To investigate the qualitative difference in myocardial hypertrophy that exists between hypertrophic cardiomyopathy (HCM) and essential hypertension (HT), we measured the mean wall thickness (MWT), the early diastolic time intervals (II_A-MVO time: from the second heart sound to the point of mitral valve opening, MVO-O time: from MVO to the O point of apexcardiogram) and the MVO-O/II_A-MVO ratio. The MWT in HCM and HT was measured by biventriculogram and echocardiogram, respectively. The MWT showed no significant difference between HT (1.31±3.0 mm) and non-obstructive type of HCM (14.8±3.7), but the MWT in obstructive type (1.08±0.24) was significantly thinner than that in HT. As the MWT increased, both II_A-MVO and MVO-O time were prolonged in both groups. But the mode of prolongation was quite different. In HT, the prolongation of the II_A-MVO time was almost always greater than that of MVO-O time. In HCM, the prolongation of the latter was greater than that of the former. The MVO-O/II_A-MVO ratio in HT was significantly greater. These findings suggest that the differences in the early diastolic time intervals between HCM and HT are not due to the magnitude of the left ventricular hypertrophy, but due to myocardial characteristics.

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In order to diagnose patients in thrombotic state, it is quite important to detect increased concentration of plasma thromboxane B₂ (TXB₂), a stable catabolite of TXA₂. To determine plasma TXB₂ levels with high sensitivity and selectivity, we employed gas chromatography-mass spectrometry (GC/MS). The trimethylsilyl (TMS) ether derivatives conventionally employed in GC/MS analysis of prostanoids are not suitable for quantitation of plasma prostanoids, because the mass spectra are deficient in ions with high intensity in the high mass range and TMS ether derivatives are sensitive to moisture. To solve these problems we employed tert-butyldimethylsilyl (t-BDMS) ether derivatives, based on the observation that t-BDMS ether derivatives afforded abundant ions at [M-57]⁺ and showed good hydrolytic stability. The reaction conditions of tert-butyldimethylsilylation were also examined to optimize the selected ion monitoring response. The t-BDMS ether derivative of prostanoids were successfully analyzed with a short capillary column with a relatively large diameter, with maintaining good separation. In conjunction with the use of reversed-phase high performance liquid chromatography as purification procedure, a sensitive and reproducible stable isotope dilution assay of plasma TXB₂ was developed. The values obtained by this method correlated well with those obtained by the radioimmunoassay we have developed.

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To evaluate the effects of lung volume changes on the body surface electrocardiogram, we performed body surface potential mapping (87 lead points) in 20 normal subjects (group N) and in 21 patients with chronic pulmonary emphysema (group CPE). P-wave, QRS, ST-segment, ST-T and QRST iso-integral maps were constructed. Group-mean maps and the mean value of the maximum (max) and the minimum (min) on each map were compared between group N and group CPE. In group CPE, the body surface distribution of the P, QRS, ST, ST-T and QRS time integrals were all positioned downwards compared with those of group N. In addition, we also detected an increase in the max of P and decreases in the min of P; max and min of QRS; and in max of ST-T and QRST integrals. It was suggested that these changes were caused by the downward shift and clockwise rotation of the heart, and also by the decreased electrical conductivity of the lungs.

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An analysis using vectorcardiography and left ventriculography was made on forty patients, 17 of whom had dilated cardiomyopathy (DCM), 14 with triple vessel coronary artery disease (CAD) and 9 control subjects. QRS deflection area vector A^^(⇾)qrs) was directed the most posteriorly in the DCM group and the second most posteriorly in the CAD group. Ventricular gradients (G^^(⇾)) were smaller in the DCM and CAD groups than in the control group and directed more posteriorly in the DCM group than in the CAD and control groups. G/Aqrs was the smallest in the DCM group and the second smallest in the CAD group. Aqrs-At Angle was the widest in the DCM group and the second widest in the CAD group. Left ventricular ejection fraction (EF) showed high correlations with the azimuth of A^^(⇾)qrs (r=0.659), with the magnitude of G^^(⇾) (r=0.720), with G/Aqrs (r=0.785) and with Aqrs-At Angle (r=-0.855). From this evidence, we conclude that the magnitude of G^^(⇾), G/Aqrs and Aqrs-At Angle have definable relationship with the impairment of left ventricular function and the Aqrs-At Angle is an especially useful parameter to detect the grade of myocardial damage in both the DCM and CAD groups.

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When estimating the pulmonary extravascular water volume (PEWV) as the lung thermal volume (LTV), by the double indicator dilution technic using heat and indocyanine green (ICG), a part of the left ventricular wall comes to the thermal equilibrium, and this leads to an overestimation of PEWV, when the samplings are made in the aortic root. In a previous study from this laboratory, this overestimation was approximately 10% of the measured LTV in the aortic root. In the present study, we evaluated the extent to which the thermal equilibrium with the aortic wall would cause LTV to slightly overestimate PEWV. For this purpose, we injected a ;mixture of the indicators into the right atrium, and recorded the indicator dilution curves at the bifurcation of the aorta (AB). We then compared this LTV with the one calculated from the indicator dilution curves recorded simultaneously in the aortic root (Ao). We obtained the following results: Firstly, the values of cardiac output (CO) from the dye dilution curve and from the thermodilution curve at two sites, Ao and AB, were all in agreement. Secondly, LTV estimated in Ao (LTV_Ao) and LTV estimated in AB (LTV_AB) were not the same, and their relationships were: LTV_AB=1.21LTV_Ao+0.44 (ml/kg), n=32, (r=0.98, p<0.001) A close agreement of CO determined at two sites indicated that there was virtually no loss of heat between the two sampling sites, Ao and AB. An excess of LTV_AB over LTV_Ao came to about 20%, and this excess appeared to be ascribable to the incorporation of the thermally equilibrated volume of the aortic wall. This finding appeared to be a challenge to the validity of estimating LTV when sampling the indicators in the distal abdominal aorta.

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The present study was undertaken to determine the central effect of adrenaline. Adrenaline was administered to the cisterna magna in urethane anesthetized rats. Following the intracisternal injections, the blood pressure dropped and reached a plateau after 15 min, the hypotensive effect continuing for at least 30 min. The heart rate also showed concomitantly with the depressor effect. The vehicle treated rats did not show any cardiovascular responses. The cardiovascular responses in the experimental rats were accompanied by an inhibition of the sympathetic nerve activity. Pressor responses to electrical stimulation of the posterior hypothalamus were partly inhibited, while pressor responses to intravenous injections of noradrenaline remained unchanged. In DOCA hypertensive rats, the depressor responses to intracisternal injections of adrenaline were augmented. These findings suggest that adrenaline in the brain could contribute to the inhibitory mechanism of the cardiovascular system accompanied by inhibition of the sympathetic nerve system, and that this mechanism may be attenuated in DOCA hypertensive rats.

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The accumulation of metabolic intermediates subsequent to impaired β-oxidation of free fatty acids has been suggested to be a cause of cellular damage and ventricular arrhythmias in the ischemic heart. The effects of verapamil on ventricular arrhythmias and free fatty acids metabolism during coronary artery reperfusion in experimental dogs were evaluated over a period of 40 minutes and followed by reperfusion for 15 minutes. One tenth mg/kg/min of verapamil was administered for 5 minutes before occlusion and followed by an infusion of 0.01 mg/kg/min to the end of the experiment. Myocardial samples were obtained from both the non-ischemic and ischemic areas after coronary artery reperfusion and then ATP, free carnitine, long chain acyl carnitine and long chain acyl CoA were measured. In the control group, 3 dogs (27%) had ventricular fibrillation and 2 dogs (18%) had ventricular tachycardia during coronary occlusion. In addition, 2 dogs (25%) developed ventricular fibrillation after reperfusion. On the other hand, all 6 dogs treated with verapamil had neither ventricular fibrillation nor tachycardia during both coronary artery occlusion and reperfusion. ATP and free carnitine levels in the ischemic area were significantly higher in the verapamil group than in the control group (ATP: p<0.01, free carnitine: p<0.01). However, there was no significant change in long chain acyl CoA levels between the control and verapamil groups. This study shows that verapamil protects against ventricular arrhythmias and has beneficial effects on the metabolization of free fatty acids. In conclusion, it is suggested that one of the antiarrhythmic mechanisms of verapamil in ventricular tachyarrhythmias may be due to the prevention of the accumulation of metabolic intermediates of free fatty acids.

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The common form of aortic atresia is associated with atrioventricular and ventriculoarterial concordant connections, but it has been very rarely found in "discordant connection" in the literature. In a 6-day-old male infant, clinical and postmortem pathologic features of this rare lesion, associated with Ebstein's and Uhl's anomaly in "congenitally corrected transposition" in situs solitus, are described. A possible pathogenesis is suggested for the concomitant presence of aortic atresia and poor-functioning, morphologic right ventricle.

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Three cases of criss-cross heart which we have observed during last five years are described. All of these cases were diagnosed by angiocardiography and two-dimensional echocardiography, and one of them was verified by autopsy. Two of them are unique among cases reported thus far. Case 1 shows ordinary criss-crossing with supero-inferior ventricle, and case 2, extreme crossing atrioventricular (A-V) valves, in which the right-sided right atrium connects to the left posteriorly positioned right ventricle through the tricuspid valve, and the left-sided left atrium to the right anterior left ventricle via a posteriorly positioned mitral valve. In case 3, the criss-cross appearance is secondary to displacement of the heart by compression caused by a diaphragmatic hernia. Findings in these cases suggest that criss-cross heart is caused not only by primary rotation of the ventricles during cardiac morphogenesiss but also by secondary rotation of a formed heart induced by extracardiac compression. The degree of rotation in these cases revealed a wide spectrum from minimal to extreme. In addition, subxiphoid two-dimensional contrast echocardiography is recommended as the only accurate method of non-invasive diagnosis of this condition.

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This study was performed to investigate spontaneous variability in VPC frequency, to determine standards for distinguishing antiarrhythmic efficacy from the spontaneous variability, and to compare the effectiveness of disopyramide, mexiletine, aprindine, propranolol, and diltiazem. Holter ECG techniques were used for this study and the population studied consisted of 182 patients having more than 1000 VPCs/day. Forty patients had ischemic heart disease, 52 had miscellaneous heart disease and 90 were free of heart disease (idiopathic VPCs). Circadian variability of VPCs can be divided into 4 types: Type D (VPCs increasing during waking hours), Type DN (small VPC changes between waking and sleeping hours), Type N (VPCs increasing during sleeping hours) and Type Ir (irregularly occurring VPCs). The incidence of Type D, DN, N and Ir was 45%, 29%, 12% and 14%, respectively. VPC frequency in the first and second recordings at a 7 up to 21 day interval was highly reproducible (r=0.951). the percent reduction in VPC frequency necessary to distinguish true drug response from spontaneous VPC variability, corresponded to 57% with 95% confidence level, and 67% with 99% confidence level. VPCs were reduced by at least 57% in 19 out of 33 patients (58%) with disopyramide, 9 of 15 (60%) with mexiletine, 11 of 18 (61%) with aprindine, 9 of 24 (38%) with propranolol and 8 of 22 (36%) with diltiazem. Concerning Prop., it is exclusively effective to the Type D VPCs (70%). Consequently, it is important to distinguish true drug effect from spontaneous VPC variability in long-term antiarrhythmic treatment. In this regard, Holter ECG techniques play a very important role in the evaluation.

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A comparison of the effects of several antiarrhythmic agents was made in a study of 70 patients - 15 with manifest Wolff-Parkinson-White (WPW) syndrome, 17 with concealed WPW syndrome, 18 with AV nodal re-entrant tachcardia, 14 with paroxysmal atrial fibrillation and 6 with paroxysmal atrial flutter - employing intracardiac stimulation and esophageal pacing. For the termination of paroxysmal supraventricular tachycardia, intravenous administration of verapamil or aprindine was more effective than that of disopyramide or aprindine was indicated especially for patients with the accessory pathways of the short antegrade refractory period, because these drugs lengthened the refractory period of the accessory pathways. For the purpose of converting atrial fibrillation or flutter to the sinus rhythm, type IA drugs such as disopyramide were indicated. However, verapamil was effective for slowing down the ventricular rate in atrial fibrillation or flutter except in cases of manifest WPW syndrome. A 6-month follow-up study showed that oral administration of verapamil was also useful for putting a stop to the attacks in 24 out of 32 patients with paroxysmal supraventricular tachycardia, while oral disopyramide prevented the recurrence of atrial fibrillation in only 4 of 10 patients.

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In 96 cases of paroxysmal tachycardia, results of chronic pharmacological assessment (CPA) were compared with acute electrophysiological-pharmacologic assessments (EPA) to evaluate the usefulness of EPA. I. Patients with sustained VT (31 cases): Sustained VT and repetitive ventricular response (RVR) could be induced in 61% and 23% respectively. More than one effective drug was found by EPA for 23 of 24 subjects. Of the 22 followed by CPA, the effectiveness of medication was excellent for 14 (64%), moderate for 1, slight for 4, and ineffective for 3 (14%). II. Patients with non-sustained VT (23 cases): RVR could be induced in 52%. Effective medication was identified by EPA for 8 of 10 patients. Of the 7 followed by CPA, the effectiveness of medication was excellent for 2(28.5%) moderate for 2, and ineffective for 3. III. Patients with PSVT (42 cases): PSVT could be induced in 90% of cases. Effective medication was found for all 31 cases which underwent EPA. Of the 23 cases followed by CPA, the chronic efficacy of drugs was excellent for 7 (30%), moderate for 5 (22%), slight for 7 (30%), and noneffective for 4 (18%). Therefore, we conclude that the usefulness of EPA differs according to the type of tachycardia. EPA is most useful in predicting chronic results for patients with sustained VT, especially when the sustained VT is readily reproducible by electrical stimulation. It is less useful for nonsustained VT and PSVT. With nonsustained VT, EPA is limited by difficulty in repeatedly inducing RVR, and by difficulty in predicting the appropriate medication for chronic oral therapy. With PSVT, even though the PSVT can be induced with greater success, EPA is limited by variations in pharmacologic effects over time, which create discrepancies between EPA and CPA.

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This study was performed to delineate the precise features and the treatment of ventricular tachycardia (VT) with acute myocardial infarction (AMI). Results indicate: 1) the incidence of VT in 310 AMI patients was 16.1% (50 patients); 2) the higher incidence of ventricular fibrillation and mortalities were observed in VT group compared with non-VT group; 3) the incidence of VT was higher in inferior infarction group (21.0%) than anterior group (13.1%); 4) more frequent VT were seen in patients with more severe heart failure; 5) two peaks of VT occurrence, on the first day and in the 4th week after the onset of AMI, were recognized especially in anterior infarction group; 6) supraventricular arrhythmias were more frequent than ventricular premature beats during one minute preceding VT; 7) the successful termination of VT was achieved in 63.9% of episodes by thump-version, 61.5% by lidocaine, 66.7% by disopyramide and 100% by mexiletine; 8) prophylactic effect on VT by class Ia antiarrhythmic agents seemed stronger than others; 9) IABP was effective to prevent VT in some cases; 10) poor prognosis was determined by frequent and later onset of VT, and combination of severe heart failure.

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Four hundred and sixty-seven cases with implantation of an artificial pacemaker were studied. The postoperative survival rate was 63% for 15 years. Seventy-two percent of type III patients of the sick sinus syndrome were free from postoperative thromboembolism and the lowest of the three types of the sick sinus syndrome. Comparing postoperative physical activity, cardiothoracic ratio and exercise tolerance time, physiological pacing was superior to ventricular pacing in hemodynamic effects and clinical symptoms. In a hundred cases of physiological pacing, complications and problems of physiological pacing were discussed. Atrial sensing failure and oversensing were observed in seven and two cases respectively. A low amplitude of atrial potential and use of unipolar atrial leads were considered to be the main causes of these complications. Bipolar lead should be used as the atrial lead to avoid such complications, because the atrial potential by bipolar leads is not less than that by unipolar leads. Atrial sensing may be more sensitive without electromagnetic interference. The fixed A-V delay time whenever the atrium is sensed or paced, often results in a ventricular fusion beat and hemodynamic change on every beat, according to the interval of atrial and ventricular contractions. The A-V delay time should be changed in accordance with atrial sensing or pacing.

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Sixty-six patients in whom atrial pacemaker (AAI) were implanted were followed for one year to 5 years for the occurrence of pacing failure, sensing problems, and later AV block. Pacing failure occurred in only one patient and sensing problems occurred in 15 patients but 10 of them improved after a change of sensing. Temporal change of AV conductivity was not recognized in the majority of patients. Eighteen patients developed transient decrease in AV conductivity. Two patients developed persistent decrease in AV conductivity and ended in clinical AV block for which the pacemaker was implanted. Out of 66 patients, 22 had a history of paroxysmal atrial flutter or fibrillation (AFF) prior to AAI implantation. They were divided into two groups. Group I consisted of 20 patients in whom paroxysmal AFF disappeared after AAI implantation. Group II consisted 22 patients in whom paroxysmal AFF persisted after AAI implantation. Electrophysioligical studies prior to the AAI implantation showed that sinus rate at control was significantly slower (36.310.1 beats per min in Group I, 57.110.8 beats per min in Group II), atrial fragmented activity zone was significantly narrower (62.732.9 msec in Group I, 88.119.7 msec in Group II), and the occurrence of PAC was less at an atrial pacing rate of 70 beats per min (8% in Group I, 67% in Group II) in Group I compared to Group II. In conclusion: When extensive electrophysiological studies prior to AAI implantation were done to select proper patients, chronic AAI pacing had few clinical problems. In addition, electrophysiological studies prior to AAI pacemaker implantation could identify the patients in whom AAI pacemaker would prevent the occurrence of paroxysmal AFF.

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