The present study examined the angiographic characteristics and prognosis of young males under 40 years of age with acute myocardial infarction (AMI) and familial hypercholesterolemia (FH). The study group was divided into an FH group (n=16) and a non-FH group (n=27). Lesion morphology was classified as complex or smooth. Overall 36 patients were followed up for an average of 9.4 years. The frequency of angiographic normal or non-obstructive culprit lesions was significantly higher in the non-FH group (p<0.01). In contrast, the incidence of complex or totally occlusive lesions was higher in the FH group (p<0.01). At 10-year follow-up, survival rates from cardiac death (FH 85% vs non-FH 100%, p=0.06), from AMI (FH 43% vs non-FH 80%, p<0.05), and from any ischemic event at a new lesion (FH 9% vs non-FH 67%, p<0.01) were all reduced in the FH group. These results suggest that the mechanism of AMI in young male patients with FH differs from that in similar aged patients without FH, and that the overall prognosis of these patients is less favorable. (Jpn Circ J 2001; 65: 247 - 250)

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Thrombus in the infarct-related artery is one of the limitations for flow restoration in primary percutaneous transluminal coronary angioplasty (PTCA) treatment for acute myocardial infarction (AMI). The present study investigated the benefit of preceding intracoronary thrombolysis (ICT) by retrospectively analyzing acute phase flow restoration in 80 AMI patients with intracoronary thrombus: 40 undergoing primary PTCA alone (primary PTCA group) and 40 treated with preceding ICT plus PTCA (combined group). Acute phase Thrombolysis in Myocardial Infarction (TIMI) grade flow was as follows: TIMI 0/1: 35.0% vs 12.5% for the primary PTCA group and the combined group, p=0.06; TIMI 2: 7.5% vs 15.0%, p=NS; TIMI 3: 57.5% vs 72.5%, p=NS). In the subgroup analysis, it was also less in the combined group among 33 patients with a left anterior descending coronary artery (LAD) lesion (42.1% vs 7.1%, p=0.08), but not among the remaining 47 with either a right coronary artery or left circumflex artery lesion. The combined therapy may potentially provide better acute phase flow restoration in AMI patients with an intracoronary thrombus in a LAD lesion.(Jpn Circ J 2001; 65: 251 - 256)

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A more durable mechanical valve may be a better choice for the tricuspid position than a bioprosthesis when the patient already has mechanical prosthesis in the left side of the heart. Eleven cases of triple valve replacement (total follow-up period, 49.5 patient years), all with mechanical valves, are reviewed to assess optimal valve selection. Nine patients had undergone a total of 12 previous cardiac surgeries. Three patients died in hospital (27.3%), but there were no late deaths among the survivors. Two cases of valve thrombosis in the tricuspid position occurred (linearized incidence: 4.04%/patient years) and 1 of these required reoperation. Because of this high incidence of valve thrombosis, the bileaflet mechanical valve is not considered to be the best choice. Even if mechanical valves are implanted in the left side of the heart, a bioprosthesis may be a better choice at the tricuspid position. (Jpn Circ J 2001; 65: 257 - 260)

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Monocyte chemoattractant protein-1 (MCP-1) plays a fundamental role in monocyte recruitment and has been implicated in atherosclerosis. The present study tested the hypothesis that increased levels of MCP-1 are associated with an increased risk for restenosis post stent implantation. The plasma MCP-1 antigen levels were measured pre-stenting, and at 24 and 48 h and 6 months post stenting in 41 patients with stable exertional angina (SEA) who had undergone successful stent implantation. Nineteen patients with chest pain syndrome were selected as a control group. Initial plasma MCP-1 antigen levels (mean ± SE, pg/ml) in the patients with SEA were significantly higher than those in the control group (852.3±51.4 vs 418.2±26.7, p<0.001). The patients with SEA were divided into 2 groups based on follow-up angiographic findings: 17 patients with restenosis (R group); 24 patients without restenosis (N group). The lesion was significantly longer in the R group than in the N group (p<0.03). Plasma MCP-1 antigen levels at pre-stenting were not significantly different between the 2 groups (820.6±69.1 in the R group vs 874.7±73.8 in the N group). Serial changes of plasma MCP-1 levels were plotted as percent changes from the initial levels (mean ± SE, %) and were significantly higher in the R group than in the N group at 48 h and at 6 months post stent implantation (104.6±4.8 vs 89.2±3.4, p<0.01, 109.6±11.2 vs 98.5±5.0, p<0.05). The study concludes that MCP-1 production at stented coronary arterial sites is associated with an increased risk for restenosis post stent implantation. (Jpn Circ J 2001; 65: 261 - 264)

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The present study, which aimed to determine the predictors of distal embolization and restenosis after stenting for vein graft disease, retrospectively analyzed 51 consecutive patients who underwent stent implantation for diseased saphenous vein grafts. Follow-up angiography was performed 6 months after the procedure and the clinical and angiographic variables were analyzed by multivariate logistic regression to determine the predictors of distal embolization and restenosis. Initial clinical success was achieved in 49 patients, 44 of whom underwent follow-up angiography and were enrolled in the retrospective analysis. Distal embolization occurred in 6 grafts (13.6%). Multivariate analysis showed that the lesion length and the total cholesterol level were independent predictors of distal embolization. Angiographic restenosis occurred in 13 (26.5%) of 49 lesions. The minimum luminal diameter and the percent diameter stenosis after stenting were associated with the occurrence of restenosis. Multivariate analysis of lesions located in the graft body identified graft age as an independent predictor of restenosis. Distal embolization can occur after vein graft stenting, especially in patients with hypercholesterolemia and diffuse stenosis. The post-stenting minimum luminal diameter and the percent diameter stenosis are predictors of restenosis. In particular, graft age is associated with the restenosis of graft body lesions. (Jpn Circ J 2001; 65: 265 - 270)

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The presence of left atrial thrombus (LAT) is associated with an increased risk of embolic stroke. However, it has yet to be established definitively whether low-intensity warfarin therapy (INR: 1.5-2.0) can prevent LAT formation in patients with nonvalvular atrial fibrillation (NVAF). The present study analyzed the clinical and transesophageal echocardiography (TEE) features of 123 such patients to identify risk factors for LAT formation and the efficacy of prophylactic low-intensity warfarin therapy. Left atrial thrombi were found in 35 patients (28%) in whom systemic hypertension (49% vs 23%; p<0.01) and ischemic heart disease (17% vs 3%; p<0.01) were more frequent. Left ventricular ejection fraction (54±14% vs 60±11%; p<0.05), left ventricular end-diastolic dimension (51±7 mm vs 48±5 mm; p<0.05), spontaneous echo contrast (2.2±0.7 vs 1.4±0.9; p<0.01), left atrial diameter (50±6 mm vs 43±7 mm; p<0.01), left atrial appendage blood velocity (22.3±8.7 cm/s vs 37.2±21.5 cm/s; p<0.01) and the incidence of left ventricular hypertrophy (37% vs 15%; p<0.01) were also significantly different between the groups. Fourteen patients received continuous warfarin therapy (target INR: 1.5-2.0) and on the follow-up TEE study the left atrial thrombus resolved in 10 (71%). There were no thromboembolic events or major hemorrhagic complications in these patients, so it was concluded that low-intensity warfarin therapy is efficacious in treating LAT formation in patients with NVAF. (Jpn Circ J 2001; 65: 271 - 274)

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Based on the results of the Cardiac Arrhythmia Suppression Trial (CAST), strategies for the treatment of tachyarrhythmias have changed rapidly. The Japanese Antiarrhythmics Long-Term (JALT) study was planned to investigate the present methods for choosing antiarrhythmic drugs, and the effects on long-term prognosis in patients with tachyarrhythmias in Japan. Following a 6-month preliminary study (JALT-1), there was a multicenter nonrandomized prospective study (JALT-2), with a 2-year follow-up, of patients with paroxysmal atrial fibrillation (PAF), sustained ventricular tachycardia (SVT) and nonsustained VT (NSVT). Four hundred fifty-five patients were registered, and 361 of them (79%) were analyzed. Cerebral infarction occurred in 10 of 193 patients (5.2%) with PAF. Transition to chronic AF was observed in 21 patients (10.9%), but in none of the patients receiving Ca antagonist therapy. Twenty-five patients died: 5 deaths were arrhythmic, 10 were because of pump failure, and 9 were noncardiac. The most significant difference in drug selection between JALT-1 and JALT-2 was the increase in the use of slow kinetic Na channel blockers for PAF and the decrease in the use of the same agents for VT in the JALT-2 study. A marked change of therapeutic strategy occurred in JALT-2 compared with JALT-1. Most patients with a poor prognosis had underlying heart diseases and heart failure, but the per annum rate of death by arrhythmia and pump failure in JALT-2 was less than that in JALT-1. (Jpn Circ J 2001; 65: 275 - 278)

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The study investigated whether patients hospitalized for unstable angina pectoris (UAP), who subsequently develop complete coronary thrombosis (acute transmural myocardial infarction (AMI)) despite medical treatment, exhibit platelet hyperaggregability in an assay system that does not employ agonist stimulation. The study comprised 89 patients with UAP (Braunwald type B). Unfractionated heparin and nitrate were administered to all patients via continuous intravenous drip together with aspirin taken orally. Citrated platelet-rich plasma (230-250 × 10³/μl) was obtained on admission and again, in some patients, following the AMI. Platelet aggregability was measured in an optically modified cone-plate viscometer that enables the detection of platelet aggregation without agonist stimulation. A continuous shear rate of 1,200/s was employed. Of the 89 patients, 85 were finally stabilized, while 4 developed an AMI accompanied by persistent ST-segment elevation with increased levels of plasma creatine kinase within 3 h after starting the treatment. The extent of platelet aggregation on admission was significantly greater in these 4 patients compared with the 85 who were stabilized (87.8±6.8%, n=4 vs 26.8±9.1%, n=85; mean ± SD). These data suggest that platelet hyperaggregability mediated mainly by fibrinogen binding to the activated glycoprotein IIb/IIIa complex occurs before a complete thrombotic occlusion and this evaluation may provide important information before the onset of myocardial infarction. (Jpn Circ J 2001; 65: 279 - 282)

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The present study examined the ability of dual-chamber (DDD) pacing to improve symptoms and exercise tolerance in patients with non-obstructive hypertrophic cardiomyopathy (HNCM). Seven patients with HNCM who had failed to benefit from pharmacotherapy participated in the study. The New York Heart Association (NHYA) functional class status and exercise tolerance, which was determined by the treadmill exercise test, were recorded and an echocardiographic observation was performed before, and 1 week, 3 months and 1 year after the implantation of a permanent DDD pacemaker. The atrioventricular delay (AVd) was determined by measuring the point of peak rapid filling velocity and maximum cardiac output (CO). Two patients were not implanted with a permanent pacemaker because their CO and blood pressure decreased or because palpitation occurred during temporary pacing. The ratio between early and late peaks of flow velocity (1.56, 1.21, 0.95, and 0.86 before implantation and 1 week, 3 months and 1 year after implantation, respectively); deceleration time (ms: 263.2, 217.6, 204.6, 187.0); peak filling rate (ml/s: 146.2, 204.0, 233.2, 243.6); NYHA functional class status (2.0, 1.8, 1.6, 1.4); and exercise tolerance (s: 203, 264, 403, 480) were significantly improved after implantation. However, left ventricular dimension, percent fractional shortening, ejection fraction, acceleration time and the isovolumic relaxation time were not changed significantly. In conclusion, DDD pacing improved symptoms and the NYHA functional class status, which is associated with improvement of left ventricular diastolic function. It is proposed that DDD pacing would be useful in patients not only with obstructive but also non-obstructive hypertrophic cardiomyopathy refractory to medical treatment, depending on the careful selection of subjects. (Jpn Circ J 2001; 65: 283 - 288)

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Medically refractory heart failure may be present in children with cardiomyopathy (CMP) or complex congenital heart disease (CHD). In adults, the surgical management of this condition is either heart transplantation or the Batista operation. From March 1995 to January 2000, a total of 6 children, aged from 1 to 16 years, with medically refractory heart failure associated with CMP or complex CHD underwent cardiac transplantation and one of them also had the Batista operation as a bridge to transplantation. One of the 6 patients died of intractable sepsis 17 days after the operation, but the other 5 were discharged with satisfactory hemodynamics. Immunosuppressive agents, including azathioprine, cyclosporin or FK-506, were given. One patient experienced moderate acute rejection, but it was controlled by FK-506, OKT-3 and solumedrol. However, another suffered from lymphoproliferative disease 8 months after transplant, but it was controlled by intravenous immunoglubulin, α-interferon and acyclovir. Cardiac function during serial follow-up (range, 1 month to 5 years) revealed normal systolic and diastolic function and none received any anticongestive medications. Almost all patients received an oversized donor heart. The left ventricle (LV) mass was remodeled, initially as an decrease and later as an increase. The patient who underwent the Batista operation was discharged 1 month after the operation with an increased LV ejection fraction (from 10% to 22%). She was successfully bridged to heart transplantation 7 months after the Batista operation. The results of cardiac transplantation in growing children are satisfactory and remain the mainstay of surgical treatment for medically refractory heart failure in these patients. However, with a shortage of donor hearts, the Batista operation may be adopted as a bridge to heart transplant with a fair response. (Jpn Circ J 2001; 65: 289 -293)

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Preexcitation in Wolff-Parkinson-White syndrome (WPW) has been reported to induce long-lasting changes in ventricular recovery properties. However, there has not been a report concerning changes in the activation - recovery interval (ARI) in 12-lead ECGs before and after catheter ablation (CA) in patients with WPW syndrome. The present study compared changes in ARIs from 12-lead ECGs with those from body surface unipolar leads before and after CA to examine whether ARIs from limb leads of 12-lead ECGs provide useful information on changes in recovery properties in addition to the ARIs from precordial leads. The study population consisted of 27 manifest WPW patients with a left- (n=18, group A) or right-sided accessory pathway (n=9, group B). ARIs in leads I, II, and III were strongly correlated with those in unipolar leads over the left lateral, left lower, and right lower chest, respectively. ARIs in leads aV_R, aV_L, and aV_F showed a significant correlation with those in unipolar leads over the right upper, left upper, and lower anterior chest, respectively. These correlations were maintained before and after CA. Furthermore, in group A, ARIs in lead V₁ tended to increase on day 7 post CA compared with before CA and on day 1. In group B, ARIs in lead III significantly decreased on day 7 compared with before CA and on day 1. These findings suggest that ARIs from the limb leads of 12-lead ECGs may represent those from unipolar leads of a particular area over the body surface, and that ARIs from 12-lead ECGs may provide useful quantitative information on changes in recovery properties before and after CA in patients with manifest WPW syndrome. (Jpn Circ J 2001; 65: 294 -299)

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Stroke volume (SV), cardiac output (CO) and systolic blood pressure (SBP) were measured during maximal symptom-limited bicycle exercise testing in 13 young patients (age, 11-26 years) with nonobstructive hypertrophic cardiomyopathy (HCM). SV was measured by impedance plethysmocardiography; %SV_end, %CO_end, and %SBP_end represent the ratio of the value at termination of the exercise to the respective value at rest. In all patients of HCM-I (the Cardiac Event Group, 3 patients) and 3 of HCM-II (the Non-Cardiac Event Group, 10 patients), the %SV_end was less than 100%. The %SV_end of HCM-I was significantly lower than the respective values of the HCM-II and Control groups. The %CO_end values of the HCM-I and HCM-II groups were each significantly lower than that of the Control. The %SBP_end values of the HCM-I and HCM-II groups were each significantly lower than that of the Control. Among the HCM patients, the %SV_end value was positively correlated with the %SBP_end value. The patients who had more severe HCM had poorer exercise-induced increases in SV and SBP. These results suggest that sudden cardiac death in young HCM patients is associated with inhibition of the increase in SV upon exercise. (Jpn Circ J 2001; 65: 300 - 304)

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The purpose of the present study was to examine the mechanisms of improvement in left ventricular (LV) diastolic function in hypertensive patients treated with cilnidipine, a new and unique calcium antagonist that has both L-type and N-type voltage-dependent calcium channel blocking actions, using pulsed Doppler echocardiography and pulsed tissue Doppler imaging. The study comprised 35 untreated patients with essential hypertension (19 men and 16 women; mean age 65±10 years). The peak early diastolic and atrial systolic transmitral flow velocities (E and A, respectively) and their ratio (E/A), and the peak early diastolic and atrial systolic motion velocities (Ew and Aw, respectively) of the LV posterior wall and their ratio (Ew/Aw) were determined in all patients before and after 1, 3 and 6 months on cilnidipine (10 mg/day). One month: Systolic and diastolic blood pressures were significantly decreased. E and E/A were significantly increased, whereas there were no significant changes in Ew and Ew/Aw. Three months: Ew and Ew/Aw were significantly increased compared to those before and 1 month after cilnidipine. Six months: E and E/A were significantly increased compared with before and 3 months after cilnidipine, and Ew and Ew/Aw were significantly increased compared with before cilnidipine. Moreover, the LV mass index was significantly decreased compared to that before cilnidipine. In summary, changes in LV diastolic performance in patients with essential hypertension following cilnidipine treatment were biphasic with an initial increase in early diastolic transmitral flow velocity and a later increase in early diastolic LV wall motion velocity. The initial and later changes can be related to an acute change in afterload and a later improvement in LV relaxation. (Jpn Circ J 2001; 65: 305 - 309)

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Several DNA variants at the lipoprotein lipase (LPL) gene locus have been found to be associated with the plasma lipid levels and the prevalence of coronary artery disease (CAD). In particular, the Ser447-termination (Ter) mutation at the exon 9 of the LPL gene has the potential to elevate the plasma high-density lipoprotein (HDL) levels, but it remains unknown in the Japanese population. The present study investigated 93 CAD patients and 96 age- and sex-matched healthy controls. The Ser447-Ter mutation was determined by polymerase chain reaction restriction fragment length polymorphism method. The allelic frequency of the Ser447-Ter mutation was 0.103 in all subjects. The Ser447-Ter (GG and CG) group was associated with significantly higher levels of plasma HDL-cholesterol (p<0.001) and lower levels of plasma triglyceride than the CC group (p<0.02). The peak particle size of low-density lipoprotein (LDL) was significantly larger in the Ser447-Ter (GG and CG) group than in CC group (p<0.05). The frequency of the Ser447-Ter genotype in GG and CG was significantly lower in CAD than in the controls (11.9% vs 26%, odds ratio = 0.38; 95% confidence interval, 0.18-0.81; p<0.02). These results suggest that the Ser447-Ter mutation of the LPL gene is associated with high plasma HDL-cholesterol levels, low plasma triglyceride levels and a larger LDL particle size. This mutation may have a protective effect against the development of CAD via its favorable lipoprotein profile. (Jpn Circ J 2001; 65: 310 - 314)

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To examine the clinical features of primary cardiac tumors, 34 patients who underwent surgical treatment from 1973 to 2000 at the Kanazawa University Hospital were analyzed and the literature was reviewed. The 34 patients were divided into 3 categories: (i) myxomas; (ii) benign non-myxomas; and (iii) malignant tumors. Twenty-three patients (70%) were diagnosed with myxomas, including 22 left atrial myxomas and 1 right atrial myxoma. Seven patients (18%) were diagnosed with benign non-myxoma tumors, including 3 hemangiomas, 1 fibroma, 1 rhabdomyoma, 1 pheochromocytoma, and 1 lipoma. Four patients (12%) were diagnosed with malignant tumors, including 2 angiosarcomas, 1 rhabdomyosarcoma, and 1 malignant fibrous histiocytoma. Among the myxoma patients, in-hospital mortality was 9% (2/23), late mortality was 10% (2/21), and no recurrent myxomas have been identified. Among benign non-myxoma patients there were no perioperative deaths; however, 1 patient died 11 years after surgery, with no linked cause. No recurrent tumors have been identified. Among malignant tumor patients, 1 patient died the day following surgery and the rest died within 14 months. Early and late results of surgery were acceptable for those patients with benign tumors, while the prognosis for patients with malignant tumors was very poor. (Jpn Circ J 2001; 65: 315 - 319)

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To clarify the autonomic nerve mechanisms whereby isoproterenol induces vasovagal reaction, 32 patients with recurrent syncopal episodes of unknown origin underwent head-up tilt testing. Syncope was induced in 11 patients by a control tilt (control/+ group). The remaining 21 patients (control/- group) underwent the procedure during isoproterenol infusion. Syncope was induced in 13 (isoproterenol/+ group), but not in the remaining 8 patients (isoproterenol/- group). High-frequency component (HF) and low-frequency component (LF)/HF, which are indices of heart rate variability, were assessed for 2-min intervals at baseline (T1) during the initial phase (T2) and at the end (T3) of tilting in each test. The ratios of HF and LF/HF at T2/T1 and T3/T2 were calculated. The HF value at T3 in the control/+ group was greater than that in the control/-group (1.47±0.91 vs 0.75±0.34; p<0.05). The HF value at T3 in the isoproterenol/+ group was significantly greater than those in the isoproterenol/- group (1.19±1.04 vs 0.43±0.23; p<0.05). The HF value at T2 in the isoproterenol/+ tended to be greater than in the isoproterenol/-group (1.30±0.85 vs 0.66±0.53; p=0.07). The ratio of HF for T2/T1 in isoproterenol/+ was greater than in the other groups (2.04±1.26 in isoproterenol/+ vs 0.58±0.39 in control/-, 0.47±0.18 in control/+ and 0.71±0.45 in isoproterenol/-; p=0.0001), whereas that of HF for T3/T2 in the control/+ group was greater than in the other groups (1.48±0.62 in control/+ vs 0.97±0.33 in control/-; p<0.05, 0.79±0.35 in isoproterenol/- and 0.88±0.37 in isoproterenol/+; p<0.01). No difference was observed in either LF/HF or the ratio of LF/HF among the groups. The early and persistent increase in parasympathetic nerve tone provoked by isoproterenol plays an important role in enhancing the vasovagal reaction during head-up tilt testing. (Jpn Circ J 2001; 65: 320 - 324)

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Left ventricular function and blood pressure responses were evaluated in 56 patients with non-obstructive hypertrophic cardiomyopathy (HCM) and 12 control subjects by using a radionuclide ventricular function monitor during supine ergometer exercise. Patients with HCM were divided into 2 groups: (i) group A had no decrease in ejection fraction (EF) during exercise; and (ii) group B had a decrease in EF during exercise. During exercise, the change in end-diastolic volume did not differ between the 3 groups. In contrast, the change in end-systolic volume differed between the 3 groups (p<0.0001). The change in systolic blood pressure (SBP) also differed significantly between the 3 groups. The change in SBP in group B was smaller than that in the control group and group A, and changes in the EF and changes in the SBP between rest and peak exercise showed a significant correlation (p<0.005). These results suggest that exercise-induced systolic dysfunction in patients with non-obstructive HCM may contribute to abnormal blood pressure response in those patients. (Jpn Circ J 2001; 65: 325 - 329)

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Calcium overload is considered to be a primary contributor to ischemia - reperfusion injury. Cardiac sarcoplasmic reticulum (SR), the main regulator of intracellular Ca²⁺ concentration under normal conditions, is a target for ischemic myocardial injury. The ryanodine receptor (RyR) is the SR Ca²⁺ release channel. Previous reports have shown that a reduction in RyR activity during global myocardial ischemia correlates with concomitant myocardial dysfunction. Crystalloid cardioplegia, a technique for myocardial protection during heart operations, reduces Ca²⁺ accumulation during global ischemia. Hence, the effects of cardioplegia on RyR in isolated rabbit hearts was investigated. The study also compared [³H] ryanodine binding before ischemia (control group), after 30 min of ischemia (either global ischemia (GI group) or cardioplegic arrest (CA group)), and after 20 min of reperfusion. The GI group, but not the CA group, showed a significant reduction in the maximum number of binding sites (Bmax) for RyR compared with the control group (Control vs GI group: after ischemia, 1.33±0.27 vs 0.83±0.12 pmol/mg protein, p<0.05; after reperfusion, 1.33±0.27 vs 0.80±0.08 pmol/mg protein; p<0.05). CA group: after ischemia, 1.22±0.20 pmol/mg protein; after reperfusion, 1.15±0.28 pmol/mg protein). The affinity (Kd) values for [³H] ryanodine binding were not different among the 3 groups at any point. The preservation of RyR numbers during cardioplegia correlated with the concomitant preservation of cardiac functions. The results indicate that number of functional RyR was much better preserved during cardioplegia than during global ischemia. It is postulated that cardioplegia-induced protection of cardiac RyR may result in the protection of SR function during ischemia - reperfusion. (Jpn Circ J 2001; 65: 330 - 334)

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In the present study, the long-term process of progression of electrical remodeling at various atrial sites, which is not well understood, was compared while monitoring continuously the electrophysiologic parameters at multi-recording sites in canine atria during continuous atrial burst pacing. A rapid pacing device was implanted in 5 dogs, and continuous atrial burst pacing (400 beats/min) was delivered at the right atrial appendage (RAA). Four pairs of epicardial wire electrodes were sutured on (1) the RAA, (2) Bachmann's bundle (BB), (3) the right atrium close to the inferior vena cava (IVC), and (4) the left atrium (LA). The distal ends of those wires were exteriorized posteriorly and used for pacing and recording. The atrial effective refractory period (AERP), AERP dispersion (AERPd), atrial conduction time (CT) and inducibility of atrial fibrillation (AF) were evaluated during burst pacing for 14 days and during the subsequent 7 days' recovery. The AERP at the LA pacing site was shorter than that at the other sites on day 0. The AERP shortening was greater in the RAA and LA sites than in the BB and IVC sites. The AERPd increased during pacing and reached the maximum level on day 3, and then decreased during the recovery phase. Prolongation of CT tended to be longer between the RAAand IVC sites than that between the other sites. The incidence of AF induction became higher in accordance with the time course of the rapid pacing phase. There was another peak of AF induction on days 7-10. In a canine chronic rapid atrial stimulation model, the progression of electrical remodeling (ie, the shortening of the AERP and the prolongation of the CT) was not homogeneous in both atria, the AERPd showed a temporal increase between days 3 and 7 and matched the increase in AF inducibility at the LA pacing site, the increase in the AERPd was mainly caused by more rapid AERP shortening at the RAA or LA sites, and the LA site always showed a shorter AERP than the other atrial sites in the control state and during the rapid pacing phase, whereas AF inducibility was higher at the LA site than the other sites. (Jpn Circ J 2001; 65: 335 - 340)

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A 70-year-old woman with acute myocardial infarction (AMI) had a narrow necked left ventricular (LV) aneurysm and pericardial effusion. Although there had been no obvious sign of pseudoaneurysm at the first operation on the 13th day after onset, LV volume increased so dramatically that dyspnea on mild exertion was induced only 2 months after the onset of AMI. She underwent Dor's operation for the expanded LV aneurysm. The histological findings of the resected tissue, which were fibrotic epicardial lesion with small myocyte islands, indicated a true aneurysm. The ultrasound manifestation of a narrow necked aneurysm with abrupt thinning of the myocardium at the hinge point may be a valuable predictor of free wall rupture in the early phase and severely progressive LV remodeling in the late phase. Such aneurysms need to be considered as high risk. (Jpn Circ J 2001; 65: 341 - 342)

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The postpericardiotomy syndrome is a well-known complication of opening and manipulating the pericardium. The occurrence of this syndrome following transvenous pacemaker insertion is very rare, and only 5 cases have been reported to date. The present patient repeated this syndrome 3 times in a short period following 3 different interventional techniques: a temporary transvenous pacemaker, a permanent transvenous pacemaker and surgical pericardiotomy. (Jpn Circ J 2001; 65: 343 - 344)

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A 31-year-old woman was admitted to hospital with loss of consciousness and generalized convulsions. Electrocardiography (ECG) showed complete atrioventricular block (AV block) with a pulse rate of 30 beats/min. Endomyocardial biopsy from the right ventricle showed massive necrosis and degeneration of myocardial cells with extensive infiltration of lymphocytes into the interstitial space. These pathological findings suggested fulminant myocarditis. Following glucocorticoid therapy, the patient became asymptomatic, but the AV block did not resolve completely and a bifocal pacemaker was implanted. However, similar symptoms recurred 7 years later. An ECG showed pacing and sensing failure linked to an increase in the pacing threshold and a decrease in the sensing threshold. Endomyocardial biopsy from the right ventricle again showed interstitial infiltration with lymphocytes and eosinophils. After glucocorticoid therapy, she became asymptomatic once more, and the improvement in the pacing and sensing failure, and cardiomegaly, was satisfactory. This patient represents a very rare case of recurrence of acute myocarditis without progression, as much as 7 years after its first occurrence. Glucocorticoid therapy was still effective in treating the recurrent myocarditis presenting with pacing and sensing failure. (Jpn Circ J 2001; 65: 345 - 348)

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Four patients had the clinical features of `ampulla cardiomyopathy', consisting of acute-onset transient left ventricular apical akinesis with basal normokinesis, normal coronary angiogram, ST-segment elevation and subsequent giant T wave inversion, which mimicked acute coronary syndrome, the onset of which occurred shortly after extreme mental stress. Myocardial necrosis was minimal, although 2 patients showed elevated serum catecholamine levels in the acute phase. Each patient underwent serial cardiac radionuclide single-photon emission computed tomography of myocardial functional sympathetic innervation, fatty acid metabolism and perfusion using I-123-metaiodobenzyl-guanidine (MIBG), I-123-β-metyl-iodophenyl pentadecanoic acid (BMIPP) and thallium-201 (²⁰¹Tl), respectively. In the acute phase, MIBG and BMIPP imaging showed an uptake defect in the apical region, whereas ²⁰¹Tl uptake was mildly decreased. When assessed semi-quantitatively, the MIBG images had higher defect scores from the acute phase throughout the year of observation compared with BMIPP, and ²⁰¹Tl. These observations suggest that the primary cause of ampulla cardiomyopathy is related to a disturbance of the cardiac sympathetic innervation. (Jpn Circ J 2001; 65: 349 - 352)

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