The presence or absence of ventriculoatrial (VA) conduction in the human heart is assessed by investigating whether 1:1 retrograde atrial capture is observed during constant cycle length ventricular pacing. In this study, a new pacing protocol for assessing VA conduction was designed in which the ventricular extrastimulus was delivered during basic ventricular and atrial simultaneous pacing (VE-VASP method). The effect of this pacing protocol on VA conduction was investigated in 12 patients who showed no evidence of VA conduction with the constant cycle length ventricular pacing method. In 5 of 12 patients, intact VA conduction was demonstrated with the VE-VASP method, while VA conduction was not observed in the remaining 7 patients. These results suggest that VEVASP method sometimes demonstrates the presence of intact VA conduction in patients who show no evidence of VA conduction during constant cycle length ventricular pacing.

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The features of ventricular arrhythmia in coronary spasm induced by ergonovine were examined to elucidate the characteristics of ventricular arrhythmia in acute myocardial ischemia. The coupling intervals and configurations of the QRS wave of the premature ventricular beats (PVBs) were extremely variable, even in the same individual and at the closer time phases. The prematurity index (R-R'/QT) of PVBs with the right bundle branch block (RBBB) pattern was significantly smaller than with the left bundle branch block (LBBB) pattern. The vulnerability index (R-R×QT/R-R') of PVBs with the RBBB pattern was significantly larger than with the LBBB pattern. The incidence of PVBs with the RBBB pattern (50.4%) was slightly larger than with the LBBB pattern (40.5%). PVBs deteriorated into ventricular tachycardias (VTs) in 29 (24.8%) of 117 cases with the RBBB pattern and in 11 (11.7%) out of 94 cases with the LBBB pattern. Thus, PVBs with the RBBB pattern were more likely to progress to VT than with the LBBB pattern. But it is difficult to assess the clinical significance of PVBs from their QRS morphology alone, because 11 (27.5%) of 40 cases of VT were initiated by PVBs with the LBBB pattern.

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Ventricular inhibited demand pacemakers (VVI) were implanted in 27 patients with complete A-V block and pacemaker arrhythmias were analyzed by Holter system ambulatory electrocardiograms and conventional electrocardiograms. With Holter ECG, 13 patients showed myopotential inhibition, 5 patients had sensing failure and premature ventricular contractions (PVC) were observed in all patients. On the contrary, myopotential inhibition and sensing failure were not detected by conventional ECG and the detection rate of PVC was only 30%. The transient recovery of A-V conduction was observed in 14 of 27 patients with Holter ECG, but was not detected by conventional ECG. The Holter system ambulatory electrocardiogram clearly demonstrated the complex cardiac arrhythmias. Therefore, it is useful for monitoring arrhythmias caused by VVI pacemakers.

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We studied the electrophysiologic effects of intravenous adenosine triphosphate disodium (ATP-2Na) on 15 patients with paroxysmal supraventricular tachycardias (PSVTs). One patient had sinus node (SN) reentry and 2 patients had intraatrial (IA) reentry. Five patients had AV nodal reentry and 7 patients had atrioventricular reentrant tachycardias (AVRTs) with accessory pathways (APs). ATP-2Na was injected during ventricular pacing (VP) in patients with AVRTs with APs. A bolus injection of ATP-2Na terminated all the PSVTs within 40 sec except in one case of IA reentry. The sites of block at the termination were the atrium in SN reentry and IA reentry, between A and H (AH) block or between H and A (HA) block in AV nodal reentry and AH block in all the AVRTs with APs. ATP-2Na during VP in patients with AVRTs with APs produced the changes of atrial activation sequences in 3 patients, induction of PSVT in 2 patients and a Mobitz type II VA block in 2 patients. The former two phenomena suggested a retrograde AV nodal block and raised the possibility of a simple test for retrograde atrial fusion during VP in patients with WPW syndrome. Chest discomfort of short duration was most commonly noted after ATP-2Na. Inosine pretreatment potentiated the effects of ATP-2Na. This combination may further alleviate the side effects of ATP-2Na, while preserving the effective action of ATP-2Na for rapid termination of PSVTs.

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Serial determinations of serum creatine kinase (CK), cardiospecific isoenzyme of CK (CK-MB), glutamic oxaloacetic transaminase (GOT) and alpha-hydroxybutylate dehydrogenase (HBD) were made in 29 consecutive patients undergoing aorta-coronary (AC) bypass grafting, and the results were compared with those in 31 patients with acute myocardial infarction (AMI). Postopera-tively, all patients had an uneventful postoperative course and there was no evidence of AMI. The time course of enzyme activity following surgery was characterized by 1) shortening of peak activity time of all enzymes except CK, 2) rapid disappearance of CK-MB, 3) prolonged normalization of GOT and HBD. Peak activities of CK, CK-MB, GOT and HBD in AC bypass patients were 801±77, 46±6, 100±9 and 718±32 IU (mean±SEM), respectively, which were equivalent to 46%, 12%, 22% and 47% of those in AMI. The degree of postoperative CK-MB elevation was influenced by the duration of the operation and the extracorporeal circulation, and the number of grafts bypassed. The peak CK-MB activity did not correlate with the CK peak. The ratio of CK-MB to CK was much smaller in AC bypass than in AMI (6.5±1.8 vs. 20.1±1.4%). It was concluded that serum enzyme elevations after AC bypass surgery largely reflected enzyme release from the skeletal muscle rather than the myocardium.

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We evaluated the treatment of left ventricular aneurysm (LVA) caused by myocardial infarction in 44 patients showing cineangiographical features of left ventricular aneurysm.
Of the 44 patients, 28 were treated non-surgically (N-S) and 16 were treated surgically (S). Combined aortocoronary bypass graft (ACBG) with aneurysmectomy was performed on 10 patients. Clinical symptoms in LVA patients were angina (34%), congestive heart failure (31.8%), arrhythmia (29.5%), mitral regurgitation. (9%), embolism (4%) and septal perforation (2.3%). Distribution of coronary arterial lesions were single vessel (isolated LAD) 29.5% and multiple vessel 59%. Parameters of LV performance measured at baseline in all LVA patients were: CI 3.05±0.64L/min/m², LVEDP 19.0±3.5mmHg, LVEDV 200.6±25.9ml, diast. wall stress 50.7±16.8g/cm², EF 0.46±0.15, LV dp/dt/p 17.8±2.1 S^-1, SWI 61±24gm/m². LV performance after surgery showed clear decreases in LVEDP, LVEDV and wall stress (p<0.05, p<0.02 and p<0.02, respectively). In contrast, EF, LV dp/dt/p and SWI increased significantly (p<0.02, p<0.1 and p<0.01, respectively). Comparison of the results of restudy with first catheterization data in the N-S group showed decreases of EF, contractility index and LV dp/dt/p, each reaching p<0.1. Residual myocardial motion 1 year after the first cineangiographic study showed a significant decrease (-12.8±26.7%) in the N-S group, whereas in the S group it significantly increased to (+60.4±52.7%). A significant difference in coefficient of variation between N-S and S groups was found. Thus, it can be concluded that aneurysmectomy or concomitant myocardial revascularization with aneurysmectomy improves left ventricular diastolic performance and increases residual myocardial viability.

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Adenosine effects on the transmembrane potential characteristics and the sarcolemmal Na⁺-K⁺ ATPase activity of human atrial myocardium were studied in tissue from 20 patients who were divided into 2 groups based on the maximum diastolic potentials (MDP) greater than or less than -60mV. Group A consisted of 10 patients with MDP of 70.84±4.20mV and Na⁺-K⁺ ATPase activity of 15.37±0.46μmole Pi/mg/hr. Ten patients with MDP of 44.54±6.24mV and Na⁺-K⁺ ATPase activity of 12.55±0.42 μmole Pi/mg/hr were included in group B. Adenosine had no effects on the electrophysiological properties and the sarcolemmal Na⁺-K⁺ ATPase activity of atrial myocardium at concentrations below 1×10-5 M in either group. Adenosine resulted in mildly altered atrial transmembranes potentials without significant effect on Na+-K+ ATPase activity at concentrations between 1×10-5 M and 5×10-4 M. However, a significant reduction of transmem-brane potentials and an apparent inhibition of Na⁺-K⁺ ATPase activity were observed only in tissue from group B. These results suggest that: 1) adenosine has no effect on the electrophysiological properties and the sarcolemmal Na⁺-K⁺ ATPase activity of human atrial myocardium at physiological concentrations; 2) adenosine induced inhibition of the sarcolemmal Na⁺-K⁺ ATPase activity in slow channel-dependent atrial tissues may be a mechanism responsible for the alterations of transmembrane potentials under unphysiological conditions; and 3) adenosine contributes to the genesis of cardiac arrhythmias during acute myocardial ischemia, which can reduce transmembrane potentials of the myocardial cells and may increase the myocardial adenosine level above its effective concentration.

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This paper reports a modification of Jacobson's method^{1), 2)} for culturing adult rat heart cells after mechanical and enzyme treatment. For heart cell dissociation, it is useful to wash tissue fragments 3 times with saline A solution after enzyme treatment, and it is important to change the medium immediately after culturing heart cells in order to prevent myocardial cells from degeneration caused by the enzyme solution and toxins in the cell debris.

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The calcium accumulating ability of mitochondria isolated both from bovine coronary artery and aorta was investigated. Coronary artery and aorta were pretreated with 0.1% collagenase. Cytochrome c oxidase activities of mitochondria isolated from coronary artery and aorta showed 25-fold and 19-fold increases, respectively, as compared with those of each homogenate, whereas NADPH-cytochrome c reductase, potassium-phosphatase and Na⁺-K⁺ ATPase activities increased less than 2-fold. This suggests that the isolation procedure is capable of obtaining a subcellular fraction highly enriched with mitochondria.
Mitochondrial calcium uptake activity of the coronary artery was approximately 250 nmoles Ca²⁺/mg protein/10min, and was markedly depressed with metabolic inhibitors such as NaN3, ruthenium red and 2, 4-dinitrophenol. Calcium uptake activity of bovine aortic mitochondria showed similar activity and a similar trend in sensitivity to metabolic inhibitors. By contrast, the onset of the calcium binding reaction of the aortic mitochondria was slower and the azide-sensitivity of the mitochondria to magnesium ATPase activity was lower than those for coronary artery mitochondria. The present study has provided a method for isolation of mitochondria with a high capacity of calcium uptake activity, which may prove meaningful for future physiological and pharmacological evaluation of mitochondrial calcium accumulation in vascular smooth muscle.

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The effects of intravertebral artery infusions of [Sar¹, Ile⁸] and [Sar¹, Thr⁸] angiotensin II on the central nervous system were studied in furosemide-treated dogs anesthetized with α-chloralose. Acute administration of furosemide led to a significant increase in plasma renin activity, plasma noradrenaline levels and heart rate, and also to a slight rise of blood pressure. In the furosemidetreated dogs, intravertebral artery infusion of either angiotensin II antagonist (250ng/Kg/min, for 30min) suppressed the furosemideinduced increases in plasma noradrenaline, heart rate and arterial blood pressure. The effects of [Sar1, Thr8] angiotensin II on the last two parameters were more pronounced than those of [Sar¹, Ile⁸] angiotensin II. Intravenous infusion of the same dose of each antagonist had little influence on the furosemide-induced increases in arterial blood pressure, heart rate and plasma noradrenaline levels. These results suggest that the central actions of angiotensin II contribute to the regulation of blood pressure through the sympathetic nervous system.

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The effects of therapeutic doses of antiarrhythmic drugs (12mg/Kg of procainamide, 2mg/Kg of disopyramide and 0.2mg/Kg of propranolol) on sinus cycle length (SCL), sinoatrial conduction time (SALT) estimated by a constant atrial pacing technique, and atrial developed tension (DT) were measured in isolated canine atria cross-perfused with heparinized arterial blood from donor dogs as well as on mean systemic blood pressure (SBP) and on heart rate (HR) in those dogs. Procainamide, which produced hypotension and bradycardia in the donor dog, did not change SACT significantly, although it increased SCL and decreased DT in the isolated atrium. However, disopyramide raising SBP slightly (but not significantly) and decreasing HR in the donor dog produced a significant prolongation of SACT and SCL and reduction of DT in the isolated atrium. Propranolol caused slight but insignificant hypotension and long-lasting bradycardia in the donor dog, accompanied by a significant increase in SCL and SACT, and decrease in DT in the isolated canine atrium. We concluded that SACT was significantly increased by a therapeutic dose of propranolol and disopyramide but was not altered by that of procainamide.

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Non-traumatic hemothorax is rare and in the case we report was due to rupture of a benign thymoma. The clinical course of the patient suggested rapid intrathoracic bleeding and emergency surgery was required to make the correct diagnosis.

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A forty-year-old man was admitted to our hospital because of dizziness, palpitations and an oppressive feeling in the precordium. Physical examination was normal. A chest roentgenogram revealed mild cardiomegaly and the electrocardiogram showed ventricular tachycardia of a left bundle branch block configuration which was terminated by the intravenous injection of procainamide. During sinus rhythm the electrocardiogram showed incomplete right bundle branch block, PQ prolongation and inverted T waves in leads V1 through V₃. Two-dimensional echocardiography revealed only moderate right ventricular dilatation. Right ventricular angio-graphy showed severe right ventricular dilatation and hypokinesis of the right ventricular apex and pulmonary artery infundibulum. From these characteristic signs we concluded that this adult patient had arrhythmogenic right ventricular dysplasia (ARVD), suggesting that this condition is not confined to children but may occur in adults as well.

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Four clinical cases of subaortic hypertrophic muscular stenosis are discussed. All four, in addition to a loud systolic murmur, had a loud systolic click. However, the timing of the click and its relationship to the phase of the carotid pulse were different in each case varying from close to medium and to distant (or midsystolic). The comparison of the sound tracing with the carotid tracing demonstrated that, in each case, a sudden change in acceleration was taking place. In one, the click coincided with the onset of the carotid upstroke; in another, with the first peak of the carotid pulse; in the third, with the trough between first and second peak of the pulse; in the last, with a sudden drop of the pulse at mid-systole caused by sudden obstruction to flow. It is concluded that the clicks were caused by rapid changes of acceleration resulting from the abnormal aortic ejection. Thus, the study of the carotid pulse and of the sound tracing are important for a non-invasive diagnosis together with the echo study of the septum and ventricular wall.

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