During the past 10 years we experienced 234 patients with atrial fibrillation, of whom 94 patients (40.2%) showed a paroxysmal form. Underlying diseases of these 94 patients were hypertension and/or coronary heart disease in 51 (54.3%), rheumatic valvular disease in 3 (3.2%), hyperthyroidism in 2 (2.1%), and miscellaneous diseases in 15 patients (16.0%). Idiopathic atrial fibrillation was found in the remaining 23 patients (24.5%). Frequency of paroxysm was variable. Paroxysm occurred only once or twice in 35 patients (37.2%) and more than 21 times in 20 patients (21.3%). Duration of a single paroxysm ranged from less than 24 hours in 49 patients (52.1%) to more than 15 days in 7 patients (7.4%). Atrial fibrillation became permanent in 19 (25.3%) of 75 patients who had been observed for a period of more than 1 year.

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Etiology of QT prolongation and T wave high voltage was studied in 90 chronic alcoholics in relation to history of alcoholism, blood chemical values, heart rate and QRS voltage with a technic of multiple regression analysis. Incidences of QT prolongation (22%), T wave high voltage in lead V₂ (9%), hypopotassemia (23%), hypocalcemia (26%) and hypomxagnesemia (28%) were high, despite these examinations were done after relatively long abstention period (35 days on average). Sinus tachycardia (19%) and QRS high voltage (S_v1+R_v5 exceeding 4mV, 41%) were also frequent. Unexpectedly, QT interval did not correlate to serum electrolytes, including calcium. Major factors associated with QT prolongation were sinus tachycardia, longer abstention period and larger amount of daily alcohol consumption. Although the reason of each association was not quite clear, alcoholic myocardial damage may be a cause of QT prolongation. Voltage of T wave in lead V₂ was sensitive to serum potassium level, but the observed tendency of hypopotassemia acted to the direction against high voltage of T wave. The sole factor positively associated with high voltage of T_v2 was high QRS voltage, which may be a manifestation of left ventricular hypertrophy.

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Eighty-nine children with rheumatic fever between 1964 and 1978 were reviewed. There were 40 males and 49 females. The first attack occurred mostly between 6 and 12 years. Arthritis was present in 62.9%; carditis, 55.1%; chorea, 19.1%. Children were followed from 20 months to 15 years (mean 61 months). Seventeen developed recurrent attacks (19.1%). On final examination, 40 had no heart disease, 30 had mild heart disease, 6 required valve surgery, 4 had died, and 9 had moderate heart disease but not operated. Chorea was present in 20 children. Six of them also had mitral insufficiency, 3 had recurrence after episode of chorea. Prompt diagnosis and treatment of streptococcal infection and penicillin prophylaxis need to be stressed. Severe carditis on initial attack and recurrence predispose to the development of severe heart disease.

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In order to evaluate left anterior descending coronary artery (LAD) lesions proximal or distal to the first septal branch and to detect geomerical change of the left ventricular (LV) chamber, esophageal and conventional echocardiographies were performed on 18 patients who had more than 75% narrowing of the LAD and on 21 normal control subjects. In the 17 LAD disease patients with adequate echocardiograms, the interventricular septum (IVS) and left ventricular anterior wall (LVAW) excursions were evaluated and used to predict the site of the angiographically determined LAD lesions. The 5 patients with distal LAD lesions had normal septal excursions. However, 4 of them (80%) had diminished or absent LVAW excursions. On the other hand, the 12 patients with proximal LAD lesions had diminished LVAW excursions and 9 of them (75%) had diminished or absent septal excursions. In the presence of coronary artery disease, reduced or absent IVS and LVAW excursion on echocardiograms strongly suggests LAD lesions proximal to the first septal brach. On the other hand, normal IVS and abnormal LVAW excursion suggests the presence of distal LAD lesions.
In normal subjects, there was good agreement between the dimension of the LV chamber from the LVAW to the left ventricular posterior wall (LVPW) measured by esophageal echocardiography and the dimension of the LV chamber from the IVS to the LVPW measured by conventional echocardiography. However, in most patients with LAD lesions, the esophageal echocardiographic dimension was larger than the conventional echocardiographic dimension, especially when asynergy was severe. The geometrical change probably explains this disparity.
Echocardiography, especially esophageal echocardiography, may be a useful noninvasive method in predicting the location of the LAD lesions and in detecting left ventricular geometrical change of patients with coronary artery disease.

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A noninvasive method for the determination of stroke volume which can be applicable even to a heart contracting asymmetrically is desired. The momentum of blood ejected from heart will be divided into 2 forms; the one is that of blood running away distally and the other is the momentum of the aortic root. SV is estimated by an equation; SVao=k×D²× Vao^1/2×AOT, where D is the diameter of the aortic root, Vao is the mean velocity of the systolic movement of anterior aortic wall, and AOT is the duration of the valve opening of the aortic leaflets. A good correlation was found between SVao and SV measured by the thermodilution method (r=0.85, p<0.001). Since the parameters used in the present method are not affected directly by the mode of cardiac contraction; symmetrical or asymmetrical, it may be useful to determine SV in man.

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The mechanism of detecting the cardiac wall motion by Cardiokymography (CKG) using a sensing coil was studied by the following experiments. 1) The precordial maps of CKG were recorded on 3 subjects. When the surface movement of the chest was eliminated by a piece of acrylic board in each subject, the amplitude of CKG was reduced to average of 22.7±2.5% of the initial amplitude (p<0.01). 2) As the content of salt was increased in water and blood above the probe, the oscillation frequency dropped slightly at first, then it went up beyond the initial value. 3) When an artificial pneumothorax was made in a dog, the amplitude was reduced. Then, by the application of an acrylic board, the wave form became flat. 4) CKG could not detect the movement of the resected canine heart containing blood in a normal saline solution. These data indicate that the capacitance was the main determinant of oscillation frequency in man and that the most significant factor of the wave form was the surface movement of the chest.

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The intrinsic cycle length of the ventricular parasystolic pacemaker may be modulated by electrotonic influence of intervening ventricular depolarizations. In order to quantify the magnitude of modulation in relation to the timing of the intervening depolarization, a curve of influence was constructed in a patient with ventricular parasystole. The current communication deals with the detailed description of a step-by-step method for the construction of the curve of influence.

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Experiments were designed to clarify what mechanisms are involved in the contraction of dog coronary artery induced by acetylcholine. Helical strips cut from the left circumflex coronary artery were suspended in a bath filled with oxygenated Krebs-Ringer solution at 37°C, and tension developments were recorded isometrically. During potassium-contrac-ture acetylcholine produced further contractions of the strips, which were significantly depressed by atropine together with phentolamine or atropine together with d-tubocurarine. In the strips prepared from dogs in which 6-hydroxydopamine was administered 2hrs before isolation of hearts, acetylcholine-induced contraction was suppressed by atropine alone. Norepinephrine produced contractions in these strips, which were blocked by phentolamine. Results indicate that acetylcholine may directly con-strict the artery through a muscarinic action and simultaneously produce norepinephrine release from sympathetic nerve endings by acting on presynaptic nicotinic receptors resulting in the contraction of the artery.

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The effect of L-carnitine on cardiac hemodynamics was evaluated in normal closed chest dogs. Extracorporeal circulation was produced to measure coronary blood flow in closed chest dogs. Coronay venous blood was introduced to the extracorporeal circuit through a polyethylene catheter wedged into the coronay sinus under fluoroscopic control and was returned to the animal through the left jugular vein. L-carnitine was infused intravenously at a constant rate of 80mg/Kg/min for 8min. Hemodynamic responses appeared within 1 to 3min of carnitine infusion and peak effects were observed nearly after 5min. Peak effects on cardiac hemodynamics after 5 to 8min of carnitine infusion were as follows. Heart rate decreased by 17% from control (p<0.05). Aortic and left ventricular pressure increased by 20% (p<0.05 and p<0.01 respectively) and peak positive left ventricular dp/dt increased by 35% (p<0.01), the mean rate pressure product as the index of myocardial oxygen consumption remained unchanged. Coronary blood flow increased by 60% (p<0.001) and coronary vascular resistance decreased by 25% (p<0.01). As the infusion of carnitine was discontinued, the effects promptly disappeared. These data suggest that L-carnitine has direct vasodilating and positive inotropic effects on cardiovascular system.

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The effect of 5-hydroxytryptamine (5-HT) on the isometric contraction, membrane potential, and membrane current of isolated bullfrog (Rana catesbeiana) atrium was investigated. 5-HT depressed the isometric contraction and this negative inotropism was atropine-resistant.
5-HT reduced both peak amplitude and duration of the action potential, but caused no detectable changes in the resting membrane potential and membrane input resistance. The final, or "secondary depolarization phase"¹⁾ in the rising phase of the action potential was found to be selectively depressed by 5-HT. These inhibitory effects on the action potential were also atropine-resistant.
A single sucrose-gap voltage-clamp experiment revealed that 5-HT caused a reduction of the slow inward (Ca⁺⁺/Na⁺) current. The membrane slope conductance near the resting membrane potential and the degree of activation of the time-dependent potassium current showed no detectable change in the presence of 5-HT.
It was concluded on the basis of the present results that 5-HT directly controlled the action potential by selectively depressing the slow inward (Ca⁺⁺/Na⁺) current. This may be responsible for the negative inotropic effect of 5-HT on bullfrog atrium.

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The effects of magnesium chloride were investigated on pacemaker activity and atrial contractility, using isolated, blood-perfused canine atrial and ventricular preparations with heparinized arterial blood led from the support dogs. Magnesium chloride injected directly into the sinus node artery produced dose-related negative chronotropic and inotropic effects in isolated right atria. In small doses (0.1-1mg), magnesium chloride caused only a negative chronotropic effect without significant negative inotropic changes. The threshold dose for inducing the negative chronotropic response to magnesium chloride was approximately 0.3-1mg, but that for the negative inotropic response 1-3mg. The duration of the negative inotropic response was usually shorter than that of the negative chronotropic response. These negative effects were not inhibited by atropine which completely blocked the acetylcholineinduced effects. Magnesium chloride also produced a dose-dependent negative inotropic effect in the isolated, blood-perfused left ventricular preparation in relatively high dose ranges. Moreover, magnesium chloride produced an uniform depression of contraction amplitude at all frequencies (2-3.5Hz) examined on the frequency-force relationship.

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Effects of calcium antagonists on the ST alternans during acute coronary occlusion were examined in dogs. The intravenous administration of verapamil at doses of 0.1mg/Kg and 0.2mg/Kg prominently attenuated the degree of ST alternans. Diltiazem at dose of 0.2mg/Kg also attenuated the degree of alternans. Dipyridamole at dose of 0.5mg/Kg did not significantly attenuate the degree of alternans. Verapamil significantly inhibited the ST-segment elevation. After verapamil, ST alternans did not occur even after a longer period of occlusion when changes in QRS complex and the ST-segment elevation were remarkable. It is possible that verapamil inhibits ST alternans by both the protecting effect against ischemic injury and a direct effect on the electrical activity of the myocardial cell membrane.

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Changes of the surface ECG and monophasic action potential induced by isoproterenol injection were investigated under normo- and hypercalcemic conditions in dogs. (1) Biphasic time course of T wave changes, initially inverted and subsequently uprightly tall, was observed after intravenous injection of isoproterenol in doses of more than 2μg. (2) Initial prolongation and subsequent shortening of the phase 2 of action potential were observed on the ventricular surface in accordance with the biphasic time course of the T wave changes on the surface ECG after isoproterenol injection. (3) Giant T wave inversion associated with QT prolongation was obtained by isoproterenol injection under hypercalcemia. (4) Marked prolongation of total duration as well as phase 2 of action potential was observed in accordance with the giant negative T wave on the surface ECG. Although the mechanism of this experimental model of giant negative T wave is not clear, this model could have important suggestions on the unknown mechanism of giant negative T wave observed in various clinical status.

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The diagnosis of atrial septal defect (ASD), persistant left superior vena cava (LSVC) and absence of coronary sinus was established by cardiac cateterization in a 20 years old female. At surgery the coronary vein ostia were located in the left atrium. LSVC was ligated and a pericardial patch was sutured around the orifices of the coronary veins and extended to the ASD to redirect the coronary blood flow into the right atrium and close the defect. The postoperative cardiac catheterization and hemodynamic studies revealed good result.

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A 17-month-old Japanese girl with an idiopathic acute myocarditis had symptoms of vomiting, slight fever, and liver enlargement, but no edema. Clinical diagnosis of acute myocarditis was not made until she had Stokes-Adams syndrome and electrocardiogram revealed complete atrioventricular block on the day of death. At autopsy, idiopathic acute myocarditis was detected diffusely in the right and left ventricles. Vomiting and liver enlargement were due to congestive heart failure.
Serial sections of the atrioventricular conduction system revealed diffuse and severe acute inflammatory changes in the right bundle and the left bundle branches, especially in the terminal portions. Acute inflammation was focally noted in the atrioventricular node and the His bundle. The complete atrioventricular block probably followed the severe acute inflammation of the bundle branches.
Our case suggests that idiopathic acute myocarditis may be underdiagnosed in babies, as there is no way to determine whether there is dyspnea and palpitation on exertion, and idiopathic fibrosis of conduction system with or without conduction disturbances in children and adults may be sequelae of healed myocarditis in babies.

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A 49-year-old female patient with dissecting aortic aneurysm and severe hypertension was reported. Aortogram revealed dissection of De Bakey type IIIb, which extended to the iliac artery and caused occlusion of the left renal artery. Peripheral plasma renin activity was extremely elevated and 1-Sar-8-Ile-angiotensin II produced a marked fall in blood pressure. The patient was treated conservatively with antihypertensive agents for about 4 years from July, 1974 to Octover, 1978 when she died suddenly in an early morning.

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