location and extent of myocardial infarction Methods: Eleven mongrel dogs were anesthetized and the chest of each dog was opened by an incision at the left 5th intercostal space and myocardial infarction was caused by ligation of the orifice or branch of the left anterior descending coronary artery. In 1 to 5 weeks after the ligation, each heart was isolated to observe directly the location and extent of infarction. Each map was based on the record of unipolar lead electrocardiograms obtained through the use of needle electrodes attached to 85 lead points on each dog's chest surface in a supine position. Maps were made twice, before and a week after the ligation of each dog with a mapping system using a mini-computer. Results: The dogs with myocardial infarction were classified into three groups according to the location and extent of infarction. Each group had its own characteristic maps, as follows . Group I (Half of the ventricular septum and the larger part of the left anterior and left lateral wall were infarcted.) 1) The negative potentials always occupied the left anterior chest surface for the entire duration of the ventricular depolarization. 2) A large part of the dorsal region was occupied by the positive potentials from the early stage. 3) There was no appearance of the maximum on the left anterior chest surface. 4) The minimum was always observed near the center of the anterior chest surface all through the ventricular depolarization,

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Following the development of CCU, rate of death due to fatal arrhythmia in acute myocardial infarction (aMI) has been markedly reduced, on the other hand, circulatory failure presents remaining problem as notorious cause of death in this clinical catastrophe. Attempt has been made to evaluate the left ventricular performance in the acute stage of myocardial infarction, in which systolic time intervals (STI) were used by non-invasive technique. The relationship of STI with prognosis was also studied, and the results were compared with those of old myocardial infarction. Materials and Methods: In 30 cases of aMI with an average age of 60.2 years, admitted to the CCU, phonocardiogram, electrocardiogram, and carotid pulse tracings were simultaneously recorded, after exclusion of cases with atrial fibrillation, left bundle branch block, and frequent supraventricular or ventricular premature beats. Diagnosis was based on clinical signs, electrocardiogram, and serum enzyme studies. Transmural infarction was noted in all cases. The tracings were recorded by a Fukuda MCM-800 polygraph and TY-303 transducer with paper speed of 100mm/sec, as early as possible on the admission day. Thereafter the recordings were performed in every morning in the CCU, then once a weak after transfer to the general ward until discharge. Recording was carried out to ensure measurement of R-R, I-II, total electromechanical systole (Q-II), and left ventricular ejection time (LVET) in 5 consecutive cycles. Using the average values, pre-ejection period (PEP) was calculated as (Q-II)-LVET, and isometric contraction time (ICT) as (I-II)-LVET, and PEP/LVET to be expressed as a percentage of the ratecorrected normal value according to Sawayama et al. Clinical signs were classified into the following two categories: Group 1: Complete absence of left ventricular heart failure (16 cases). Group 2: Definite left ventricular heart failure with dyspnea, auscultatory and chest x-ray abnormalities, including those requiring digitails administration though left ventricular failure was not always evident (10 cases). Death occurred during hospitalization in 4 cases, all with heart failure. These were classified in a separate group.

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