In 2 patients with complete heart block, characteristics of retrograde conduction and the localization of orthograde conduction block were studied. In patient 1, retrograde conduction was demonstrated during both A-V junctional rhythm and ventricular pacing. The sinus and retrograde P waves seemed to utilize and compete for the A-V conduction system. The time from QRS complexes to retrograde P waves was longer during ventricular pacing than during A-V junctional rhythm by approximately 65 to 110msec. 1:1 ventriculoatrial conduction could be elicited at the ventricular pacing rate between 70 and 100 beats per minute. The time interval between the pacemaker impulse and the retrograde P wave became progressively longer as the pacing rate increased. The V-A conduction showed Wenckebach phenomenon with 5:4 conduction ratio at the rate of 110/min, and that with 3:2 conduction at 120/min, respectively. The His bundle electrogram demonstrated a complete heart block due to AH block. In patient 2, electrocardiogram during a Stokes-Adams attack showed complete heart block and an escape rhythm with retrograde P waves. The QRS complexes of the escape rhythm were normal in configuration and duration, indicating an A-V junctional origin. At the time of His bundle recording, ECG showed 1:1 atrioventricular conduction. Although PA, AH and HV times were all within normal limits without any intervention, AH time developed a Wenckebach periodicity in response to atrial pacing rate of 90 beats per minute or higher. Therefore, it was presumed that the complete heart block demonstrated during a Stokes-Adams attack had been due to AH block. These studies indicate that a retrograde V-A conduction could occur in the presence of orthograde A-V block due to AH block. Possible mechanisms of retrograde V-A conduction in the presence of complete orthograde AH block were discussed, and unidirectional block at the A-V junction seemed to be the most probable mechanism operating in our patients.

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The effects of amyl nitrite on systolic murmurs and hemodynamic alterations in the elderly have been studied with amyl nitrite test using 2 phonocardiographic amplifier channels and 2 microphones of the same frequency response. From the simultaneous recording at the aortic and apical region, the alteration of the amplitude of systolic murmurs in both areas after inhalation of amyl nitrite was checked. In Germany, we named this method with 2 microphones as "Doppel Amyl-nitrit Versuch".
Mechanocardiographically the time intervals such as HR, Q-I, Q-IIi, ET, ETi, PEPi were checked. The following observations were made: Alterations of systolic heart murmurs were divided in 4 different groups, namely, (1) increased murmurs in both regions, the apex and base (group I), (2) decreased murmurs in both areas (group II), (3) increased murmurs at aortic area and decreased murmurs at the apex (group III), (4) others: i.e. increased murmurs only at the apex, and decreased murmurs only at the apex or base (group IV).
The results support the opinion that the effects of amyl nitrite in the elderly is not as conspicuous as in children. Amyl nitrite test using double microphones may be useful to differentiate the origin of some murmurs as the Gallavardin phenomenon.
The Gallavardin phenomenon is the more common in the older patients. Furthermore, apical murmurs may also be conducted often to the base of the heart, especially when the left ventricle and ascending aorta are dilated (anti-Gallavardin mechanism). Under some conditions the systolic murmur of mitral incompetence may have its maximum intensity at fourth or third left ICS.

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5μCi/Kg ¹³¹I-MAA was injected into the right coronary arteries in Cases 1, 2, and 3 under the diagnosis of right coronary artery fistula, and in Case 4 under the diagnosis of Bland-White-Garland syndrome. The results were compared with the angiocardiogram and right heart catheterization. When a fistula is small and cardiac cavity at the opening is not visualized by the angiocardiogram, coronary perfusion scanning successfully disclosed the location of fistula and influence of coronary circulation.

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The subclavian arterial blood flow as a parameter of cardiac output was measured in 7 patients with ischemic heart disease (3 acute myocardial infarction, 3 angina pectoris, 1 variant form of angina pectoris) and 5 normal subjects. The measurement was continuously and non-invasively made, utilizing the Doppler ultrasonic flowmeter technique before, during and after exercise. The exercise was performed in the upright position on a bicycle ergometer for 3 min at the work load of 230Kpm/min. In 3 normal subjects, oxygen consumption at various work loads was also measured by the Douglas bag simultaneously with the subclavian arterial blood flow.
In normal subjects, the subclavian arterial blood flow steeply increased soon after the beginning of the exercise and promptly returned to the preexercise level after the termination of the exercise. While in patients with ischemic heart disease, the increase in the subclavian arterial blood flow during the exercise was slow, and the time required to return to the preexercise level was significantly prolonged. Light to moderate exercise under the work load of 230Kpm/min increased both the subclavian arterial blood flow and oxygen consumption nearly in the same ratio. With stronger exercise, the increase in oxygen consumption was by far larger than in the blood flow.
Continuous measurement of the subclavian arterial blood flow by the Doppler ultrasonic technique is supposed to be a useful method for the evaluation of cardiac function.

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In the management of Ischemic Heart Disease (IHD) patients the exercise tests are indispensable for the evaluation of severity, coronary reserve capacity or their functional capacities. In the case of cardiac rehabilitation, it is very important to gain the data about patients' cardiac activities (H.R., ECG, workload, etc) not only in the laboratory testing process but also in their daily lives directly. The latter is also the exercise test in the broad sense, and the need for such a test has been recognized by clinicians. We have been utilizing the H.R. value refering to ST, T changes on the exercise test to evaluate and control the IHD patients. Fortunately, by the aid of recent advances of the electronics, we have become able to devise so compact an apparatus as can be carried in their daily lives without worries. These are H.R. Alarm, H.R. Memo. and ECG Memo. In addition to them, the ergometer with a computer for treating the fundamental data in the rehabilitation program has been devised.
The Check-Alarm-Training system (CATS) is composed of these apparatuses and considered to be very useful for the management of cardiac patients in their daily lives.

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In the dog heart-lung preparation (HLP) M & B 17, 803A (0.5mg) prevented the development of epinephrine-halothane induced ventricular fibrillation and epinephrine-halothane-aortic pressure induced ventricular tachycardia. M & B 17, 803A in the dose used produced a blockade of effect of epinephrine on the heart rate, aortic pressure and cardiac output. Suppression of ouabain-induced multifocal ventricular tachycardia was achieved with a dose 16 times greater than the beta receptor blocking one, and the duration of suppression was 90min. Pretreatment of the HLP with 4mg of M & B 17, 803A increased both the toxic and lethal dose of the cardiac glycoside and changed the mode of death from ventricular fibrillation (seen in control experiments) to cardiac arrest. It is concluded that M & B 17, 803A is an effective antiarrhythmic agent against catecholamine induced and digitalis induced cardiac arrhythmias. Further, neither the suppression of cardiac glycoside-induced arrhythmia nor protection against toxic doses of the glycoside is related to the beta receptor blocking activity of such agents.

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The direct and beta adrenergic blocking effect of M& B 17, 803A was investigated in the isolated supported dog heart preparation (ISHP) in the presence of a constant coronary blood flow. Administration of graded doses of norepinephrine into the coronary arteries produced a dose-dependent increase in the heart rate, myocardial contractile force, left ventricular systolic pressure and coronary artery perfusion pressure. The myocardial oxygen consumption was increased significantly (p<0.05) by each dose of norepinephrine. Pretreatment of the ISHP with 0.3mg/Kg of M & B 17, 803A produced a generalized myocardial depression and an increase in coronary artery perfusion pressure, whereas the smaller dose (0.15mg/Kg) of the blocking agent was without any effect. Both the doses of M & B 17, 803A produced a competitive blockade of the effect of norepinephrine on the myocardial hemodynamics and oxygen consumption. M&B 17, 803A thus appears to be a potent agent that blocks the beta receptors, and has a significant myocardial depressant activity.

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The effect of bradykinin on afferent cardiac sympathetic nerve fibers has been examined. Using anesthetized dogs, the action potentials of the fibers were derived from either the 2nd or 3rd thoracic communicating ramus of the left side. Excitation of the afferent fibers was observed following administration of bradykinin acetate dissolved in physiological saline on the left ventricular wall. The minimum concentration required for excitation was 50-100ng/ml. The fibers were excited rhythmically synchro-nous with myocardial contraction and/or relaxation. However, no significant augmentation of myocardial contraction was produced by the agent. Bradykinin-induced excitation of the fibers was significantly reduced by pretreatment with acetylsalicylic acid. The results suggest bradykinininduced sensitization of the receptor sites of the afferent fibers for normal modality of left ventricular motion.

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The conduction system of a case of systemic lupus erythematodes with incomplete atrioventricular block and atrial flutter was studied histopathologically with complete serial sectioning. It was highly suggestive that incomplete interruption of the atrio-AV nodal junction by fibrosis based on connective tissue change of systemic lupus erythematodes corresponded to the AV block and focal hemorrhage into the internodal tract was related to the terminal atrial flutter.

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An autopsy case was presented of isolated myocarditis (Fiedler's myocarditis) which was probably affected by fatal generalized infection of 2 rarely encountered infective agents, namely, infectious mononucelosis and cytomegalic inclusion disease.

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