Effects of a single administration of captopril on plasma and urinary vasopressin (AVP) were examined in 8 normotensive (NT) female volunteers, 17 patients with essential hypertension (EHT) and 2 patients with primary aldosteronism (PA). Orally-administered captopril (25 mg) had no effect on plasma AVP levels in the three groups. However, urinary excretion of AVP decreased significantly after use of captopril in both NT and EHT subjects (-57% and -67%, respectively), and also in Pa subjects. The magnitude of reduction in urinary AVP was significantly correlated with the pretreatment levels of plasma renin activity (r=0.85) and plasma aldosterone concentration (r=0.88) in NT subjects. Such correlation was not found in EHT subjects. These results suggest that captopril decreases AVP secretion in both normotensive and hypertensive subjects, but the relation of the magnitude in AVP reduction by captopril to the peripheral renin-angiotensin system might be different.

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In this study, we monitored changes in the mixed venous blood oxygen saturation (Sv^^-O₂) level of 45 patients with acute myocardial infarction and compared these results to the traditional parameters. The Sv^^-O₂ level was found to correlate well with the clinical course of patients and their hemodynamic conditions. The mean Sv^^-O₂ level of the group having congestive heart failure (53.3±8.4%) was found to be statistically lower than those without (69.8±5.6). Furthermore, patients whose Sv^^-O₂ level was lower than 60% were found to be at greater risk for heart failure and a very high mortality rate. Patients were classified into four subsets according to Forrester's hemodynamic classification; their Sv^^-O₂ levels were 70.7±4.1% (I: 23 cases), 54.7±6.9% (II: 8 cases), 55.8±9.4% (III:10 cases), and 47.0±8.0 (IV: 4 cases), respectively. A reverse relationship between pulmonary capillary wedge pressure and Sv^^-O₂ having a correlation coefficient of r=-0.64 was observed, and a logarithmic curvilinear relation between cardiac index Sv^^-O₂, stroke volume index Sv^^-O₂, and left ventricular stroke work index Sv^^-O₂ was also evident. When the decrease in the Sv^^-O₂ level was more than 5%, it always showed a significant decrease in the cardiac index. This study suggested that continuous monitoring of the Sv^^-O₂ level revealed simultaneous changes in the hemodynamic state, which lead to the assistance and aid for treating patients with critical conditions of acute myocardial infarction. In such circumstances, it was noted that the Sv^^-O₂ level should be maintained above 60% in order to stabilize the hemodynamic state.

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Deflection area vectors of QRS (A^^→qrs) and T (A^^→t) and ventricular gradient (G^^→) calculated from vectorcardiographic leads were compared in single vessel coronary artery diseases divided into subgroups of normokinetic, hypokinetic and akinetic by left ventriculography. In the LAD group, A^^→qrs shifted posteriorly, A^^→t were smaller and shifted to the right and G^^→ were smaller and shifted posteriorly or to the right. In the RCA group, A^^→qrs were smaller and shifted upwards, A^^→t shifted upwards and G^^→ were smaller and shifted upwards. In the LCx group, A^^→qrs shifted upwards, A^^→t shifted anteriorly and upwards and G^^→ were smaller and shifted upwards. Decreased magnitude and directional change of G^^→ reflect the severity and location of myocardial damage.

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We measured increments of peripheral venous pressure induced by dynamic leg exercise (ΔVP) in 10 healthy subjects (Group C) and 70 patients with heart diseases which primarily affect the left-side of the heart. None of the subjects showed apparent symptoms of left- or right-sided heart failure. The patients were divided into 2 groups on the basis of ΔVP, namely, Group N (ΔVP<35 mmH₂O, n=30, normal reaction) and Group H (ΔVP≥35 mmH₂O, n=40, abnormal reaction). We measured the increments of plasma concentrations of noradrenaline (ΔNA_PH) and adrenaline (ΔA_PH) with infusion of phentolamine (PH). Parallel studies with nitroglycerin and prozosin supplied strong evidence that ΔNA_PH was brought about mainly by the blockade of α₂-receptors at the sympathetic nerve terminals. Thus, we estimated the degree of sympathetic nerve activity from the central nervous system by opening using PH the negative feed-back loop for noradrenaline (NA) release at the sympathetic nerve terminals, and this degree of sympathetic nerve activity was compared with the degree of ΔVP. The results obtained were 1) there was a rough overall correlation between ΔVP and ΔNA_PH in the subjects of Groups C, N and H, and 2) ΔNA_PH was significantly higher in Group H than in Groups C and N. These results suggest that much reliance can be placed on the measured increment of plasma NA concentration in response to the administration of PH in assessing the degree of enhanced sympathetic nerve activity in the patients with "latent" left-sided heart failure.

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Polysomnography was carried out in 11 adult outpatients with stable chronic heart failure (CHF) due to valvular heart disease in order to investigate respiratory abnormalities during sleep. The subjects consisted of 6 males and 5 females and their ages ranged from 54 to 76 years. A coexisting central dominant sleep apnea syndrome (SAS) was found in 4 males, 3 of whom had evidence of nasal obstruction. A successful mitral valve replacement in one patient with central dominant SAS was associated with a reduction in the frequency of sleep apnea. The results suggest complications caused by respiratory abnormalities should sleep are common and should be considered in the management of patients with CHF.

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We examined whether dobutamine infusion during reperfusion modifies myocardial infarct size in a rabbit ischemia-reperfusion model. Prior to the infarct size study, the hemodynamic response to dobutamine.5, 10, and 15μg/kg/min i.v. was evaluated in the rabbit model. Ten μg/kg/min of dobutamine increased the left ventricular dp/dt max by 34.0±4.9% (n=7) and the myocardial blood flow from 0.86±0.16 to 2.19±0.57 ml/min/g without change in the collateral blood flow (n=4). The heart rate, systolic and diastolic blood pressures were elevated by only 4.7±1.0%, 9, 4±3.0%, and 8.0±3.7%, respectively (n=7). In the infarct size study, a coronary branch was occluded for 30 min and then reperfused. Seventy-two hours after reperfusion, the myocardium supplied by the occluded artery (area at risk, AAR) and the infarcted area were determined by fluorescent particles and histology (hemotoxylin-eosin and modified Mallory's staining), respectively. In the dobutamine treated group (DB group), 10μg/kg/min of dobutamine were infused for 30 min starting immediately after reperfusion, and a comparable volume of saline was infused in the control group. Hemodynamic parameters and the size of AAR were comparable in the control and DB groups. Myocardial infarct size, expressed as the percentage of AAR, was 45.1±3.9% in the control (n=11) and 40.2±2.4% in the DB group (n=10), which was not significantly different. These findings indicated that the isotropic dose of dobutamine administered during reperfusion did not cause myocardial necrosis by disturbing the recovery process of the myocardium from ischemic injury.

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In order to determine whether isovolumic relaxation period (IRP) reflects left ventricular relaxation under different afterload conditions, 17 anesthetized, open chest dogs were studied, and the left ventricular pressure decay time constant (T) was calculated. In 12 dogs, angiotensin II and nitroprusside were administered, with the heart rate constant at 90 beats/min. Multiple linear regression analysis showed that the aortic dicrotic notch pressure (AoDNP) and T were major determinants of IRP, while left ventricular end-diastolic pressure was a minor determinant. Multiple linear regression analysis, correlating T with IRP and AoDNP, did not further improve the correlation coefficient compared with that between T and IRP. We concluded that correction of the IRP by AoDNP is not necessary to predict T from additional multiple linear regression. The effects of ascending aortic constriction or angiotensin II on IRP were examined in five dogs, after pretreatment with propranolol. Aortic constriction caused a significant decrease in IRP and T, while angiotensin II produced a significant increase in IRP and T. IRP was affected by the change of afterload. However, the IRP and T values were always altered in the same direction. These results demonstrate that IRP is substituted for T and it reflects left ventricular relaxation even in different afterload conditions. We conclude that IRP is a simple parameter easily used to evaluate left ventricular relaxation in clinical situations.

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A 40-year-old female with arrhythmogenic right ventricular dysplasia (ARVD) demonstrated a reduced motion of the left ventricular (LV) apex. Specimens of LV free wall, obtained by endomyocardial biopsy, histologically revealed prominent interstitial fibrosis with sparse distribution of myosytes. The myosytes were hypertrophic and disrupted with loss of myofibrils. This is a case of ARVD, where LV involvement was histologically verified.

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Much remains unknown about the conditions surrounding the occurrence of prehospital sudden cardiac arrest. We have investigated the clinical characteristics and predictors of survival in a total of 90 consecutive patients in whom sudden cardiac arrest (SCA) happened to occur during their hospitalization in general wards over the past 19 years. The types of arrhythmia present at the time of SCA were ventricular fibrillation (in 46% of cases), ventricular tachycardia (19%), and bradyarrhythmia (35%). The underlying causes were coronary artery disease (45%), cardiomyopathy (20%), and valvular disease (14%). SCA showed a circadian pattern, with many cases during the day and few at night. Prodoromal symptoms included chest pain (16% of patients), dyspnea (11%) and palpitations (2%). Of the total of 90 subjects, 26 (29%) were discharged from hospital alive, and SCA recurred in 24% of these. The 5-year survival rate was 52%. The most important predictors of survival examined were initiation of cardiopulmonary resuscitation, NYHA class, and time of SCA. Of those in whom cardiopulmonary resuscitation was initiated within 1 min, 52% were discharged alive, but all of those not receiving it within 10 min died.

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Of 383 patients with vasospastic angina who were followed for a period of 3.2±0.1 years, 9 (2%) died suddenly from cardiac causes. Calcium antagonists had been given to 98% of our patients. Only one patient who died suddenly had a fixed coronary stenosis of 75% or greater. Eight of the 9 patients showed ST segment elevation during anginal attack at rest, and 3 patients showed ST segment elevation at both anterior and inferior leads. Sudden death occurred in 6 of 41 patients (12.5%) who were documented to have multivessel coronary spasm, but in only 3 of 342 patients (1%) who had single vessel spasm (p < 0.01). Serious arrhythmia occurred during anginal episode in 3 of 9 patients who died suddenly (53%) and in 52 of 374 who did not (14%). These results suggest that the frequency of sudden cardiac death was rather low in Japanese patients with vasospastic angina. The risk of sudden death was increased in patients with multivessel spasm and serious arrhythmia during anginal attacks but not these with fixed coronary stenosis.

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The long-term prognosis for 314 patients with hypertrophic cardiomyopathy (HCM) and 82 with dilated cardiomyopathy (DCM) was investigated in an attempt to elucidate clinical variables predicting sudden death (SD). In the patients with HCM, 68% of cardiac deaths occurred suddenly and unexpectedly. Variables associated with an increased risk to SD were young age (< 30 years), reduced fractional shortening (< 35) and elevated left ventricular end-diastolic pressure (&ges; 20 mmHg). Eight of the 10 patients who died suddenly during or immediately after strenuous exercise were less than 30 years old, and the collapse tended to be associated with exercise-induced ST-depression. In contrast, SD occurring during mild activities, resting or sleep was mainly observed in those aged 30 years or more. Ventricular tachycardia was observed on electrocardiographic monitoring in 24% of those 30 hand, no SD was found in patients with apical hypertrophy nor in those 50 years or more. These observations suggest that HCM patients at a young age, with impaired left ventricular systolic and diastolic function, have an increased risk to SD. Since exercise-induced myocardial ischemia rather than ventricular arrhythmias appears to be the more likely mechanism for SD for those under 30 years old, restriction of strenuous exercise should be strongly advised for these patients. For those aged from 30 to 50 years, ventricular tachycardia should be controlled by antiarrhythmic agents for the prevention of SD. In patients with DCM, 24% of all cardiac deaths were attributed to SD. Although no variables reliably predicted SD, it was of note that only one patient out of 26 with SV₁+RV₅&ges;35 mm died suddenly. Whereas ven-ventricular arrhythmias are known to be a contributing cause for SD, the prognostic significance of ventricular tachycardia on electrocardiographic monitoring in predicting SD has not yet been established. In addition, antiarrhythmic agents often precipitate hemodynamic deterioration. It therefore appears that use of antiarrhythmic agents is not a therapy of first choice and that primary treatment should be focused upon improvement in ventricular function in order to prevent SD in patients with DCM.

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The purpose of this study is to investigate the long-term prognosis of ventricular tachycardia (VT) mainly with respect to sudden death (SCD) in patients with ischemic heart disease (IHD), idiopathic cardiomyopathy (ICM), miscellaneous heart disease (MHD) and idiopathic ventricular tachycardia (IVT). The study included 117 patients with VT (80 male, 37 female). The number of patients with IHD, ICM, MHD and IVT was 14/40 (35%), 4/17 (24%), 6/25 (24%) and zero (0%), respectively. The other having had syncope in IHD, ICM, MHD and IVT was 19/40 (48%), 7/18 (39%), 6/26% (23%) and 6/33 (18%), respectively. Out of the 19 IHD patients with syncope, 15 had had ventricular fibrillation (VF), which was induced by a disopyramide injection. In IVT, the patients with syncope had a significantly higher VT rate than those without syncope (p < 0.01). There were no significantly differences in the electrocardiographical high risk parameters for SCD, the age, follow-up periods, the presence or absence of VF and ejection fraction between the SCD and the surviving groups. Consequently, it is suggested that IVT is not related to SCD but careful attention should be paid to syncope when the rapid VT rate is observed although VT with organic heart disease is closely related both to SCD and syncope. In addition, it is considered that the above electrocardiographical parameters and so on were not always independent predictors of SCD among the patients having VT.

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Thirty nine cases, in which sudden cardiac death (SCD) was suspected, were studied to evaluate the mechanism and the prediction of SCD i arrhythmia-patients using electrophysiological studies (EPS). The 39 cases (28 male and 11 female) were located by surveying 2098 patients who underwent EPS for the evaluation of arrhythmias. Age at time of EPS ranged from 4 to 86 years, average 50.5 years. Time from EPS to death was 2 to 163 months, average 27.9 months. Underlying heart disease was: dilated cardiomyopathy in 11, old myocardial infarction in 5, ischemic heart disease in 5, hypertensive heart disease in 5, valvular heart disease in 3, hypertrophic cardiomyopathy in 2, arrhythmogenic right ventricular dysplasia in 1, myocarditis in 1, sarcoidosis in 1, cor pulmonale in 1, and no obvious heart disease in 4. Fifteen had a permanent pacemaker implanted. SCD in cases without a permanent pacemaker (24 cases): 2 had chronic complete A-V block (one BH block, one HV block), 1 had advanced A-V block (HV block), 3 had bundle branch block with first degree HV block, 9 had ventricular tachycardia (VT), 3 had sick sinus syndrome (SSS), 3 had paroxysmal atrial flutter, 1 had WPW syndrome and praxysmal atrial fibrillation, 1 had paroxysmal atrial tachycardia, and 3 had premature ventricular beats and first degree HV block. SCD in cases with permanent pacemaker (15 cases): 5 had SSS, and 10 had A-V block. In 3 of the 5 with SSS and 7 of the 10 with A-V block, VT was found before pacemaker implantation. In our study, brady and tachyarrhythmias coexisted in 25 cases (64%). Twenty two of these were ventricular arrhythmias. Therefore, the coexistence of bradyarrhythmias with ventricular arrhythmia (especially VT), and the treatment of VT as well as bradyarrhythmias are thought to have great clinical importance.

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To evaluate the mechanism of sudden death in childhood and the physical activity levels at the onset of sudden death, we studied the following items: (1) the incidence and the circumstances surrounding sudden death at school in Kanagawa Prefecture, (2) high risk heart diseases detected among healthy school children by heart disease screening, (3) sudden cardiac death or near miss seen in outpatients with heart disease except congenital heart disease. Among total 15, 156, 346 school children, sudden death was observed in 97 subjects (M:77, F:20). Annual incidence of sudden death was 6.4 per 10⁶. Of the 97 subjects, acute heart failure of unknown etiology was found in 60 (62%), cardiovascular disease in 18 (19%), cerebral vascular accidents in 14 (14%) and heat stroke in 5 (5%). Of the 78 subjects (M:64, F:14) considered as sudden cardiac death, 62 (79%) died during sports activities, and 16 (21%) died at rest. Of the 62 subjects, 29 died during track and field activities and 7 while swimming, both in physical education classes. Eighteen died during athletic club activities and 8 during extracurricular activities. Consequently, 54 subjects (87%) died in the presence of a school teacher. Of the 18 subjects with cardiovascular disease, 9 (hypertrophic cardiomyopathy in 3, myocarditis in 3, Kawasaki \disease in 2 and long QT in one) were diagnosed initially by the autopsy study. Latent high risk heart disease, detected among presumably healthy school children by the heart disease screening program, were the following: hypertrophic cardiomyopathy, long QT syndrome, Kawasaki disease and some arrhythmias (ventricular tachycardia, sick sinus syndrome, A-V block and atrial fibrillation). Follow-up observations of outpatients with heart disease revealed the same results as the heart disease screening program. In order to prevent sudden death at school, the following recommendations should be observed: 1) sports directors should learn "sports medicine in childhood", including primary cardiovascular resuscitation, 2) and accurate heart disease screening program should be operated to detect latent high risk heart disease, advise on adequate medical treatment, and help ensure an appropriate selection of sports activities, 3) comprehensive autopsy studies should be performed.

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From 1982 to 1986, 1230 sudden death cases were autopsied in Osaka Medical Examiner's Office. Among them, 810 cases were sudden cardiac deaths (SCD) including coronary heart disease (77%), cardiomyopathy (7%), valvular disease (3%). All SCD cases were dead within 24 hours of the appearance of the fatal symptoms, and most of them (72%) were considered instantaneous death. Many of the fatal symptoms began in bed (31%), at bath (17%), at toilet (8%), or at work (8%). Thirty-four percent of them were thought by themselves or by their families to be healthy before the death. Hypertension (38%), coronary heart disease (13%) and diabetes mellitus (11%) were the major past history recorded. Microscopic observation of the hearts of 200 cases autopsied in 1986 showed various cardiac lesions: hypertrophy, strophy, degeneration of myocytes, cellular and fatty infiltrations of the interstitium. According to their cardiac lesions and degrees of severity of coronary sclerosis, patients who died suddenly were divided into 8 groups as follows: 1. myocardial infarction (41) 2. myocarditis (6) 3. hypertrophic cardiomyopathy (19) 4. chronic ischemia with severe coronary sclerosis (65) 5. chronic ischemia with moderate coronary sclerosis (27) 6. small vessel disease (18) 7 amyloidosis (1) 8. unknown (23). These results suggest that coronary heart disease and hypertension play an important role in SCD.

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