The purpose of the present study was to examine noninvasively the myocardial performance before and after hemodialysis in 40 patients of chronic renal failure. Using systolic time intervals, the following results were obtained. l ) Left ventricular ejection time was shortened significantly. The reduction of circulating blood volume estimated by the body weight change seemed to be responsible for this finding. 2) Pre-ejection period seemed to be a sensitive indicator of the left ventricular performance in hemodialysis. 3) The less the circulating blood volume, the less the suppression of cardiac performance. 4) Left ventricular function in patients without cardiomegaly was improved. 5) Left ventricular function tended to improve in the young age group . The present study demonstrated that the left ventricular performance tended to be suppressed in older age patients, in patients with cardiomegaly and in the cases with excessive removal of circulating blood volume during dialysis. The significance of noninvasively obtained left ventricular hemodynamic parameters in patients with hemodialysis was discussed.

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Correlation of asynergies on the left ventriculogram with the transverse and frontal plane QRS loops recorded by the Frank lead system was investigated in 276 cases with a significant occlusive lesion of the left anterior descending coronary artery (luminal narrowing of 75% or more). Among the 97 cases with akinesis or dyskinesis in the anterior and/or septal segments, 84 satisfied the transverse plane VCG criteria for anterior myocardial infarction. Of the remaining 13 cases, 6 were diagnosed to have high lateral myocardial infarction based on the frontal plane VCG findings. Six of the 7 cases that were not diagnosed as having myocardial infarction evidenced concomitant akinesis in the inferoposterior segment. Of the 24 cases which had akinesis or dyskinesis localized in the apex, 10 showed a VCG pattern of anterior and/or high lateral myocardial infarction. Among 92 cases with hypokinesis in the anterior and/or septal segments, only 16 had VCG findings of anterior and/or high lateral myocardial infarction. There were no significant differences in the frequency of "bite" between these patients and the normal control group.

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Effects of high frequency (HF) stimulation on membrane potential were examined in ventricular muscle and Purkinje fibers, which were isolated from canine and rabbit hearts, by using microelectrode techniques. When the stimulating frequency of preparations was increased abruptly from basic frequency (BF, 0-30/min) to high frequency (HF, 60-150/min), the maximum diastolic potential (MDP) of both ventricular muscle and Purkinje fibers decreased with each beat and reached a minimal value (initial depolarization). Then, MDP gradually increased beyond the steady state level at BF (hyperpolarization). On returning the stimulating frequency from HF to BF, a further terminal hyperpolarization ensued, and finally MDP decayed back to the control level within several minutes. The intensity of MDP change (both depolarization and hyperpolarization) was apparently greater in ventricular muscle than in Purkinje fibers. A significant increase of threshold current for excitation and a slight increase of membrane input resistance were also observed at the hyperpolarized period after HF stimulation. Lowering the temperature of the perfusate from 37°C (control) to 31°C or 26°C led to an augmentation of initial depolarization and also a decrease in the intensity of ensuing hyperpolarization. The decay time of the hyperpolarization after HF stimulation was much prolonged. In the presence of ouabain, HF stimulation caused a monotonic decline in MDP and no hyperpolarization was recorded during and after HF stimulation. These results suggest that an active ion transport through the sodium pump contributes significantly to the electrical properties of ventricular muscle as well as the Purkinje fibers when the firing rate of the fibers is abruptly changed.

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Open heart surgery under aortic cross-clamping is often required, but coronary reperfusion injury after release of aortic cross-clamping is unavoidable irrespective of applications of various protective methods to the myocardium. The anterior descending branch of the left coronary artery of mongrel adult dogs was occluded for 2 hours and then reperfused. The protective effects of intra-aortic balloon pumping (IABP) and of a calcium antagonist "diltiazem hydrochloride" (diltiazem) on the decreased reperfusion of ischemic, border and normal areas were examined by measuring the regional myocardial blood flow (RMBF) using a radioactive microsphere method. Diltiazem could increase significantly the RMBF in the border area. IABP induced a significant increase in the RMBF of the same area more than Diltiazem, with the increase in the endocardial layer tending to be superior to that in the epicardial layer. The results suggested that diltiazem is very effective for reducing the coronary reperfusion injury. It is also suggested that IABP is even more effective than diltiazem because it increases the RMBF significantly and, moreover, has a tendency to increase the blood flow in the endocardial layer which is poor in collateral vessels and thus vulnerable to ischemia.

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Morphological changes associated with recurrent reduction of blood flow in the partially constricted common carotid artery and that in the ipsilateral cerebrum were examined angiographically in anesthetized beagle dogs. During the recurrent reductions of carotid flow, spasm and small and multiple defects indicating platelet aggregates or thrombi in the constricted carotid segment were observed in 8 and 5 of 20 preparations, respectively. Also, large defects indicating thrombi were observed at the outlet of the constricted segment in the other 2 preparations. During the reduction of cerebral flow, spasm was observed in the internal carotid artery and cerebral arteries in 9 and 8 preparations, respectively. Also, obstruction of the cerebral arteries with "cut-off" sign indicating emboli was observed in the other 2 preparations. The changes appeared singly or in combination. It is suggested that spasm, platelet aggregates, thrombi and/or emboli were responsible for the recurrent reduction of carotid and cerebral blood flow.

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A microscopical study of the AV conduction system using a serial sectioning method, was performed on 81 autopsied hearts with blocks anywhere in the AV conduction system, 44 with miscellaneous arrhythmias, and 65 control hearts without arrhythmia. Pre-blockade hypertrophy in the AV conduction system was seen in 38%, 38%, 50-58% corresponded respectively to 3° AV block, 1-2° AV block and bundle branch block (including left hemiblock). Post-blockade hypertrophy was also observed in 58%, 38% and 42-25% of the above mentioned types of blocks respectively. Hypertrophy anywhere in the AV conduction system was seen in 77%, 42%, 78%, 39%, 30% and 74% of the cases with blocks, sick sinus syndrome, pre-excitation syndrome, other arrhythmias, normal hearts and hypertrophied hearts without arrhythmia, respectively. Hypertrophy of the proximal AV conduction system to the bundle of His was specific for arrhythmia group, whereas hypertrophy of the bundle branches occurred in either hypertrophy without arrhythmia or in bundle branch block. Hypertrophy of the Purkinje cells was remarkable in sudden cardiac death by clinically-proved ventricular fibrillation. Incidence of sclerosis of the AV node artery was high in the arrhythmia group, especially the highest (90%) in the sudden death group.

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Atrioventricular (AV) conduction was studied in isolated, perfused rabbit hearts. Total AV interval was subdivided into the intraatrial, intranodal and His-Purkinje conduction times. Concentrations of Ca, K and Na in the control perfusate were 2.4, 4.5 and 144.8 mM, respectively. Generalized ischemia or hypoxia almost selectively depressed intranodal conduction, engendering a second degree block. Low Ca (0.8 mM) slightly prolonged the intranodal conduction time, whereas high Ca (4.8-7.2 mM) caused a greater prolongation of this interval, often causing intranodal block. High Ca-induced depression of intranodal conduction was antagonized by high K (7.5 mM). Verapamil (0.5-1.0 mg/L) produced a second degree intranodal block. Subsequent elevation of Na concentration to 172 mM (but not high Ca) restored a 1 : 1 conduction. Tetrodotoxin (2-10 mg/L) did not affect, whereas low Na ( 108.6 mM) severely depressed intranodal conduction. These results suggest that (1) AV nodal conduction is most vulnerable to reduced oxygen supply, (2) an optimal Ca concentration for AV nodal conduction exists, (3) high K counteracts high Ca-induced depression of AV nodal conduction, and (4) slow Na current may play a major role in generating AV nodal action potentials. Voltage clamp experiments on the AV node substantiated some of these observations.

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In 45 (25%) of 182 patients with various cardiac arrhythmias, dual A-V nodal pathways (DPWs) were diagnosed with atrial extrastimulus technique at least at one or more basic cycle lengths and/or after intravenous administration of atropine (1 mg). The jump of discontinuous A₁A₂, H₁H₂ curve of these 45 ranged from 25 to 235 (92±56) msec and the jump of A₁A₂, A₂H₂ curve ranged from 40 to 260 (107±55) msec. The fast pathway FRP (functional refractory period), slow pathway FRP, fast pathway ERP (effective refractory period) and slow pathway ERP was 464±87 msec, 532±91 msec, 404±96 msec and 328±70 msec, respectively. DPWs were demonstrated in 10 (59%) of 17 patients with paroxysmal supraventricular tachycardia (PSVT), 3 (5%) of 55 with WPW syndrome, 2 (20%) of 10 with paroxysmal atrial fibrillation, 11 (29%) of 38 with sick sinus syndrome, 10 (38%) of 26 with first degree and/or second degree A-V (AH) block, none of 3 with second degree HV block, 3 (27%) of 11 with bundle branch block and 6 (27%) of 22 with the other cardiac arrhythmias. In 17 patients with PSVT, seven demonstrated A-V nodal reentrant tachycardia. Six of these 7 had evidence of DPWs. In the other 7 of the 17, concealed accessory pathway was demonstrated. Three of these 7 had DPWs, which did not constitute the reentrant circuit. Twenty-eight of 45 patients (62%) with DPWs had one or more electrophysiological abnormalities suggesting A-V nodal dysfunction: 1) prolonged AH interval (>130 msec) during sinus rhythm (10 patients), 2) atrial pacing rates of 130 or less inducing A-V nodal Wenckebach periods (24 patients), 3) prolonged A-V nodal ERP or slow pathway ERP (>400 msec) (8 patients), and 4) prolonged A-V nodal FRP or fast pathway FRP (>500 msec) ( 16 patients). However, in most patients, atropine improved A-V nodal dysfunction. We consider that DPWs are a common electrophysiological finding and have a strong association not only with PSVT but also with A-V nodal dysfunction.

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Electrophysiological studies were performed on 34 patients whose reentrant circuit of paroxysmal supraventricular tachycardia (PSVT) involved normal atrioventricular (AV) conduction system as the antegrade limb and either overt (25 patients) or concealed (9 patients) accessory AV pathway as the retrograde limb. The diagnosis of this mechanism was made by one or more of the following: 1) eccentric retrograde atrial activation sequence; 2) effect of bundle branch block on ventriculoatrial (VA) conduction time; 3) paradoxically premature atrial capture; 4) atrial capture by premature ventricular stimulation when His bundle was refractory during PSVT; 5) no significant prolongation of VA conduction time with retrograde atrial activation sequence identical to that of PSVT during incremental and premature ventricular stimulation; 6) shortening of cycle length with constant H-V and V-A intervals after atropine administration. The participation of accessory pathway in PSVT circuit should be decided by as many of the above-mentioned findings or procedures as possible for optimal therapy. Electrophysiological studies have led to the recognition that accessory pathway, functionally silent during antegrade conduction, is responsible for some patients with PSVT. If the mechanisms of PSVT were more carefully analyzed, the recognition of PSVT cases involving accessory pathway would increase.

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Ventricular pre-excitation was experimentally produced in mongrel dogs. Their ECG and epicardial maps were analyzed. Forty-two cases of W-P-W syndrome were operated on between 1969 and May, 1980. The relationship between ECG, particularly the delta wave and localization of the accessory conduction pathway (ACP) was analyzed. The usefulness and meaning of pre-operative examinations such as vectorcardiography, echocardiography, body surface mapping, intracavitary potential study, and cardiac pacing, were presented and discussed. As an intraoperative study, epicardial mapping was indispensable and was the most accurate method in determining the ACP. Endocardial potential study was another meaningful method in certain cases. Detachment of the atrium from the ventricle with an incision along the annulus and at the opposite of the pre-excitation area resulted in complete correction in 32 out of 34 cases between 1973 and May, 1980. Six cases of multiple ACPs were also corrected, although 4 needed a second operation. Indications for surgery of the W-P-W syndrome should be extended further in view of the high success and safety rate of the surgery.

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This study was designed to detect reflection of epicardial breakthrough to body surface isopotential maps by recording epicardial and body surface maps simultaneously, and to estimate changes in epicardial breakthrough associated with complete and incomplete blocks induced by compression of the main stem of the right bundle branch or trans-sectioning of the lateral branches. In the control, epicardial breakthrough appearing on the right ventricular surface was well detected on the body surface maps as a bend of isopotential lines localized at the mid sternum at 11.5±1.6 msec (n = 5) after QRS initiation. At complete block immediately after compression of the main stem, the localized bend shifted inferiorly to the left at 17.8±1.8 msec (n = 5) after QRS initiation, suggesting appearance of the left ventricular epicardial breakthrough. With progression of recovery from the compression, in addition to epicardial breakthrough on the left ventricle, the breakthrough on the right ventricle became detectable again with a delay of 5 msec, and then the former was faded away as time progressed. After trans-sectioning of the lateral branches, sequential changes in the body surface maps were almost the same as in complete block of the main stem but they lapsed about 43 msec (n = 5) shorter in comparison with the complete block. In conclusion, detection of the localized bend of the isopotential lines on the body surface can provide diagnosis of the site and degree of the right bundle branch block in detail.

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There still exist many questions to the human intraventricular conduction system, especially morphology of left ventricular (LV) conduction system. In the present study, LV conduction system was examined by serial histological examinations, and based on these results experimental and clinical subdivision block of the left bundle branch (LBB) were studied electrophysiologically and histopathologically. 1 ) Reconstruction of the human LBB: Human LV conduction system of 14 hearts showed much variability. LV conduction system was a diffuse fan like structure broadly distributed over the left septal surface and always covered diffusely mid-septal area. 2) Experimental subdivision block of the LBB: In the discrete block of the septal Purkinje network (11 dogs), the activation time in the apical area prolonged from 20.0±4.9 msec to 24.5±4.9 msec (p<0.05), and the QRS loop tended to be displaced anteriorly. In the discrete block of the left posterior division (9 dogs), the activation time showed slight prolongation in the posterior basal area, but the QRS waves of the scalar ECG did not change significantly. In the block of the left posterior division and septal Purkinje network ( 11 dogs), epicardial activation delay was observed in a relatively wider area from the apex to the posterior basal area. The maximum QRS vector in the frontal plane shifted rightward (p<0.05). 3) Prominent anterior QRS force (PAF) in clinical electrocardiogram: PAF was observed frequently in patients with ischemic heart disease (12.4%) and diabetes mellitus (8.5%). Serial histological examination of a patient with PAF showed marked fibrosis in the mid-septal fibers in association with fibrosis of the right bundle branch and posterior part of the LBB. Intermittent PAF was observed in supraventricular premature beats suggesting that PAF might be due to intraventricular conduction disturbances as well as left anterior or posterior hemiblock. This intermittency also supports the existence of this new type of divisional block of the LBB. New concepts of intraventricular conduction disturbances must be established including the conduction disturbances of the mid-septal fibers of the LV conduction system.

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Analysis of conduction characteristics within the ischemic myocardium and the incidence of ventricular arrhythmias for the first 30 minutes of coronary artery ligation identified two phases of ventricular arrhythmias with different electrophysiological mechanisms. The first phase appearing during 2-10 minutes (immediate ventricular arrhythmias: IVA) was closely related to the degree of epicardial delay and thus considered to be initiated by reentry within the ischemic epicardial zone. In contrast, the second or delayed phase (12-30 minutes, delayed ventricular arrhythmias: DVA) of ventricular arrhythmias appearing independently from epicardial delay was suggested to originate from the subendocardial Purkinje network, since endocardial activation of the ischemic zone consistently preceded the QRS complexes of ventricular arrhythmias. Measurements of myocardial adenosine triphosphate (ATP) contents demonstrated that in animals developing a profound myocardial ischemia by 3-5 minutes, epicardial delay was not observed and thereby IVA was not initiated. In contrast, epicardial delay and IVA were associated with a significant, but milder or slower ischemic process. At the time of DVA, myocardial ATP contents were at extremely low levels for both groups with and without DVA, supporting the concept that DVA is not originated from the ischemic myocardial cells, but from Purkinje fibers depressed secondarily by surrounding ischemic myocardial cells.

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