To evaluate the effect of the duration of fasting on myocardial fluorine-18-fluorodeoxyglucose (FDG) uptake and distribution, 16 FDG-positron emission tomography (PET) studies were performed in 7 normal volunteers under three different conditions: glucose loading, 6 h fasting and overnight fasting. In the glucose-loaded condition, all subjects had good image quality, and myocardial metabolic rates of glucose (MRGlc) were significantly higher than those in the other two conditions. In the 6 h and overnight fasting conditions, image qualities varied according to MRGlc. Although there were visually distinct regional differences with MRGlc ranging from 0.05 to 0.15 μmol/min per g, these differences were not impressive by a quantitative analysis. The ranges of MRGlc in these two fasted conditions overlapped each other. There was a significant negative linear correlation between MRGlc and serum free fatty acid levels. Thus, MRGlc and image quality in fasted normal subjects varied with the extent of the fed-to-starved transition under clinical fasting conditions (6 h to over-night), and this transition does not depend solely on the duration of fasting. These findings may explain the heterogeneity in FDG studies under fasting conditions. (Jpn Circ J 1996; 60: 319 - 327)

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Due to the increase in life span and the decrease in mortality associated with aortic surgery, many geriatric patients now undergo surgery for abdominal aortic aneurysms (AAAs). Therefore, we studied our surgical results for AAAs in an elderly population to assess the value of such operations. Twenty-six patients aged 80 years or older underwent surgery during an 11-year period from 1984 to 1994 at our institutions, and their outcomes were compared with those of 212 younger patients. The ratio of ruptured to non-ruptured AAAs Was significantly higher in the older patients (aged 80 years or older) than in the younger patients (aged 79 years or younger), and aneurysm size in cases of non-rupture was greater in older patients than in younger patients. For octogenarians with non-ruptured AAAs, the survival rate was 85.7% at 5 years, compared with 43.6% at 3 years for those with ruptured AAAs, and these figures were not significantly different from those in younger patients. The present findings support the value of our active surgical approach for octogenarians with AAAs. We believe that an aggressive approach for octogenarians will decrease the incidence of ruptured AAAs and contribute to better patient survival. (Jpn Circ J 1996; 60: 328 - 333)

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Background: To clarify the physiological significance of the pulmonary artery index (PAI), we examined the relationship between PAI and physiological properties of the pulmonary vascular bed. We also examined the limitations of PAI in practical use. Methods and Results: We examined the relationships between PAI and pulmonary vascular resistance (Rp), pulmonary arterial compliance (Cp), and the time constant (RC) of pulmonary circulation in 50 patients with congenital heart disease with decreased pulmonary blood flow, PAI was significantly related to Cp and RC (r=0.67, r=0.63, respectively). These correlations became more significant when we excluded patients in whom the central pulmonary arteries were disproportionately dilatated in contrast to the peripheral pulmonary arteries (r=0.80, r=0.70, respectively). Conclusions: PAI reflects the state of the pulmonary vascular bed, especially when the peripheral arteries develop in proportion to the central pulmonary artery. (Jpn Circ J 1996; 60: 334 - 340)

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Adenosine appears to mediate the preconditioning-induced reduction in infarct size in rabbits and dogs, but little is known about the role of adenosine in preconditioning-induced protection against ischemia-induced arrhythmias. We compared the effects of preconditioning induced by 2 cycles of 5 min of global ischemia and 2 cycles of 5 min of perfusion with either adenosine (100 μmol/L) or the adenosine A1-selective agonist 2-chloro-N6-cyclopentyladenosine (CCPA, 100 nmol/L) in protecting against ischemia-induced arrhythmias in Langendorff-perfused rat hearts. Preconditioning reduced the incidence of ventricular tachycardia (VT) from 100 to 58% and the incidence of sustained VT or ventricular fibrillation (VF) from 92 to 33%. Perfusion with adenosine reduced the incidence of VT from 100 to 55%, the incidence of VF from 67 to 9% and the incidence of sustained VT or VF from 92 to 9%. CCPA reduced the incidence of sustained VT or VF from 92 to 25%. These interventions provided a true reduction in the severity of arrhythmias, rather than merely a delay in the onset. Our results suggest that the stimulation of A1 receptor by adenosine is involved in triggering ischemic preconditioning-induced protection against ischemia-induced arrhythmias in rats. (Jpn Circ J 1996; 60: 341 - 348)

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The purpose of this study was to determine whether thromboxane A₂ (TXA2) is involved in the development of ventricular arrhythmias produced by coronary artery occlusion. Ventricular arrhythmias were induced by coronary artery occlusion in 66 male Sprague-Dawley rats. Rats were separated into 4 groups, and saline (n=19) or CV4151 (a TXA2 synthetase inhibitor)(10 mg/kg, n=14; 30 mg/kg, n=15; or 100 mg/kg, n=18) was injected intravenously 5 min before coronary artery occlusion. The antiarrhythmic effect of CV4151 was assessed in terms of the number of ventricular premature complexes (VPCs), the combined duration of ventricular tachycardia (VT) and ventricular fibrillation (Vf) , the incidence of Vf, and the mortality rate within 30 min after occlusion. The total number of VPCs was as follows; control: 1789±330 beats: 10 mg/kg group: 1289±302 beats: 30 mg/kg group: 1008±229 beats: 100 mg/kg group: 986±275 beats, with no significant differences between groups. The incidence of Vf was significantly reduced in the 30 mg/kg and 100 mg/kg groups, as was the combined duration of VT and Vf and the mortality rate. Our results indicate that the TXA2 synthetase inhibitor CV4151 reduces the incidence of lethal arrhythmias induced by coronary artery occlusion in rats. (Jpn Circ J 1996; 60: 349 - 354)

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Cardiopulmonary bypass (CPB) per se alters many factors simultaneously, including free radical generation, which suggests that conventional hyperoxic CPB may produce oxidative injury in the infantile heart and lung. This study tests the hypothesis that CPB provokes oxidative cardiopulmonary changes and pulmonary endothelial dysfunction in immature piglets that can be prevented by free radical scavengers. We studied 15 2- to 3-week-old piglets. Five served as a control without CPB. Ten piglets underwent 60 min of CPB with a membrane oxygenator (Sarns). In 5 of these 10, the bypass prime was supplemented with N-mercaptopropionylglycine (MPG: 80 mg/kg) plus catalase (50,000 U/kg), whereas the others were not treated. Pre- and post-bypass cardiopulmonary function was measured in terms of left ventricular end-systolic elastance [Ees] by a conductance catheter, the arterial/alveolar pO₂ ratio (a/A ratio) and static lung compliance. Conjugated dienes (A233 nm/mg lipid) were measured to detect lipid peroxidation in heart and lung tissue, and myocardial antioxidant reserve capacity [malondialdehyde (MDA) production in cardiac tissue incubated with the oxidant t-butyl hydroperoxide (t-BHP)] was assessed to detect oxidative changes. Pulmonary vascular resistance (PVR) and transpulmonary nitric oxide (NO) production were measured to assess pulmonary endothelial injury. Myocardial antioxidant reserve capacity was significantly reduced after 60 min of CPB, compared to control animals (MDA 779±100 vs 470±30 nmol/g protein, p<0.05 at t-BHP 2.0 mmol/L), without evidence of lipid peroxidation or myocardial dysfunction. Pulmonary vascular resistance after CPB was dramatically increased (83±12 to 212±30, p<0.05) without any change in lung function. In parallel to pulmonary vasoconstriction, NO production was significantly decreased after CPB (from 8.8±1.4 to 2.5±0.5 mmol/min/kg, p<0.05). The addition of antioxidants (MPG+catalase) to the prime significantly improved myocardial antioxidant status (MDA: 604±30 vs 779 ±100 nmol/g protein, p<0.05) and pulmonary vascular resistance (114±29 vs 212±30, p<0.05 vs no-treatment group). In conclusion, the present study confirms that 1) Cardiopulmonary bypass produces substantial oxidative stress in normal immature myocardium, as assessed by reduced antioxidant reserve capacity; 2) CPB impairs pulmonary endothelial function, characterized by NO production, resulting in pulmonary vasoconstriction; and 3) These deleterious effects can be prevented by the addition of antioxidants (MPG/catalase) to the pump prime. (Jpn Circ J 1996; 60: 355 - 363)

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We report a patient with Brugada syndrome who developed sustained mono-morphic ventricular tachycardia (SMVT). The patient was a 29-year-old man who experienced recurrent episodes of palpitation and syncope after drinking alcohol. Electrocardiogram showed right bundle branch block and ST-segment elevation in precordial leads V_1-3 without Q-Tc prolongation. Organic heart disease and coronary artery disease were excluded by noninvasive and invasive tests. Ventricular fibrillation was induced by the application of a single extrastimulus to the right ventricular outflow tract. During isoproterenol infusion, SMVT of left bundle branch block morphology (240/min) was induced by the application of a single extrastimulus to the right ventricular apex. SMVT also developed spontaneously. Pace mapping disclosed that SMVT originated at the free wall of the right ventricular outflow tract. Head-up tilt test and an alcohol provocation test both induced similar SMVT that was associated with hypotension and near syncope. SMVT was not terminated by intravenous administration of lidocaine, procainamide or adenosine triphosphate (10 mg), but was terminated by propranolol. Thus, a beta-adrenoceptor-mediated mechanism appears to play an important role in SMVT in this patient. The site of origin of SMVT might be closely related to the lesion that causes ST-segment elevation . (Jpn Circ J 1996; 60: 364 - 370)

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Autonomic nervous dysfunction has recently been considered to be an etiological factor in syncope and sudden death in cases of hypertrophic cardiomyopathy. However, the precise mechanism is still unknown. A 73-year-old woman with obstructive hypertrophic cardiomyopathy was hospitalized with complaints of impaired consciousness; faintness 3 to 4 h after meals, lightheadedness while walking, and syncope during and after defecation and micturition. Faintness was induced by alimentary hypoglycemia related to gastrectomy performed 5 years previously. Lightheadedness and syncope were accounted for by autonomic nervous failure combined with an impairment of α1-adrenoceptor in vasoconstriction and the carotid sinus hypersensitivity which accompanied preceding events such as abdominal pain, defecation and micturition, which could enhance the vagally-mediated baroreceptor reflex. (Jpn Circ J 1996; 60: 371 - 376)

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A 50-year-old Japanese male was admitted with a 1 month history of progressive shortness of breath, palpitations, and intermittent low-grade fever. On admission, a musical diastolic murmur (sea-gull murmur) was heard on the 3rd left sternal border. Blood studies showed an accelerated erythrocyte sedimentation rate, and positive C-reactive protein. Retrograde aortography revealed severe aortic regurgitation. At the operation, the aortic wall was remarkably thickened, and the aortic valve commissures between the right and left coronary cusps and between the left and non-coronary cusps had completely detached from the aortic wall. The aortic valve was replaced with a St Jude Medical valve using pledgeted sutures. Histologic studies of the aorta and aortic valve revealed no evidence of any pathologic changes. Echocardiography performed 82 days after aortic valve replacement showed severe paravalvular leakage and valve detachment. At the reoperation, the prosthetic valve was detached from the extremely edematous and fragile native aortic annulus. There was no vegetation or abscess formation. Aortic root replacement with the Cabrol technique was performed using a composite graft in which the prosthetic valve was placed 1 cm above the proximal extremity to reduce the tension on the suture line and the aortic annulus. Histologic study of the aorta after the reoperation showed non-specific inflammatory disease. The patient, who received steroid therapy, has recovered without any signs of graft detachment or pseudoaneurysm formation. (Jpn Circ J 1996; 60: 377 - 381)

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Acute infectious myocarditis is primarily by viruses and bacteria, but sometimes by rickettsia. Tsutsugamushi disease is a febrile illness caused by Rickettsia tsutsugamushi, and has been prevalent in Korea since 1985. Characteristics of tsutsugamushi disease are fever, rash and eschar. Tsutsugamushi myocarditis is rare. Cardiac involvement may include ST-T changes, PR prolongation, mild mitral regurgitation, and perivascular inflammation with myocardial necrosis. We describe here a 50-year-old woman who complained of fever, orthopnea and chest pain. Work-up of the patient revealed abdominal scar, positive tsutsugamushi antibody, congestive heart failure with severe mitral and tricuspid regurgitation, persistent atrial standstill on electrophysiologic study, junctional rhythm and ST-T changes mimicking anterior myocardial infarction and myocardial inflammation with perivasculitis on endomyocardial biopsy. The patient's condition improved with doxycycline and inotropics. Persistent atrial standstill during was found at the one-year follow-up. (Jpn Circ J 1996; 60: 382 - 388)

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