The present study attempted to determine the lowest temperature at which the slow atrioventricular nodal pathway responds to heating and the temperature necessary for successful ablation of the slow pathway in patients with atrioventricular nodal reentrant tachycardia (AVNRT). The study group comprised 23 consecutive patients (14 women, 9 men) with symptomatic AVNRT. Radiofrequency current was delivered at the slow pathway potential recording site using a HAT 200S catheter ablation system. Successful radiofrequency ablation of the slow pathway was achieved in all 23 patients. Junctional beats, suggesting the response of the slow pathway to temperature, were detected in 62 of the total 136 applications. The temperature measured at the first junctional beat was 45.4±4.2 °C. The maximum temperature required for the successful ablation of AVNRT ranged from 45 to 88°C. There were no complications except for 1 patient with transient atrioventricular (AV) block. There were no recurrences of AVNRT during follow-up. The lowest temperature at which the slow pathway was responsive to heat was quite similar to that for accessory pathways or the AV junction. However, the temperature required for the successful ablation of AVNRT differed markedly among the patients. (Jpn Circ J 1999; 63: 427 - 432)

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The familial form of hypertrophic cardiomyopathy (HCM) is attributed to mutations in the genes for contractile proteins, but the etiology of non-familial form remains unknown. This study was designed to examine the clinical features, histopathologic changes, and hepatitis C virus (HCV) genomes in patients with HCM associated with HCV infection. Anti-HCV antibody was present in the sera of 9 of 65 patients (13.8%) with HCM versus 2.41% in a control population of voluntary blood donors in Japan, a statistically significant difference (p<0.0001). Among these 9 patients, 6 had ace-of-spades-shaped deformities of the left ventricle with apical hypertrophy. Myocardial fibrosis was found in all patients, and mild cellular infiltration was observed in 5 patients. Type 1b HCV RNA was present in the sera of 5 of the 9 patients. The copy number of HCV was 5.5×10 ³-8.6×10⁵ genomes/ml serum, and multiple clones of HCV were detected in the sera of each patient by an analysis of the hypervariable regions using fluorescent single-strand conformation polymorphism. Positive strands of HCV were found in the hearts of 5 patients, and negative strands in the hearts of 2 patients. A high prevalence of HCV infection was found in patients with HCM, particularly of the apical variety, suggesting that HCV is an important causal agent in the pathogenesis of the disease. (Jpn Circ J 1999; 63: 433 - 438)

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Pulmonary thromboembolism (PTE) is considered an uncommon disease in Japan and there are not any reported prospective studies on the incidence of PTE in Japan. The objective of the present study was to determine the number of patients with PTE per year in a prospective study using a questionnaire. Letters were sent to clinical departments in university schools of medicine or medical colleges, and to hospitals with more than 100 beds. The diagnosis of PTE was to be confirmed by (1) pulmonary artery stenosis or occlusion on pulmonary angiography, (2) mismatch of pulmonary perfusion scintigraphy and pulmonary ventilation scintigraphy, (3) changes on pulmonary perfusion scintigraphy performed twice, or (4) autopsy. The questionnaire elicited 2,341 replies (the withdrawal rate was 40.7%). In 231 hospitals, 237 patients were diagnosed definitely during the study period of 2 months from 1 August to 30 September 1996. From this it was estimated that there are 3,492 (95% confidence interval: 3,280-3,703) patients with PTE per year, which implies that the incidence is 28 persons per 1,000,000 people per year, confirming that PTE is rare in Japan. (Jpn Circ J 1999; 63: 439 - 441)

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Global left ventricular (LV) pump function is generally preserved in patients with hypertrophic cardiomyopathy (HCM). However, it is unknown whether regional myocardial contractility is impaired, especially in nonhypertrophied regions. The purpose of this study was to evaluate regional LV myocardial contraction in patients with HCM using magnetic resonance (MR) spatial modulation of magnetization (SPAMM) myocardial tagging. The study group comprised 20 patients with asymmetric septal hypertrophy (HCM group) and 16 age-matched normal patients (control group), and data were collected using transthoracic M-mode and 2-dimensional echocardiography, and MR SPAMM myocardial tagging. The systolic strain ratio, maximum systolic strain velocity, and time from end-diastole to maximum systolic strain (ΔT) in the anterior, ventricular septal, inferior and lateral regions for 2 LV short-axis sections at the levels of the chordae tendineae and papillary muscles were measured at 50-ms intervals by MR myocardial tagging. The end-diastolic anterior and ventricular septal wall thicknesses and LV mass index were significantly different between the HCM and control groups. The systolic strain ratio for all 4 walls, particularly the anterior and ventricular septal regions, was significantly lower in the HCM group. In the HCM group, the maximum systolic strain velocity was significantly lower and ΔT was significantly shorter for all 4 walls, particularly the anterior and ventricular septal regions. The standard deviation for the ΔT, calculated from the ΔT for the 8 regions of the 2 LV short-axis sections, was significantly greater in the HCM group. In conclusion, regional LV myocardial contraction is impaired in both hypertrophied and nonhypertrophied regions, and systolic LV wall asynchrony occurs in patients with HCM. (Jpn Circ J 1999; 63: 442 -446)

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Recent observations have shown that plasma levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) correlate with cardiac function or prognosis in heart failure patients. However, relatively little is known about changes in their plasma concentration during commonly occurring physiological states such as fatigue. Therefore, this study was designed to examine the physiological changes of plasma ANP and BNP concentrations using a chronic sleep-deprivation model. Bicycle ergometer cardiopulmonary exercise tests were performed in 10 healthy volunteers (mean age: 22.7 years). Blood samples for measuring ANP and BNP were drawn during the resting state and immediately after each exercise test. Cardiac output (CO) was measured during the exercise test by the impedance method. The study conditions were designed as follows: (A) a day following a period of normal sleep (control state) and (B) a day preceded by 1 month during which sleep lasted <60% of normal (chronic sleep-deprived state). Results were as follows. (1) Peak oxygen uptake and peak CO decreased during the sleep-deprived state compared with the control state. (2) There was no difference between peak heart rates measured during exercise under the 2 conditions. (3) Plasma ANP concentration during exercise increased significantly during the control state, whereas only a tendency toward increase was observed during the sleep-deprived state. (4) Plasma BNP concentration during exercise tended to increase in the control state compared with the resting state, whereas there was no difference in plasma BNP between after exercise and resting state in the sleep-deprived state. These results indicate that changes of ANP or BNP induced by exercise tended to be decreased by chronic sleep deprivation. (Jpn Circ J 1999; 63: 447 - 452)

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This study was designed to test the hypothesis that Gadolinium-diethylenetriamine pentaacetic acid (Gd-DTPA)-enhanced magnetic resonance images (MRI) reflect the severity of ischemic injury during the acute and chronic phases of myocardial infarction (MI). Twenty-nine patients with their first acute MI underwent Gd-DTPA-enhanced MRI in the first week (4.2±0.3 days) and at 1 month after onset. Pairs of left ventriculograms were compared with Gd-DTPA-enhanced magnetic resonance images, classified into 3 pattern groups: hyper-enhancement, with and without a central hypo-enhanced region (P1 and P2, respectively), and non-enhancement (P3). In the acute phase of MI, P1 was found in 10, P2 in 11, and P3 in 8 patients. One month later, the image pattern had changed from P1 to P2 in a single patient, from P2 to P3 in 4 patients, and had remained identical in the others. Patients with P3 showed improvement of anterior wall motion in the 1-month follow-up study, and had higher TIMI flow grades and lower peak creatine kinase values than those without recovery. Thus, Gd-DTPA-enhanced magnetic resonance images, closely reflecting the severity of myocardial injury, are useful in predicting myocardial functional recovery after MI. (Jpn Circ J 1999; 63: 453 - 458)

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The effect of exercise intensity on gas exchange kinetics was investigated during exercise and recovery, as well as the relationship between the kinetics during exercise and recovery. Twenty-three patients with a history of anterior myocardial infarction performed low-intensity (38.7±8.3 W) and high-intensity (68.8±15.0 W) exercise for 6 min. The time constants of oxygen uptake (VO₂), carbon dioxide output (VCO₂) and minute ventilation (VE) were significantly prolonged during high intensity exercise compared with low-intensity exercise (61.2 ±8.6 vs 52.3±10.3 s, p<0.005 for the time constant of VO₂). The time constant of VO₂ was similar during exercise and during recovery from exercise of high (61.2±8.6 vs 66.2±12.2 s) as well as low intensity (52.3±10.3 vs 55.0±10.1 s). However, the time constants of VCO₂ and heart rate were significantly shorter during recovery than during exercise. The time constants of VCO₂ and VE were significantly longer than that of VO₂ during both exercise and recovery. In the present study, it was found that (1) the gas exchange kinetics were influenced by the intensity of exercise; (2) the kinetics during recovery did not necessarily reflect the kinetics during exercise except for VO₂; and (3) the kinetics of VCO₂ and VE were delayed as compared with the VO₂ kinetics. These characteristics should be taken into account when using gas exchange kinetics to estimate cardiopulmonary responses to exercise in patients with left ventricular dysfunction. (Jpn Circ J 1999; 63: 459 - 466)

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The present study investigated whether corrected QT (QTc) dispersion could play a role as a marker of ventricular arrhythmias and sudden cardiac death after acute myocardial infarction (MI). The study included 76 males and 24 females with a mean age of 60±11 years. Standard 12-lead ECGs were recorded during the recovery phase (15±9 days) after the onset of MI. The QTc was calculated according to Bazett's formula and QTc dispersion was calculated as the difference between the maximum and minimum QTc intervals. Patients were divided into 2 groups: 21 patients (group A) had a QTc dispersion of ≥80 ms, and the other 79 patients (group B) had a QTc dispersion of <80 ms in the recovery stage (15±9 days). Clinical, angiographical, and Holter monitoring data, and prognosis (mean follow-up period 29±18 months) were compared between these 2 groups. The frequencies of early coronary reperfusion and recanalization of infarct-related vessels during the recovery phase were significantly higher in group B than group A. The left ventricular ejection fraction was also higher in group B than group A (51±12 vs 43±12%, p=0.0029). There were no significant differences in the number of premature ventricular contractions, the percentage of patients with repetitive ventricular arrhythmias, or in the frequency of sudden cardiac death during the follow-up period between the 2 groups. In summary, QTc dispersion in the recovery stage is not a useful marker for ventricular arrhythmias or sudden cardiac death after acute MI, although increased QTc dispersion may correlate with an ineffective early coronary reperfusion and with the degree of depressed left ventricular function. (Jpn Circ J 1999; 63: 467 - 470)

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Probucol decreases and bezafibrate increases plasma high density lipoprotein-cholesterol (HDL-C) levels in humans. This study was performed to determine whether the HDL-C-lowering effects of probucol could be reversed by treatment with bezafibrate in hypercholesterolemic rabbits. Forty-nine normolipidemic Japanese White rabbits were divided into 5 groups [group 1: normal chow; group 2: 0.2% cholesterol (Ch) diet; group 3: 0.2% Ch and 1% probucol diet; group 4: 0.2% Ch and 1% bezafibrate diet; group 5: 0.2% Ch and 1% probucol plus 1% bezafibrate diet] and treated for 8 weeks. Plasma lipids, cholesteryl ester transfer protein (CETP) activity in the lipoprotein-deficient plasma fraction, CETP mRNA in liver tissue and plasma drug concentrations were investigated. Serum total cholesterol (TC) increased after the rabbits in groups 2, 3, 4 and 5 were fed Ch, but overall, no significant differences were observed in serum TC and triglyceride (TG) among these groups. Serum HDL-C levels increased (p<0.01) in the bezafibrate-treated group, but a significant (p<0.05) reduction in HDL-C was observed in both the Ch + probucol (group 3) and Ch + probucol plus bezafibrate (group 5) groups; no significant difference was observed between groups 3 and 5. Significant correlation (p<0.01) was found between serum low density lipoprotein cholesterol (LDL-C) levels and plasma probucol concentrations in groups 3 and 5, but no correlation was found between plasma concentrations of probucol/bezafibrate and serum HDL-C levels. CETP activity in the lipoprotein-deficient plasma fraction increased in the Ch-, Ch + probucol-, and Ch + probucol and bezafibrate-fed groups (groups 2, 3 and 5, respectively), whereas a significant reduction in this activity was observed in the Ch + bezafibrate-fed group (group 4). An analysis of covariance showed that the CETP activity responded more sensitively to drug treatment than did the serum HDL-C level. CETP mRNA in liver tissue was assessed by Northern blotting at 8 weeks, but no changes were observed among the 5 groups. Probucol decreased and bezafibrate increased serum HDL-C levels, through CETP activity without affecting liver CETP mRNA levels, and the decrease in HDL-C levels produced by probucol could not be reversed by bezafibrate. (Jpn Circ J 1999; 63: 471 - 477)

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Although the enhancement of tissue plasminogen activator (tPA) induced thrombolysis by ultrasound has been reported to be augmented by ultrasound contrast agents (UCA), few data exist regarding its process. The present study evaluated the effect of a galactose based UCA on the efficacy of ultrasonic enhancement of tPA thrombolysis and observed the serial changes in the acoustic property and histopathology. A catheter-type transducer capable of ultrasound emission in both continuous (CW) and pulsed wave (PW) was used. The tPA thrombolysis was studied in 30 artificial white thrombi, which were assigned to 4 study groups based on insonation modes and with and without UCA. Each sample was suspended in 100 ml saline in a beaker. Five minutes after tPA (8000 U) administration, ultrasound was applied for 10 min. For the UCA-treated groups, UCA (0.25 g) was added 5 min after the start of ultrasound exposure. The alteration of the thrombus was monitored with echography. Weight reduction of the thrombus was -25±6% in PW and -30±7% in CW, which was significantly enhanced by UCA treatment, -40±3% (p<0.005) in PW+UCA and -43±7% (p<0.005) in CW+UCA. The area of thrombus echo image minimally decreased with ultrasound alone (-12±6%: PW, -23±11%: CW). In the UCA groups, UCA induced a remarkable reduction of size (-36±3%: PW+UCA, -43±7%: CW+UCA) with a high-echo intensity in the superficial layer of the thrombus, where multiple cavity formation was observed by light microscope. UCA markedly enhanced the effect of ultrasound on tPA thrombolysis. The altered acoustic property and corresponding histological microcavity formation in the shallow layer within the thrombus suggests that UCA augmented infiltration of tPA into the thrombus. (Jpn Circ J 1999; 63: 478 - 484)

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Although thinning of the ventricular wall due to infarct expansion (septal aneurysm) may contribute to ventricular septal rupture (VSR), spatial factors predisposing to this mechanical complication have not been fully demonstrated. To identify the morphologic predictors of VSR, a retrospective postmortem study was performed on 17 hearts with acute anteroseptal myocardial infarction, comprising 7 with VSR and 10 without rupture. Infarct size and the extent of wall thinning were quantified. Wall thinning was defined as a decrease of less than 50% of thickness of the noninfarcted wall. The total infarct size did not differ among the groups. In the free wall (FW), the infarct was smaller in hearts with VSR than in those with a ruptured FW (p<0.05) or no rupture (p<0.01). The septal involvement was more extensive in patients with VSR than in those with FW rupture (p<0.05). Septal thinning was more extensive in hearts with VSR than in those with FW rupture (p<0.05) or non-rupture (p<0.05). A combination of a small infarct of the FW and a large septal infarct may contribute to the formation of septal aneurysm, which is believed to predispose to VSR. The presence of a small infarct of the anterior septum may be another setting for postinfarction septal rupture. (Jpn Circ J 1999; 63: 485 - 489)

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A report is presented of a liquefaction necrosis of mitral annular calcification in a patient with chronic renal failure and secondary hyperparathyroidism who had been managed by hemodialysis for 11 years. The mass was echogenic with an echo-lucent area inside, high density on computed tomography and low intensity on magnetic resonance imaging. The uptake of gallium-67 (⁶⁷Ga)-citrate and the bone agent technetium-99m-methylene diphosphate (^99mTc-MDP) was seen in the mass. These findings were compatible with liquefaction necrosis of the mitral annular calcification. After treatment with low calcium concentration hemodialysis, the size of the mass reduced with disappearance of the echo-lucent area on the echocardiography and there was no uptake of ⁶⁷Ga-citrate or ^99mTc-MDP. Liquefaction necrosis might be the early and reversible form of mitral annular calcification. When a tumorlike echogenic mass at the base of mitral leaflets is seen in patients with predisposing factors for mitral annular calcification, consider the possibility of this specific form of mitral annular calcification in order to avoid any unnecessary surgical intervention. (Jpn Circ J 1999; 63: 490 - 492)

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An electrophysiological study and a provocative test of coronary artery spasm was attempted in a 68-year-old man who was having syncopal attacks and chest pain. His electrocardiogram had the characteristics of Brugada syndrome and ventricular fibrillation (VF) was induced by programmed electrical stimulation. ST-segment elevation became exaggerated by procainamide, which could not prevent the induction of VF. Coronary angiography revealed no stenotic lesions, and spasm in the left coronary artery was induced by intracoronary administration of acetylcholine with similar chest pain to that experienced before. Under treatment with diltiazem and flecainide, which suppressed the induction of VF, the patient experienced no recurrence of symptoms despite persistent ST-segment elevation. No previous reports have described coronary spasm associated with Brugada-type ECG abnormalities, and patients with syncope should be evaluated carefully. (Jpn Circ J 1999; 63: 493 - 495)

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A 16-year-old boy was diagnosed with idiopathic postural orthostatic tachycardia syndrome (POTS) during head-up tilt testing. During a passive tilt, the patient's heart rate (HR) increased by 30 beats/min within 5 min. After 25 min of tilting, his HR further increased to 133 beats/min and he began to complain of lightheadedness and weakness without hypotension. Power spectral analysis of HR variability during the tilt test revealed that the ratio of low and high frequency powers increased with the onset of orthostatic intolerance. Propranolol (10 mg every morning) dramatically alleviated his clinical symptoms, and he has been asymptomatic with gaining weight after discontinuing his crowded train commuting. (Jpn Circ J 1999; 63: 496 - 498)

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A 30-year-old Japanese woman was admitted to hospital for dyspnea. She had a history of corrective surgery for a large atrial septal defect and partial anomalous pulmonary venous drainage, which had produced cyanosis in her infancy. However, her cyanosis continued postoperatively. Angiography revealed a double inferior vena cava (IVC), with the left IVC connected with the hemiazygos vein and the right IVC with the left atrium through a very small orifice. Most of the blood from the 2 IVCs flowed into the superior vena cava via the distended azygos and hemiazygos veins. Pulmonary arteriography revealed no abnormal structures. Pulmonary arterial pressure was normal. There was marked pulmonary venous oxygen desaturation. Perfusion lung scintigraphy revealed multiple segmental perfusion defects. These findings suggested the presence of diffuse microscopic pulmonary arteriovenous fistulas bilaterally in the lungs. The patient appears to be the first reported adult case of microscopic and diffuse arteriovenous fistulas. Neither resection of the arteriovenous fistulas nor corrective surgery for the diversion was indicated, and heart-lung transplantation might be the only treatment able to relieve her dyspnea. (Jpn Circ J 1999; 63: 499 - 501)

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