The left ventricular function of patients with essential hypertension was examined during exercise and isoproterenol (ISP) infusion echocardiography. Twenty-eight hypertensive patients without cardiac hypertrophy (Group NH), 20 patients with cardiac hypertrophy (Group HH), 7 patients with cardiac dilatation (Group D), and 13 normotensives (Group N), were studied during multistage exercise using a supine bicycle ergometer. In addition, 23 hypertensives (Group NH: 13 patients, Group HH: 10 patients) and 10 normotensives were studied during ISP infusion (0.005 μg/kg/min, and 0.01 μg/kg/min, respectively, for 5 min). To assess the left ventricular function, an M-mode echocardiogram was utilized at rest and during exercise and ISP infusion. At rest, the isovolumic relaxation time (IRT) of each hypertensive group was significantly longer than that of Group N. IRT of Group HH and Group D was significantly longer than that of Group NH. Only the shortening fraction (SF) of Group D was significantly smaller than that of Group N. During exercise the SF increased in all groups, and only the SF of Group D was significantly smaller than that of Group N at a load of 75 W as well as at rest. The SF of Group HH tended to be smaller. There was no significant difference in peak negative dD/dt (-dD/dt) between any of the groups at rest; however, the -dD/dt of Group HH was significantly smaller than that of Group N during ISP infusion. We concluded that left ventricular diastolic function was disturbed in each hypertensive group at rest. Diastolic dysfunction worsened in Group HH and Group D. Only the left ventricular systolic function of Group D was already depressed at rest. Furthermore, unmanifested systolic dysfunction of the left ventricle seemed to be present in Group HH, because SF during exercise tended to be smaller and -dD/dt during ISP infusion was significantly smaller than that of Group N.

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Trends of mortality from cerebrovascular disease from 1985 to 2000 were projected by a semi-logarithmic linear regression analysis based on the deaths and population by sex and age from 1973 to 1982. crude death rates from cerebrovascular disease and cerebral hemorrhage in particular will continue to decrease but the change in death rate from cerebral infarction will remain relatively small. In the period from 1985 to 2000, the death rate from cerebral hemorrhage will decline sharply, and the death rate from cerebral infarction also is expected to decline steadily in every age group. These declines will lead to the decrease in age-adjusted death rates from these cerebrovascular diseases. The average change in the number of the deaths from 1982 to 2000 is minus 3.7% per year for cerebral hemorrhage and plus 0.8% per year for cerebral infarction. The slight increase in deaths from cerebral infarction will be due primarily to an increase in the over 80 year old population. As a result, the proportion of the deaths from cerebral infarction among all types of cerebrovascular diseases will continue to increase in Japan. These future declining trends hopefully can be further modified by improvement in dietary habits and better treatment of high risk groups.

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We report a case of idiopathic giant cell myocarditis accompanied by asymmetric septal hypertrophy. A 64-year-old woman was admitted because of dyspnea. There was no past history of hypertension or heart disease and no family history of hypertrophic cardiomyopathy. Laboratory examinations revealed general inflammatory changes and mild elevation of serum CK and GOT. The clinical course was fulminant and the patient died of heart failure one day after admission. On autopsy, symmetric septal hypertrophy was revealed and the pathohistological examination revealed panmyocarditis with mononuclear cell infiltration, interstitial edema, necrosis of myocytes, and giant cells. The inflammatory changes were most severe in the ventricular septum with asymmetric septal hypertrophy. The extent of myocardial fibers with disarray was within normal limits. Thus, the asymmetric septal hypertrophy appeared to be due to marked interstitial edema and inflammatory cell infiltration in the septum. This case suggests that myocardial inflammation and edema may cause thickening of the ventricular wall during the course of acute myocarditis.

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We report the induction of pneumopericardium by forced coughing during coronary arteriography in a 31-year-old male with anterior chest pain. The patient had no underlying disease and pneumopericardium could be reproduced by forced coughing. To our knowledge, there has been no report in the literature of pneumopericardium induced during coronary arteriography.

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In order to clarify the role of Purkinje fibers in the occurrence of reperfusion arrhythmias, endocardial mapping was performed on perfused canine hearts by attaching 42 close bipolar electrodes to the endocardial surface of the left ventricular septum. Reperfusion with oxygenated Krebs-Ringer solution following 30 min of coronary occulusion induced ventricular tachycardia (VT) in 14 out of 23 preparations. These VT degenerated into ventricular fibrillation (VF) within 1 min after the reperfusion in all but 3 cases. Endocardial mapping revealed that the excitations during VT were always initiated by the Purkinje activities and that myocardial excitations were expanded in a centrifugal manner through Purkinje-muscle junctional area. Furthermore, this excitation pattern was preserved, in the early phase of VT, even though the propagation pattern was distorted. VF was always induced by reperfusion following 30 min of ischemic condition, that is, coronary perfusion with a hyperkalemic (K=10 mM), acidic (pH=6.8) and hypoxic (PO₂=20-40 mmHg) solution (4/4 cases). Elimination of hyperkalemia from the ischemic condition markedly prevented occurrence of VF (1/6 cases) during reperfusion but it did not affect occurrence of VT (4/6 cases); this implies that hyperkalemia causes the onset of VF but has less effect on the occurrence of VT. It has been separately confirmed by micro-electrode experiment, using the dissected papillary muscle of the canine right ventricle, that abnormal impulse formation during re-oxygenation was triggered in Purkinje fibers around Purkinje-muscle junction.

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Cardiotonic steroids cause single ventricular cells to exhibit transient depolarization after a train of driven action potentials or, in voltage clamp experiments, transient inward current after a depolarizing clamp pulse. Transient depolarization or transient inward current was eliminated by an intracellular injection of EGTA. Transient depolarization was elicited by an intracellular injection of CaCl₂, even in the control Tyrode's solution. Together with transient depolarization or transient inward current, digitalis intoxication promoted spontaneous oscillatory, fluctuations in membrane potential or in membrane current. Their power spectra peaked at frequencies of 3-4 Hz and coincided well with the frequency of repetitive injections of EGTA and decreased in amplitude by caffeine with a shift toward higher frequencies. These results suggest that an oscillatory release of Ca from intracellular storage sites is the common basis underlying both the transient events and the spontaneous fluctuations in membrane potential or current. The Ca-sensitive current, measured by intracellular Ca injection, flowed inwardly at negative potentials and reversed polarity at around -22 mV. Therefore this current component is carried by more than one ion.

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Delayed afterdepolarization (DAD) and triggered-activity (TA) were induced in dog and guinea pig papillary muscles in low K⁺, high Ca²⁺ solutions. A single or train stimuli with higher rate than basic rhythm produced TA or accerelated triggered automaticity. A bigeminal rhythm was also elicited by train stimulations. Amplitude of DAD showed dual dependence on cycle length of basic stimuli and became larger at the shorter (less than 350 msec) and at the intermediate (between 500-800 msec) cycle length. Incidence of TA also increased at these zones of cycle length. The coupling interval of TA had a direct relation to basic cycle length or coupling interval of premature stimuli, at certain ranges of intervals, but outside of these zones, inverse or no relation to the latter were found. The transient inward current in single ventricular myocytes revealed similar type of cycle length dependent changes to those of DAD and TA. Termination of TA by premature stimuli could not be obtained consistently at fixed zone of coupling intervals. These characteristics are somewhat different from those of reentry and can be used as differential signs between TA and reentry.

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Under normal circumstances, excitation of the heart spreads from the endocardial site to the epicardial site via the Purkinje fiber. The purpose of this study is to observe whether the transmural unidirectional block exists near the current induced local clamp during sustained ventricular tachycardia. Twelve open chested dogs were used and the local transmural electrograms were taken by three plunge electrodes consisting of two pairs of bipolar ones which were located at the epicardial site and the endocardial site respectively. Evidence of the unidirectional block was detected by means of excitation order between the endocardial site, the epicardial site and the conduction direction. We used the concept of intrinsic deflection for documentation the conduction direction, i.e., an opposite change of the initial deflection of the local electrogram indicates a reversal of direction. Ventricular tachycardia was induced by a current with 3-5 mA to the midwall of the myocardial muscle. Results showed that 1) the change of conduction order and the reverse direction of conduction were seen simultaneously, and 2) ventricular tachycardia was converted to ordinary rhythm by the incision at the epicardial site of myocardium. These results may prove that the unidirectional block is the major qualification for the detection of re-entry.

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Locally-induced digitalis arrhythmia was produced to study whether antiarrhythmic drugs suppress arrhythmia by directly acting on the abnormal impulse generation or by suppressing Na channels of normal myocardium to make it unresponsive to abnormal impulses. Dogs were thoracotomized and the anterior descending artery (ADA) was isolated and autoperfused with arterial blood from the carotid artery. Forty μg and an additional 10 μg every 20 min of ouabain was injected directly into the ADA produced ventricular tachycardia originating from the digitalis intoxication. Locally injected class 1 antiarrhythmic drugs, including tetrodotoxin, were effective in suppressing this arrhythmia. However, when intravenously applied lidocaine was prevented from reaching the ADA area, lidocaine was not effective in suppressing this arrhythmia. We conclude that class 1 drugs produce anti-arrhythmic effect by directly suppressing the digitalis toxicated area, not by suppressing the normal myocardium.

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The effect of procainamide on ventricular vulnerability to fibrillation was studied in 13 anesthetized open-chest dogs. Epicardial electrograms were recorded through forty bipolar electrodes placed on the surface of exposed ventricles. Ventricular fibrillation (VF) was induced by sequential extrastimulation. The number of extrastimuli required to induce repetitive extrasystole (RE) or VF were defined as repetitive extrasystole threshold (RET) or ventricular fibrillation threshold (VFT). The epicardial electrograms at the onset of ventricular arrhythmia were divided every 100 msec after the last extra-stimulation, and the ratio of recordings with activation time of more than 50 msec during each divided period was defined as "chaotic score". Intravenous injection of procainamide at the does of 20 mg/kg failed to increase RET but successfully increased VFT from 4.4±0.9 to 7.0±1.8 in hearts with necrosis. Procainamide significantly reduced chaotic score from 36±12% to 14±7% at 5 sec after the induction of ventricular arrhythmias. We concluded that the antifibrillatory action of procainamide is based on reduction of the number of chaotic multiple reentries, but not on the prevention of reentry per se.

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To clarify factors affecting thee prevalence of ventricular premature contraction (VPC) in patients with stable ischemic heart disease, daily profiles of VPC prevalence were studied in 92 patients using continuous 24-hour electrocardiographic recordings. VPCs in patient groups with effort angina and inferior infarction showed similar daily profiles. However, a significant relationship between VPC prevalence and heart rate was observed in inferior infarction group, while patients with resting angina exhibited another relationship between the two parameters. Higher prevalence rate of VPCs in the early morning in patients with resting angina suggested the contribution of cardiac autonomic nerve activity to the increased frequency of VPCs, while constant frequency of VPCs during the day in anterior infarction group provided no influences on heart rate, effort, and autonomic nerve activity on the VPC prevalence. Age, sex, left ventricular ejection fraction, and nitrates and diltiazem used for the treatment of angina pectoris did not affect the daily profile of VPC prevalence in any patient groups. These results indicated that the clinical and pathophysiological differences of ischemic heart disease, even in stable patients, showed the different distribution of VPC prevalence within a day which is due, in part, to the varied activities of cardiac autonomic nerves.

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The clinical importance of triggered activity as a cause of arrhythmias is uncertain. We assumed that ventricular premature contractions (VPCs) caused by triggered activity could be increased at higher heart rates and be suppressed by calcium channel blockers and beta-adrenoceptor blockers. Thus, we evaluated VPC frequency as a function of underlying heart rate and examined the efficacy of diltiazem and atenolol on VPCs, using 24 hour ECG recording. Plots of VPC frequency vs. heart rate were made at 1-beat/min intervals for all heart rates recorded for at least 5 min during 24 hours. Diltiazem (90-180 mg/day) and atenolol (50 mg/day) were given orally for 4 weeks, respectively in 36 and 16 patients with VPCs of more than 2000/day. Patterns of relationship between VPC frequency and heart rate observed before diltiazem therapy included: 1) an increase of VPCs at higher heart rates (positive correlation) in 16 patients, 2) an increase at low heart rates and a decrease at high heart rates (bidirectional correlation) in 13 patients, 3) an increase at low heart rates and flat curve at high heart rates ( positive-flat correlation) in 5 patients, 4) a linear decrease (negative correlation) in 1 patient, and 5) flat curve (flat correlation) in 1 patient. The patterns of correlation in patients treated with atenolol were positive in 6, bidirectional in 7, positive-flat in 2 and negative in 1. Both drugs significantly reduced the VPC frequency per 24 hours for patients with a positive correlation (P group), but induced no significant change for those with the other patterns of correlation (NP group). At the 70% VPC suppression level, diltiazem was effective in 9 of 16 patients of P group and only 1 of 20 patients of NP group (p<0.01); atenolol was effective in 5 of 6 patients of P group only 1 of 10 patients of NP group (p<0.05). Both drugs reduced the slope of a positive correlation. These results suggest that: 1) VPCs which increase at higher heart rates may be related to triggered activity, and 2) an evaluation of VPC frequency as a function of heart rate predicts the response of VPCs to diltiazem and atenolol, and probably to other calcium antagonists and beta blockers.

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We investigated the recognition of late potentials in patients with and without organic hear diseases and spontaneous ventricular arrhythmias. None of the normal subjects had late potentials and patients with ventricular arrhythmias but no organic heart diseases, also had no late potentials as well as patients with idiopathic ventricular tachycardias. Late potentials in patients with idiopathic cardiomyopathy were noted more frequently in the dilated type than in the hypertrophic type, especially in those with high grades of ventricular arrhythmias. Patients with old myocardial infarctions had a higher rate of late potentials recognition in cases of sudden death or ventricular tachycardias. On the other hand, we observed lower rates in patients during early stage of acute myocardial infarction in spite of the evidence of a higher rate of ventricular electrical instability. There was no association between ejection fractions, wall motion scores and late potentials. However, a higher recognition of late potentials was found in patients with inferior or posterior myocardial infarction and ventricular aneurysm. We concluded that the late potential must be evaluated in each of the different groups of organic heart diseases in order to estimate the clinical value of ventricular arrhythmias.

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Right ventricular endomyocardial biopsies were performed in patients with repetitive ventricular tachycardia (VT; 8 patients) or ventricular premature beats (1 patient) which showed left bundle branch block morphology in electrocardiograms. These 9 males patients ranging in age from 21-55 years (mean 37.7 years) revealed enlargement and/or asynergy of the right ventricle in the ventriculogram. Randomly selected biopsied patients with dilated cardiomyopathy (DCM; 18 patients) and chronic right ventricular overloading (14 patients) who did not show the above-described arrhythmias served as controls. A histopathological analysis revealed advanced myocardal interstitial fibrosis associated with an increase in fatty tissue in 8 of the 9 patients (89%). Moreover, advanced hypertrophy of myocytes (grades 2 or more of our criteria), disarrangement of muscle bundles and endocardial thickening were prominent with incidences of 75%, 75% and 78%, respectively. Incidence of all findings was more pronounced in the ARVD group. suggestiveness of post-myocarditic change in the biopsied specimen was high in 1 patient, showing a lower incidence (12%) than the DCM group (17%). From these results, we can conclude that different etiological factors may be the based of these pathological changes. We believe that the presence of a large amount of fatty tissue within the myocardial tissue is an important element in the etiology of ventricular arrhythmias as it has also been recognized in patients with non-ARVD idopathic ventricular tachycardia in our biopsy series.

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