(Jpn Circ J 1997; 61: 807 - 813)

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To examine the relationship between overwork and the occurrence of sudden death, the relation between occupation and seasonal variation in sudden death was studied. A total of 8481 cases of sudden death (among subjects aged over 24 years) were selected from all deaths between 1984 and 1986 in the Niigata Prefecture, Japan, based on a death certificate survey. Sudden death was defined as death within 24 h of the onset of the underlying disease. We divided subjects into 4 groups according to the occupation of the householder: agricultural workers, employees, the self-employed, and other occupations . As the incidence of sudden death in the `other occupation' group did not show any significant seasonal variation, this group was considered to be a control group. Among young to middle-aged men (25-65 year old), the incidence of sudden death was higher than in the control group for agricultural workers in April and September and for employees in March and September. However, in older men (over 65) the incidence for agricultural workers was higher only in April. Among women, there was no such spring rise: in the incidence of sudden death in any occupational group. The months featuring a high incidence of sudden death coincided with the busiest occupational months only for people who were actually working and not for those who had already retired. (Jpn Circ J 1997; 61: 814 - 818)

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To investigate whether autonomic nervous dysfunction exists and to determine the relationship between autonomic nervous activity and ventricular arrhythmias in clinically stable patients with hypertrophic cardiomyopathy (HCM), we studied heart rate variability (HRV) in 21 patients with HCM and 10 age-matched healthy control subjects. Patients were divided into 2 groups: HCM I (14 patients without nonsustained ventricular tachycardia, defined as 3 or more consecutive ventricular premature beats) and HCM II (7 patients with nonsustained ventricular tachycardia). HRV was measured on 24-h ECG monitorings using both non-spectral and spectral methods (fast Fourier transform, FFT). We assessed autonomic nervous activity based on high-frequency (HF; 0.15-0.40 Hz, an index of parasympathetic nervous activity) and the low- to high-frequency power ratio (L/H ratio; an index of sympathetic nervous activity) during daytime and night-time separately. There were no significant differences in any index of HRV between the HCM I and control groups. HF in the HCM II group was significantly lower than that of both the HCM I and control groups during the day and at night, whereas the L/H ratio at night-time was significantly higher in the HCM II group than in the HCM I and control groups. These data demonstrate that, in clinically stable HCM patients without nonsustained ventricular tachycardia, autonomic nervous activity was not different to that of healthy control subjects, whereas in HCM patients with nonsustained ventricular tachycardia, parasympathetic nervous activity was reduced throughout the 24-h period, and sympathetic nervous activity at night was increased compared with healthy control subjects. Thus, HCM patients with nonsustained ventricular tachycardia have to be treated even if they do not exhibit significant clinical manifestation. (Jpn Circ J 1997; 61: 819 - 826)

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Indium-111 antimyosin antibody imaging (a tracer of myocardial necrosis) and thallium-201 imaging (a tracer of myocardial perfusion) were compared in patients with myocarditis and dilated cardiomyopathy. The distribution of each tracer and antimyosin/thallium-201 overlapping were evaluated with single-photon emission computed tomography (SPECT). Scintigraphic data were classified into 5 patterns according to the distribution of both images and were compared with histologic findings of endomyocardial biopsy: AM-D, intense and diffuse antimyosin uptake and no perfusion abnormality (active myocarditis); AM-L, localized antimyosin up-take and no perfusion abnormality (active myocarditis); HM, no antimyosin uptake with or without perfusion abnormality (healed myocarditis); DCM-NH, diffuse antimyosin uptake and inhomogeneous thallium-201 uptake (dilated cardiomyopathy); DCM-PD, diffuse or localized antimyosin uptake and myocardial perfusion defect(s) (dilated cardiomyopathy). Patients with dilated-phase hypertrophic cardiomyopathy were frequently found in the DCM-PD group. Taken together, comparative antimyosin/thallium-201 SPECT images are useful for evaluating the activity of myocarditis and ongoing myocardial damage even in areas with no perfusion in patients with dilated cardiomyopathy. (Jpn Circ J 1997; 61: 827 - 835)

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Adenosine triphosphate (ATP) is reported to be released mainly from presynaptic vesicles and cardiomyocytes. The released ATP, which can be degraded to adenosine, may cause coronary vasodilation. However, there is no clear evidence that ATP is degraded to adenosine and causes coronary vasodilation in humans. The present study was undertaken to test whether intracoronary administration of ATP increases myocardial adenosine levels and coronary blood flow. In 11 patients, 3 doses of ATP (0.1, 0.2, and 0.4 mg) were injected into the left anterior descending coronary artery. The velocity of coronary blood flow was measured by Doppler flow probe, and the adenosine concentration in the coronary sinus blood was measured. We also continuously infused ATP (0.2 mg/min) for 1 min in another 10 patients. Coronary blood flow increased dose dependently soon after injection of ATP, Coronary arteriovenous differences in adenosine concentration increased [from 21±15 to 178±15 pmol/ml (p<0.05) 10 sec after the injection of ATP (0.4 mg)] and there were marked reductions in both aortic blood pressure and heart rate. The adenosine levels returned to baseline 20 sec after the injection of ATP, and aortic blood pressure and heart rate also recovered, although coronary blood flow remained increased. Furthermore, continuous infusion of ATP for 1 min increased coronary blood flow velocity and coronary arteriovenous differences in adenosine concentration from 25±14 to 71±13 pmol/ml (p<0.05) in 10 patients. These results indicate that intracoronary administration of ATP immediately increases coronary blood flow and the adenosine concentration of coronary venous blood, which returns to the baseline level thereafter, The differences in the time courses of increases in coronary venous adenosine levels and coronary blood flow after ATP injections suggest that vasodilatory mechanisms other than adenosine, eg, nitric oxide and prostaglandins, may also be involved in the ATP-induced coronary vasodilation. ATP may be used as a cardioprotective agent as well as adenosine. (Jpn Circ J 1997; 61: 836 - 842)

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This study was conducted in an attempt to clarify whether preinfarction angina has an ischemic preconditioning effect. The subjects of this study were Killip class I patients who had suffered a first acute myocardial infarction (MI) as a result of total occlusion of the proximal left anterior descending coronary artery without development of collateral vessels and multivessel coronary artery disease. All subjects achieved successful reperfusion [thrombolysis in myocardial infarction (TIMI) flow grade 3] through intracoronary thrombolysis with single-chain urokinase-type plasminogen activator (SCU-PA). Subsequently, they received the same drug therapy and remained free of reocclusion. The patients were divided into those who experienced a new onset of prodromal angina within 24 h before the onset of acute MI [PA(+) group] and those who had a sudden onset of acute MI without the preceding angina [PA(-) group]. They were further divided according to the time interval from the onset of acute MI to reperfusion (within 1 h, 1-2 h, 2-3 h, 3-4 h, and 4-7 h). In addition, the left ventricular ejection fraction (LVEF), Ieft ventricular end-diastolic volume index (LVEDVI), and the amount of creatine kinase (CK) released (ΣCK) were compared in these 2 groups at reperfusion time. The results of this study showed that ΣCK was significantly lower in the PA(+) group than in the PA(-) group (1,850 mIU vs 3,583 mIU) when reperfusion was induced within 1 h after the onset of acute MI. When reperfusion was induced 1-2 h after the onset of acute MI, ΣCK tended to be lower in the PA(+) group than in the PA(-) group (3,677 mIU vs 5,261 mIU). Once the time to reperfusion exceeded 2 h, there was no significant difference in ΣCK between these 2 groups. On the other hand, there were no significant differences in LVEF and LVEDVI between these 2 groups at any reperfusion time. In conclusion, preinfarction angina had a preconditioning effect (reduction in ΣCK) , but this effect was lost once the time interval from the onset of acute MI to reperfusion exceeded 2 h. (Jpn Circ J 1997; 61: 843 - 849)

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Severe myocardial dysfunction, characterized by global hypokinesis, or akinetic areas with hypokinesis of the remaining wall, and a very low ejection fraction (EF), has been considered to be a contraindication for coronary revascularization (CABG). However, myocardial scintigraphy and echo-stress data have shown that hypo- or akinetic areas can regain their contractility. Therefore, we expanded the indications for CABG, and performed operations even upon patients who were waiting for a heart transplant. Between January 1993 and June 1995, among 352 patients who underwent CABG, 85 had highly depressed left ventricular function. Their resting EF was lower than 0.35, and in 27 it was lower than 0.25. Viable areas of myocardium were found in all of the patients through the combination of scintigraphy and dobutamine-echocardiography: these areas depended on significant coronary lesions. The mean age of the patients was 48.2 years (range 33-62 years); angina was present in 62 patients. A mean of 3.1 grafts/patient were implanted; enoximone was used in all but 5 patients upon weaning from cardiopulmonary bypass; intra-aortic baloon pump was used in 9 cases. Operative mortality was 10.6% (9 patients), due to low-output syndrome in 5, acute myocardial infarction in 2, cerebral damage in 1, and respiratory failure in 1. At the 6-month follow-up, EF was improved in all but 7 patients, in whom it remained unchanged. Scintigraphic and echocardiographic tests revealed good function in most of the areas that had been previously recognized as hypo- or akinetic. These results suggest that the indications for standard myocardial revascularization can be expanded, and a promising option can be offered to patients who may otherwise be destined to wait for an uncertain transplantation. (Jpn Circ J 1997; 61: 850 - 854)

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Spontaneous asynchronous contractile activity caused by spontaneous release of calcium ions (Ca²⁺) from the sarcoplasmic reticulum (SR) is thought to be the cause of deterioration of ventricular function under conditions of calcium overload. We examined whether dantrolene sodium, which can inhibit Ca²⁺ release from the skeletal SR, improves the systolic and diastolic function of calcium-overloaded hearts. In isolated hamster left ventricles, the concentration of Ca²⁺ in the perfusate ([Ca²⁺] _o) was increased from 1 mmol/L to 7 mmol/L in 1-mmol/L steps in the absence (control, n=6) and presence of dantrolene sodium (11.8 μmol/L, n=5). Left ventricular developed pressure and its maximum rate of rise (max dP/dt) increased with an increase in [Ca²⁺]_o up to 4 mmol/L, and decreased with a further increase in [Ca²⁺]_o. In the presence of dantrolene sodium, developed pressure and max dP/dt increased up to 5 mmol/L [Ca²⁺]_o. Thus, dantrolene sodium improves Ca²⁺ tolerance. In isolated ventricles perfused with 1 mmol/L [Ca²⁺] _o, dantrolene sodium decreased developed pressure by 33.7±7.4% and max dP/dt by 37.4±5.6% (mean±SEM, n=8) at 1 mmol/L [Ca²⁺]_o. In contrast, at 5 mmol/L [Ca²⁺]_o. ('calcium-overloaded state'), dantrolene sodium increased developed pressure by 6.8±2.6% and max dP/dt by 14.4±5.7%, and decreased the end-diastolic pressure by 5.3±1.9% (n=8) . Dantrolene sodium partially suppressed the spontaneous contractile activities observed microscopi-cally on the epicardium of ventricles perfused with 5 mmol/L [Ca²⁺] _o. Dantrolene sodium improved the Ca²⁺ tolerance of left ventricles and exerted positive inotropic effects and decreased diastolic stiffness in calcium-overloaded hamster left ventricles by suppressing spontaneous contractile activity. (Jpn Circ J 1997; 61: 855 - 863)

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The effects of cardiac sympathetic nerve (CSN) stimulation on the left ventricular end-systolic pressure-volume relationship (ESPVR) and plasma norepinephrine (NE) concentration in arterial blood were studied in dogs. In 12 anesthetized and open-chest dogs, left ventricular pressure and volume were measured simultaneously with a microtip catheter and a conductance catheter, respectively. The ESPVR values were constructed from pressure-volume loops during a brief occlusion of the inferior vena cava before and after a 40-sec train of electrical CSN stimulation. The slope (E_max) of the ESPVR Iine was significantly greater after CSN stimulation than before CSN stimulation (p<0.05) for both right and left CSN stimulation. The increased E_max values after right and left CSN stimulation were not significantly different from each other. In 5 dogs, time courses of E_max, Ieft ventricular systolic pressure, heart rate, and plasma NE concentration after CSN stimulation were studied. Left ventricular systolic pressure and heart rate returned to the baseline more rapidly than E_max and arterial plasma NE concentration. There was a positive, Iinear correlation between E_max (y) and arterial plasma NE concentration (x), shown as y=3.3×10^-3x+3.1 (n=30, r=0.86, p<0.05). These results imply that cardiac contractile enhancement is reflected in arterial plasma NE concentration in conditions in which CSN is activated. (Jpn Circ J 1997; 61: 864 - 871)

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A 72-year-old man was admitted with palpitations caused by sustained ventricular tachycardia. He had been followed for 27 years, with admissions on 7 occasions, on account of ventricular tachycardias, atrial fibrillation, and congestive heart failure. Electrophysiologic examination detected 2 points of origin of ventricular tachycardia in the right and left ventricles. During the examination a myocardial infarction led to death. At autopsy, most areas of the right ventricle and the left ventricular apex were found to have been replaced by fatty tissue, pointing to severe fatty infiltration into the myocardium. Thus, this patient represented a unique cause of arrhythmogenic right ventricular dysplasia (ARVD) with severe fatty degeneration causing progression of ARVD . It is important that a diagnosis of ARVD is made carefully and rigorously in elderly subjects. (Jpn Circ J 1997; 61: 872 - 876)

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Blade atrial septostomy (BAS) for pulmonary hypertension has increased long-term survival and is an effective and palliative preliminary to heart and/or lung transplantation. We treated an 18-year-old woman with severe pulmonary primary hypertension whose symptoms had worsened as a resulted low cardiac output. The patient's right ventricular pressure was 150/23 mmHg, cardiac index (CI) 1.0 L/min per m², and she showed signs and symptoms of severe primary pulmonary hypertension. We performed BAS successfully, paying particular attention to the following points. To maintain pulmonary blood flow after creating an atrial right-to-left shunt, the patient was infused intravenously with packed red blood cells and volume expander. Oxygen delivery was also increased by the transfusion of packed red blood cells. To avoid unacceptable hypoxemia immediately after the procedure, the atrial septum was initially incised with a very small-blade catheter. Nine months after the BAS, catheterization revealed a decrease in mean pulmonary arterial pressure to 73 mmHg and an increase in CI to 2.5 L/min per m². Thirteen months after the BAS, the patient died as a result of progressive worsening of right-sided heart failure. We concluded that BAS could be successful in patients with severe pulmonary hypertension providing attention is paid to the patient's condition and that BAS is an effective therapy for prolonging survival. (Jpn Circ J 1997; 61: 877 - 881)

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We describe the novel karyotype of a 33-year-old woman with severe mental retardation and multiple cardiac anomalies, including patent ductus arteriosus, a ventricular septal defect, pulmonary atresia, and an overriding aorta. Her karyotype was 46, XX, add(17)(pl3). The short arm of chromosome 17 was slightly elongated owing to the deletion of the distal portion of that chromosome and the addition of extra material from another chromosome. Miller-Dieker syndrome is characterized by a patent ductus arteriosus, Iissencephaly, and the deletion of chromosome 17pl3.3; however, as the patient's brain surface appeared normal on computed tomography, Miller-Dieker syndrome was excluded. The breakpoint in her chromosome 17 was probably located distal to band 17pl3.3. In fact, fluorescence in situ hybridization analysis demonstrated that band 17pl3.3 was intact. To date, genes distal to 17pl3.3 have not been implicated in cardiac anomalies. This patient probably carries a novel deletion on the short arm of chromosome 17. (Jpn Circ J 1997; 61: 882 - 885)

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