Little attention has been paid to the atrial fibrillatory waves (f waves) in paroxysmal atrial fibrillation. The present study attempted (1) to compare the f wave size in paroxysmal atrial fibrillation with that in persistent fibrillation, and (2) to examine whether the f wave size can predict the development of persistent from paroxysmal atrial fibrillation. The size of the f waves was measured in 60 patients with paroxysmal atrial fibrillation of non-rheumatic etiology (group A), 87 patients with persistent atrial fibrillation of non-rheumatic etiology (group B), and 34 patients with persistent atrial fibrillation of rheumatic etiology (group C). The f wave size in group A was 1.1±0.1mm (mean±SE) which was significantly smaller than 1.6±0.1mm in group B and 2.2±0.2mm in group C (p<0.01, respectively). Among patients with paroxysmal atrial fibrillation, persistent atrial fibrillation developed in 9 of 19 patients (47.4%) with f wave size of 1.2mm or more, and only in 5 of 41 patients (12.2%) with f wave size of less than 1.2mm. These results indicate that paroxysmal atrial fibrillation generally has smaller f waves than persistent atrial fibrillation, but that the presence of larger f waves indicates potential development of persistent atrial fibrillation.

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The purpose of this study was to investigate multivariable cardiovascular responses to a non-mathematical mental task. Fiftytwo subjects, 8 to 69 years of age, were monitored at rest and while attempting to solve a Raven's matrix test without prodding or pressure from the experimentors. Adults (≥18 years) had higher blood pressures (BP) and longer pre-ejection periods (PEP) at rest than did the children. Women had higher resting heart rates (HR) than men. The task induced significant increases in systolic and diastolic BP and HR in adults and children, with the adults exhibiting larger BP responses. During the stressful stimulus significant decreases in left ventricular ejection time occurred in men and women, and significant increases in forearm blood flow occurred in men. The stability in PEP during the stressful period when both BP and HR were increased is evidence of enhanced contractility brought on by the stress. In general, men and women responded similarly. Thus, even a mild, non-mathematical stress of short duration elicits the multiple cardiovascular responses, including increases in BP, HR, muscle blood flow, and contractility, which are observed with more threatening tasks.

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Thirty-six patients with the angiographic diagnosis of left ventricular mural thrombus were reviewed. All had a history of myocardial infarction. In 9 of these patients (25%), coronary neovascularity was related to a left ventricular mural thrombus. Although no relationship was found between either the size of the mural thrombus or the duration of illness and the neovascularity, the incidence of neovascularity was low in a group taking anticoagulants. Arteriographic characteristics of the neovascularity in the present cases are:
1) In all cases, the neovascularity arose from the left anterior descending coronary artery.
2) The neovascularity consisted of a hypervascular region in the same location as the mural thrombus. It was observed as a dense mass of small vessels penetrating the left ventricle in a form resembling a toothbrush.
3) The neovascular region had no veins and it extended through the narrow gap of the thrombus to communicate with the left ventricle.
Histological studies were consistent with coronary arteriography. The demonstration of neovascularity by coronary arteriography suggests either that the thrombus is relatively new or that a new thrombus is further organized on the old thrombus. This seems to be useful information from a therapeutic viewpoint.

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The surgical correction of the transposition of the great arteries (TGA) is divided into three procedures by the methods of switching i.e., (1) intra-atrial, (2) intra-ventricular, and (3) via the great arteries. Arterial correction is considered as an ideal technique physiologically as well as anatomically. With the above in mind, twenty formalin-preserved hearts of TGA were used to carry out the following studies: (1) feasibility of coronary artery relocation, (2) feasibility of switching of the aorta and pulmonary trunk, (3) feasibility of the conduit procedure, and (4) effect of left ventricular hypoplasia.
The Jatene operation in which coronary artery relocation was needed proved feasible in 20% of the cases. The Damus-Kaye-Stansel operation seemed feasible in 45% of the cases. Hypoplasia of the left ventricle was suspected in 3 of the cases that belonged to Group 1 according to Kidd's classification.

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Electron microscopic studies of chordae tendineae of the mitral valve were carried out in 17 patients who underwent mitral valve replacement due to a spontaneously isolated rupture of chordae tendineae. The normal chordae, used as the control group, were obtained at autopsy from 5 patients who died from extracardiac causes and were compared with the ruptured chordae. In all patients with chordal rupture, scanning electron microscopy showed perforations of the chordae tendineae, with extensive desquamation and disruption of the endothelial cells and wide-spread destruction of the collagen fiber bundles in the central collagenous core. These pathological findings were not observed in the normal chordae from the control group. Transmission electron microscopy showed that the ruptured chordae were characterized by heterogeneous collagen fibrils with intrinsic structural alterations and disorganization in fibril arrangement. There was a wide variation in the diameters of collagen fibrils which always showed abnormal morphology, with abnormally large, peculiarly shaped fibrils. Apparent loss and/or a disordered arrangement of the typical periodicity of the fibrils were frequently observed. In addition, various degrees of degenerative changes of collagen tissue were often present. These abnormalities were never seen in the fibrils of the normal chordae, and were observed consistently in both the fibrils of the ruptured chordae and in the macroscopically intact chordae in the group with spontaneous rupture of chordae tendineae. These results suggest that a defective organization of collagen into fibrils and fibers, associated with secondary degeneration of collagen within the central collagenous core of the chordae tendineae, are important pathogenetic mechanisms for spontaneously isolated ruptures of chordae tendineae.

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Aldosterone responses to angiotensin II were evaluated in normal subjects in 3 conditions, (1) with suppression of neither ACTH secretion nor angiotensin II, (2) with suppression of ACTH by dexamethasone, and (3) with suppression of both ACTH and angiotensin II by combined administration of dexamethasone and captopril. Baseline levels of plasma aldosterone were significantly lowered by administration of either dexamethasone or both dexamethasone and captopril. Aldosterone responsiveness to angiotensin-II was not altered by suppression of ACTH secretion. However, the responsiveness was significantly enhanced during suppression of both ACTH and angiotensin II. These results suggest that aldosterone response to angiotensin II in normal man is not dependent upon endogenous ACTH secretion, but to an action of angiotensin II on the pituitary gland to release ACTH. The combined administration of dexamethasone and captopril may be a useful maneuver to assess more precisely the reactivity of the adrenal cortex to angiotensin II in man.

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The effects of intravenous administration of several quinidinelike antiarrhythmic drugs (bunaftine, monochloroacetyl ajmaline, lidocaine, mexiletine, disopyramide, aprindine, diphenylhydantoin, procainamide) on left ventricular performance, evaluated by systolic time intervals (STI), were studied in 100 patients with atherosclerotic heart disease. The STI were measured: the pre-ejection period (PEP), the isometric contraction time (ICT), the left ventricular ejection time (LVET), corrected LVET (LVETc), and the PEP/LVET ratio. The degree of impairment of left ventricular performance was maximal after aprindine and disopyramide administration. This was demonstrated by significant increases in the PEP, ICT, and PEP/LVET and by significant decreases in LVET and LVETc, in patients in both III-IV and I-II NYHA classes. Bunaftine, monochloroacetyl ajmaline, and lidocaine induced a less marked impairment of myocardial performance, since the PEP, ICT, and PEP/LVET increases were not significant compared to controls in patients in NYHA class I-II, and since no variation of LVET and LVETc were observed. Mexiletine effects on myocardial performance appear to be intermediate between these groups of drugs. Diphenylhydantoin and procainamide, considered separately because of their effects on heart rate and blood pressure which are not possessed by the other drugs, induced significant increases of PEP in NYHA class III-IV patients. However, the effects of these 2 drugs on myocardial performance may have been understimated, due to the concomitant hemodynamic effect of these drugs.

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Surface isopotential maps were recorded immediately before and 1 week after production of myocardial infarctions in 15 dogs. Difference maps were made by subtracting pre-infarction maps from time-equivalent post-infarction maps, and the electrophysiological basis of the difference maps was examined.
The dogs were classified into 4 groups according to the location and extent of the infarction. Difference maps of these groups displayed an area with significant surface potential defects due to infarction. These changes were observed during specific phases of ventricular activation and in specific portions of the chest surface, depending on the location and extent of the infarction. These findings were well accounted for by the hypothesis that difference maps reflect the loss of activation fronts as a result of the infarction.

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The effect of trapidil on depressed cardiac function was investigated in 5 dog heart-lung preparations. Trapidil at a dose of 60mg improved cardiac function which had been severely depressed by 70±32 (S.D.) mg of sodium pentobarbital. This dose of trapidil, however, produced no significant increase in heart rate. The results suggest that trapidil would be useful in the treatment of heart failure.

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This study was conducted to determine whether or not a low concentration of carboxyhemoglobin influences the extent and severity of myocardial ischemia caused by coronary ligation. In 10 dogs, electrograms were recorded from 6 epicardial electrodes mounted on the anterior surface of the left ventricle and distributed over the area normally perfused by the lighted branch of the left anterior descending coronary artery. The magnitude of ST segment elevation of the 6 sites in each animal was determined for 15min after ligation. This elevation was used as an index of the presence and severity of myocardial ischemic injury. Ligation alone increased ∑ST elevation, summed from 6 sites, from 2.06±0.34mV (SEM) to 24.89±2.14mV (SEM). Carbon monoxide inhaled prior to ligation increased the severity and extent of ischemic injury and the magnitude of ST segment elevation in the area peripheral to the ischemic area more than did ligation alone. These changes occurred without elevation of heart rate or arterial pressure. It was concluded that a low background concentration of carboxyhemoglobin at the time of ligation increased the extent and severity of myocardial ischemic injury.

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The effects of hypoxia on the conduction of excitation in ventricular muscle were examined. Transmembrane action potentials and isometric tension of isolated rabbit papillary muscle were monitored simultaneously. When the preparations were exposed to hypoxia, the action potential duration (APD) shortened progressively and conduction velocity, assessed by the interval between two action potentials, decreased appreciably. This conduction delay was always accompanied by an increase in resting tension (RT). The upstroke velocity of the action potentials, however, was virtually unaffected by 60min of hypoxia. When the perfusate was reoxygenated, the APD, conduction velocity and RT recovered. The conduction delay and elevation of RT due to hypoxia were prevented by verapamil or a low [Ca]₀ medium and were potentiated by isoproterenol. These results suggest that a cytoplasmic Ca⁺⁺ accumulation, resulting in intercellular electrical uncoupling, may contribute to the conduction delay during hypoxia.

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The effects of propranolol treatment on adrenoceptor reactivity and on cardiac myosin ATPase activity have been studied. Eight mongrel dogs weighing 8 to 14Kg were given propranolol orally 3 times daily (10mg/Kg/day) for 2 weeks. Although the levels of propranolol were effective and there was a significant decrease in resting heart rate, there was no evidence of a rebound adrenoceptor hypersensitivity after abrupt withdrawal of propranolol treatment. The responsiveness of cardiovascular systems to 1-isoproterenol (1-ISO) was significantly attenuated 15hrs after the last medication, but it did not differ from the premedication levels 6 days after discontinuation of medication. The effects of 1-ISO on adenylate cyclase activity in the myocardial membrane preparations were not significantly different between the 3 groups (no medication, 1 day and 6 days after discontinuation). With propranolol treatment, though a rise in total plasma catecholamine (norepinephrine, epinephrine, dopamine) levels was the predominant change, there were no definite changes in respective catecholamines. Serum triiodothyronine (T₃) increased during medication in 7 of the 8 animals and decreased after medication. Calcium-activated and K⁺-activated myosin ATPase activity in the inner and outer layers of the left ventricular wall were uniform in unmedicated dogs, and propranolol produced no significant effects. No reliable evidence for propranolol withdrawal syndromes was provided in the present study.

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Differences in the relaxing effects of nifedipine, a so-called calcium antagonist, were studied in smooth muscle from different arteries of dogs. The common carotid artery (Car A), celiac artery (Cel A), superior mesenteric artery (SMA), renal artery (RA), femoral artery (FA), and coronary artery (Cor A) were helically cut, and their developed isometric tensions were recorded. High potassium contraction was induced in these strips, and, at the peak of developed tension, nifedipine (10^-6M) was added. Relaxation curves induced by nifedipine were analyzed by a curve fitting method into two to three exponentials.
The general form of the equation is At=2or3∑i=1A_0ie^-kit. The k value shows the rate of relaxation; i.e., the larger the value the faster the relaxation. The relaxation was faster in the order of RA, SMA, Cor A, Cel A, Car A, and FA. The value of (A_0i/2or3∑i=1A_0i)×100 shows the fraction of tension in each component of the relaxation curve A_0ie^-kit. The fraction of tension distributed to the faster relaxation exponentials [A₀₂e^-k2t(+A₀₃e^-k3t)] in each smooth muscle was larger in the order of RA, SMA, Cor A, Car A, FA, and Gel A.

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When the ventricle is electrically stimulated at a faster rate, the cessation of the drive is followed by a temporary suppression of automaticity (overdrive suppression). The effects of lidocaine and verapamil on overdrive suppression were studied in dogs. Lidocaine slowed the ventricular escape rate and prolonged the pause following overdrive; occasionally, it was about twice the next succeeding RR interval. On the contrary, verapamil influenced neither the ventricular escape rate nor the pause following overdrive. It is suggested that lidocaine not only suppresses the automaticity of ventricular escape pacemaker but also induces exit block and that the spontaneous depolarization of the ventricular pacemaker is not slow channel-dependent.

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This report documents a case which showed type A, type B and intermediate patterns of pre-excitation on different days. A vagotonic maneuver and digitalis induced a type A pattern, while exercise, atropine and isoproterenol caused a type B pattern of activity. A gradual transition from type A to B was demonstrated with vectorcardiograms. Despite the variations in the QRS morphology, the direction of the initial vector was not altered and was directed straight anteriorly. In this case, an accessory pathway may be located in the posterior paraseptal region or the lateral free wall of the left ventricle, and a variable size of pre-excited area may have caused type A and type B patterns of pre-excitation.

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This report describes a 45-year-old man who suffered from hemolytic-uremic syndrome. In his autopsy findings, kidney arteriolar walls showed marked hyaline degeneration and interlobular arteries were occluded by severe intimal proliferation. No vascular changes were found in other organs. There were no arteriosclerotic changes in either main branches from the aorta or the aorta. These vascular changes are correspond well with the early features of malignant nephrosclerosis without any clinical findings of malignant hypertension. This type is called primary malignant nephrosclerosis by Bohle et al. We would like to point out the significance of this case in the re-consideration of the pathogenesis of malignant nephrosclerosis.

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Three patients with mitral regurgitation (MR) associated with aortitis syndrome are presented. All had multiple lesions of the large sized arteries, calcification of the aorta, mild inflammatory findings, a chronic course, and congestive heart failure.
MR was observed by ventriculography in all 3 patients. Case 1 had mitral valve prolapse and secondary systemic hypertension. Case 2 showed mildly thickened mitral valve leaflets and had moderate aortic regurgitation (AR). Case 3 had massive AR. The grade of MR was moderate in Cases 1 and 2, and massive in Case 3. The left ventricle was moderately dilated in Cases 1 and 2 but contracted sufficiently and symmetrically in all 3 patients. Other than the prolapse, no significant mitral valve deformity or left ventricular asynergy was evident by ventriculography. The incidence of MR was 3.1% of 128 patients with aortitis syndrome observed in our clinic.
MR may be found in the late stage of aortitis syndrome. It may be caused by a mild valvular lesion related to aortitis syndrome and be exacerbated by increased hemodynamic loads such as those which occur in secondary hypertension and AR.

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Oral administration of prostaglandin E₂ resulted in marked clinical and hemodynamic improvement in patients with hypoplastic left heart syndrome. A lessening of metabolic acidosis and an increase in blood pressure were evident. These results indicate that the ductus arteriosus was effectively dilated by oral prostaglandin E₂ in patients with ductus-dependent systemic circulation, as in the case of ductus-dependent pulmonary circulation. Surgical risk will also be reduced by pretreatment with oral prostaglandin E₂.

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