Background The prevalence of Brugada-type electrocardiogram (ECG) in schoolchildren remains unclear. This study aimed to further investigate this condition. Methods and Results We studied the prevalence of Brugada-type ECG in 20,387 children (10,434 males and 9,953 females, 9.7±3.2 [SD] years old) during a school health examination in Kanagawa Prefecture, Japan, in 2002. We considered right bundle-branch block and ST-segment elevation of the J point of ≥0.1 mV in leads V₁ through V₃ as Brugada-like ECG, and an ECG was considered to be Brugada-type when the 12-lead ECG fully meet the criteria for the Brugada syndrome as recently published in a consensus report. Only 2 children (0.0098%, 95% confidence interval (CI): 0 to 0.023%) completely conformed to the criteria for Brugada-type ECG. Brugada-like ECG was found in 11 (10 male) of 20,387 children (0.054%, 95% CI: 0.022 to 0.086%). The prevalence in males was significantly higher than that in females, even in children (0.096% vs 0.010%, p=0.012). Stratified according to age, there was tendency for the prevalence of Brugada-like ECG to increase up to puberty (first graders, 0.01%; fourth graders, 0.05%; seventh graders, 0.08%; tenth graders, 0.23%; p=0.068). Conclusion The prevalence of Brugada-type ECG in Japanese children was much lower than that reported in the adult population. (Circ J 2004; 68: 275 - 279)

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Background The purpose of this study was to use the findings of a fibrinolysis and subsequent transluminal trial (FAST-3) to evaluate the association between the target time for obtaining a thrombolysis in myocardial infarction (TIMI)-3 flow after arrival at the emergency room with acute myocardial infarction (AMI) and the degree of myocardial salvage. Methods and Results The FAST-3 trial was administered to 100 patients suffering from AMI. Ranges in the door-to-TIMI-3 flow time (D-T3-time: TIMI-3 flow after arrival at the emergency room) according to quartile were as follows: 30-54 min (quartile 1), 55-77 min (quartile 2), 78-120 min (quartile 3) and 121-330 min (quartile 4). Peak creatine kinase (CK), peak CK-MB, and peak troponin-T values increased in a stepwise fashion across the increasing quartiles of D-T3-time. The left ventricular enddiastolic volume index at 30 days after the start of treatment showed low values for quartile 1. In multiple logistic regression analyses for independent predictors of myocardial damage, the adjusted odds ratios for myocardial damage (peak CK >3,000 U/L) in quartiles 3 and 4 of the D-T3-time were 4.0 (95% CI: 1.0-16.1) and 7.0 (95% confidence interval (CI): 1.4-36.0), respectively. Conclusions These findings suggest that physicians should monitor the D-T3-time for at least 55 min. (Circ J 2004; 68: 280 - 285)

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Background Endothelial dysfunction leads to atherosclerosis and the hypothesis of the present study was that the systemic circulatory response during exercise would be a manifestation of endothelial dysfunction. Methods and Results The circulatory response to exercise of 1,214 apparently healthy people (946 men, mean age 51.2±10.3; 268 women, mean age 52.7±10.1) was investigated, as well as the number of coronary risk factors. Systemic vascular resistance (SVR) was calculated from heart rate, blood pressure and oxygen uptake at rest and at maximal exercise during a ramp protocol using a bicycle ergometer. SVRs at rest (1,751-2,001 (dynes · s · cm^-5) in women and 1,528-1,564 in men) did not significantly differ among the groups by number of coronary risk factors. At maximal exercise, however, they were lower in the group with fewer risk factors; that is, among women 929 (dynes · s · cm ^-5) with no risk factor to 1,305 with 5 risk factors; among men 793 with 1 risk factor to 1,170 with 6 risk factors. Conclusions Those with more coronary risk factors showed a lower but lengthier reduction in SVR during exercise. This weak circulatory response to exercise is a manifestation of deteriorated circulatory function in coronary high-risk subjects. (Circ J 2004; 68: 286 - 293)

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Background Reduced variability of the ventricular response interval (VRI) has been reported to predict adverse prognosis in patients with atrial fibrillation (AF). To examine whether it could be related also to the quality of the daily life of patients with AF, the relationships between VRI variability and exercise tolerance, one of the markers for quality of life, were determined in patients with persistent AF. Methods and Results Thirty-one patients with idiopathic AF were included in the present study. Holter monitoring results and symptom-limited treadmill exercise testing were correlated in these patients without medications for the rate control of AF. The VRI variability, both the SD of the mean R-R interval (SDNN) and the SD of the 5-min mean R-R interval (SDANN), showed significant positive correlation with the exercise capacity (r=0.583, p=0.0004, and r=0.543, p=0.0013, respectively), whereas age, left ventricular ejection fraction and body mass index did not have any significant relationships. Multiple regression analysis revealed that increased SDNN was the only independent predictor of good exercise capacity during the treadmill exercise testing. Conclusions Increased VRI variability, independently of other clinical variables, can predict good exercise capacity in patients with idiopathic AF, thus being a new sensitive maker for quality of life in AF. (Circ J 2004; 68: 294 - 296)

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Background Inflammation is believed to predict coronary heart disease (CHD) in healthy subjects and in patients with atherosclerosis. We investigated the association of high sensitivity C-reactive protein (HS-CRP) and other inflammatory markers on cardiovascular outcome, and carotid atherosclerosis in hypertensive patients. Methods and Results We conducted a cross-sectional study of 122 hypertensive patients and compared them with 64 normotensive volunteers. We measured circulating levels of HS-CRP, white blood cells (WBC), albumin, fibrinogen, erythrocyte sedimentation rate, and interleukin-6, and examined the associations with traditional risk factors of CHD, carotid atherosclerosis, and a 10-year risk of CHD, based on the risk prediction algorithm of the Framingham model. The mean of blood pressure (BP) of the hypertensive patients was 163/102 mmHg (normotensives; 118/79 mmHg). The 10-year risk of CHD was higher in the hypertensive patients (9.3±7.3%) compared with the normotensive volunteers (4.3±4.2%). Albumin and HS-CRP were significantly higher in the hypertensive patients. Multivariate analysis showed that among markers, only HS-CRP was associated with 10-year risk of CHD (β=0.13, p=0.03). The BP, body mass index, high-density lipoprotein, WBC count, fibrinogen, and cardiac hypertrophy increased across quartiles of HS-CRP. There was no association between HS-CRP and carotid atherosclerosis in subjects with hypertension and normotension. Conclusion A higher HS-CRP level was associated with a higher risk score of CHD, but not with carotid atherosclerosis, in patients with hypertension. (Circ J 2004; 68: 297 - 303)

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Background The hepatocyte growth factor (HGF) is a multifunctional cytokine with cardioprotective properties and potent myogenic activity for vascular endothelium. In patients after acute myocardial infarction, exercise training has the beneficial effects on cardiovascular adaptations. We hypothesized that exercise induces HGF production in those patients. If this hypothesis is correct, HGF production may be associated with clinical parameters of cardiovascular function. Methods and Results In 20 patients after acute myocardial infarction, HGF levels in the pulmonary artery (HGF_PA) and aorta (HGF_Ao) were determined at rest and during supine submaximal exercise, with cardiac output (CO) measured by catheterization. Exercise-induced HGF production was calculated by using the following equation: [(HGF_PA -HGF_Ao) × CO during exercise] - [(HGF_PA -HGF_Ao) × CO at rest]. On a separate day, peak oxygen uptake (VO₂) was determined during a symptom-limited upright cardiopulmonary exercise test. Exercise increased HGF production (from 1.6±3.0 to 9.0±6.3 μg/ml, p<0.001). Exercise-induced HGF production was inversely related to peak VO₂ (r=-0.664, p<0.01) and positively related to levels of brain natriuretic peptide (BNP), a biochemical marker for post-infarction ventricular remodeling (r=0.686, p<0.01). Conclusions Exercise significantly increases HGF production. This phenomenon may play an important role in post-infarction patients, particularly with reduced exercise tolerance and elevated BNP levels. (Circ J 2004; 68: 304 - 307)

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Background Unstable plaque and coronary arterial thrombi sometimes induce a no-reflow phenomenon after intervention whereby there is sufficient reperfusion. The greater susceptibility of the right coronary artery to development of large thrombi makes successful reperfusion more difficult, therefore the characteristics of the pathological images of coronary arterial thrombi according to the infarct-related coronary artery were investigated. Methods and Results Coronary arterial thrombi were extracted from 77 patients with acute myocardial infarction (AMI) using a thrombectomy catheter. The 36 patients had a thrombus containing atherosclerotic cells. Platelets, fibrin, and neutrophils were seen in all cases. The mean ratios of structural components of thrombi were 51.0±29.5% (mean ± SD) of the platelet component, 19.9±25.7% of the erythrocyte component and 11.9±22.5% of atherosclerosis component. Erythrocyte-rich thrombi and mixed thrombi mainly composed of erythrocytes were seen in 14 of the 30 cases involving the right coronary artery, 6 of the 35 cases in the left anterior descending artery, 2 of the 11 cases of the left circumflex artery, and in the 1 case of saphenous vein bypass graft. There was significantly more erythrocyte component in the thrombi from the right coronary artery (28.7±30.1%) than in those from the left coronary artery (12.1±18.4%). Conclusion Coronary artery thrombi in AMI are composed principally of platelets. Atherosclerotic cells were identified within thrombi from some patients. In the right coronary artery there were many more thrombi that were rich in erythrocytes than in thrombi from the left coronary artery. (Circ J 2004; 68: 308 - 314)

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Background The present study examined the impact of an 8-week cardiac rehabilitation (CR) program on physiological outcomes and health-related quality of life (HRQOL) of patients with acute myocardial infarction (AMI). Methods and Results A total of 124 consecutive AMI patients were divided into a supervised outpatient CR group (n=82) and a non-CR group as a control (n=42). Peak oxygen uptake, handgrip strength, and knee extension muscular strength were used as physiological outcome measures. HRQOL outcomes were assessed by the Medical Outcome Study Short Form 36 (SF-36). CR group patients performed both aerobic exercise and moderate resistance training from 1 month (T1) to 3 months (T2) after AMI onset. Age, sex, body mass index, medications, and ejection fraction were similar in both groups. Significantly greater increases in overall physiological outcomes from T1 to T2 were measured in the CR group compared with those of the non-CR group. There were also significantly greater improvements in 4 of the 8 SF-36 health status subscales (physical functioning, role-physical, general health, and vitality) in the CR group compared with the non-CR group. Conclusions Eight weeks of exercise training have specific effects on improvement in HRQOL and physiological outcomes in Japanese patients. (Circ J 2004; 68: 315 - 320)

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Background The incidence of stroke in patients suffering atrial fibrillation (AF) is increased when left atrial enlargement occurs. Recently, the platelet adhesive molecule, von Willebrand factor (vWF), located in the atrial endocardium, has been shown to be increased in patients with a variety of heart diseases compared with patients who have no cardiac problems. Methods and Results We investigated the expression of vWF mRNA and protein in the endocardium as a possible prothrombotic alteration of AF in association with atrial structural remodeling. Atrial appendage specimens were obtained during either heart surgery or at an autopsy from AF patients with and without underlying heart disease. The immunohistochemical and in situ hybridization signals for vWF in the endocardium were well correlated and varied widely among the individual atrial appendages examined. The increased expression of vWF in the endocardium was associated with enlarged left atrial dimensions in mitral valvular disease or increased myocyte diameters in the underlying myocardium. Platelet adhesion/aggregation on the endocardium was always found under the fresh thrombi and was colocalized with strong vWF staining, but not necessarily with fibrinogen and/or fibrin staining. Conclusions Endocardial overexpression of vWF may occur during the process of atrial structural remodeling contributing to the thrombotic predilection of AF in association with underlying heart disease. (Circ J 2004; 68: 321 - 327)

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Background Prevention of restenosis after coronary stenting is clinically important. We compared amlodipine and quinapril to determine which is more effective in preventing restenosis after stenting. Methods and Results Immediately after successful coronary stenting of 101 lesions in 63 consecutive patients, the patients were randomly divided into 2 groups: 32 patients with 48 lesions were administered amlodipine 5 mg/day (group A), and 31 patients with 53 lesions were administered quinapril 10 mg/day (group Q). Lesions were assessed by quantitative coronary angiography (QCA) before and immediately after stenting and in the follow-up phase. Intravascular ultrasound (IVUS) could only be performed on 20 lesions in group A and 16 lesions in group Q throughout the follow-up period. We analyzed each lesion at 5 sites. In the follow-up phase, the minimal lumen diameter in group A was significantly larger than that in group Q (1.88±0.64 mm vs 1.52±0.53 mm, p<0.01). In the follow-up phase, the neointimal area (stent area - lumen area) in group A was significantly smaller than that in group Q (1.9±0.5 mm² vs 2.7±0.8 mm² at the middle portion of stent, p<0.01). Conclusion These QCA and IVUS findings suggest that amlodipine has beneficial effects in inhibiting neointimal hyperplasia in stented lesions compared with quinapril. (Circ J 2004; 68: 328 -333)

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Background Although it has been reported that coronary artery bypass grafting (CABG) for multivessel disease markedly improves several parameters of signal-averaged electrocardiography (SAECG), its beneficial effect on SAECG is variable. The hypothesis of the present study was that the presence of diabetes mellitus (DM) affects the improvement in SAECG after CABG. Methods and Results Pre- and post-operative SAECGs were recorded in 100 consecutive patients who underwent complete surgical revascularization. Changes in the following parameters were compared between the diabetic (n=43) and non-diabetic (n=57) patients: filtered QRS duration (dQRS), root mean square voltage in the terminal 40 s of the QRS complex (RMS40), and duration of the terminal low-amplitude signal lower than 40 μV (LAS40). Although baseline characteristics and the occurrence of late potentials were similar in both groups, quantitative improvements in the SAECG parameters after CABG were significantly greater in non-diabetic than in diabetic patients (dQRS: 109±22 ms vs 102±19 ms in diabetics and 106±21 ms vs 88±11 ms in non-diabetics; p=0.028, RMS40: 55±46 μV vs 65±38 μV in diabetics and 50 ±37 μV vs 76±37 μV in non-diabetics; p=0.037, LAS40: 31±20 ms vs 26±17 ms in diabetics and 32±12 ms vs 17±8 ms in non-diabetics; p=0.007, respectively). Conclusions The presence of DM limits the CABG-induced improvement in SAECG. In diabetic patients, therefore, perioperative changes of the SAECG must be interpreted with caution. (Circ J 2004; 68: 334 - 337)

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Background Sleep-disordered breathing may adversely affect heart function, and thereby contribute to the progression of heart failure. A study was undertaken in patients with idiopathic cardiomyopathy to document the characteristics of sleep-disordered breathing. Methods and Results Thirty-five patients with a diagnosis of idiopathic cardiomyopathy, comprising 20 patients with dilated cardiomyopathy (DCM) and 15 patients with hypertrophic cardiomyopathy (HCM), underwent overnight polysomnography. Of these 35, 16 (80%) of the DCM patients and 7 (47%) of the HCM patients had sleep-disordered breathing. Central sleep apnea - hypopnea syndrome (CSAHS) was seen in 10 DCM patients, but not in the HCM patients, and obstructive sleep apnea - hypopnea syndrome (OSAHS) was seen in 6 DCM patients and 7 HCM patients. CSAHS was seen in DCM patients with a low left ventricular ejection fraction. HCM patients with OSAHS had a significantly greater body mass index (BMI) than those without OSAHS and CSAHS (27.6±3.8 vs 22.0 ±4.0 kg/m², p<0.05). DCM patients with OSAHS had a larger BMI than those with CSAHS (29.3±5.8 vs 24.2±4.0 kg/m², p<0.05) and those without OSAHS and CSAHS (29.3±5.8 vs 21.3 ±3.1 kg/m², p<0.05). Conclusions Sleep-disordered breathing is common in patients with idiopathic cardiomyopathy; half of DCM patients had CSAHS, which was closely associated with obesity. (Circ J 2004; 68: 338 - 342)

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Background The present study examined whether the very low frequency (VLF) power of heart rate variability (HRV) is predictive of clinical prognosis in patients with congestive heart failure (CHF). Method and Results The study recruited 54 consecutive CHF patients with emergency admission because of exacerbation of pulmonary congestion. Holter monitoring was performed after improvement of pulmonary congestion. The frequency components of HRV were calculated in the frequency domain (VLF, low frequency (LF), high frequency (HF), total power (TP) and the ratio of LF to HF power). The left ventricular ejection fraction was calculated, and plasma brain natriuretic peptide (BNP) and norepinephrine were also measured at discharge. Within a mean follow-up period of 19.8 ±11.7 months, 18 patients experienced cardiovascular events; 7 patients died and 11 patients required rehospitalization because of worsening of CHF. In univariate analysis, diabetes mellitus (DM), BNP and New York Heart Association (NYHA) functional class were significant as risk factors for cardiac events. VLF power, LF power and TP were the strong predictors for cardiac events in HRV. In multivariate analysis, VLF power predicted cardiac events independently of LF power, TP, DM, BNP and NYHA functional class (chi-square = 6.24, p=0.01). Conclusions VLF power is an independent risk predictor in patients with CHF. (Circ J 2004; 68: 343 - 347)

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Background GIK-²⁰¹Tl imaging reportedly improves the detection of viable myocardium, so the present study evaluated whether it can detect myocardial viability after acute myocardial infarction (AMI). Methods and Results Resting ²⁰¹Tl and ^99mTc-pyrophosphate (PYP) dual single photon emission computed tomography (SPECT) and ²⁰¹Tl SPECT after ²⁰¹Tl with GIK (10% glucose, insulin 5 U, and KCl 10 mmol) infusion (GIK-²⁰¹Tl) were performed in 25 AMI patients within 10 days of admission. GIK-²⁰¹Tl SPECT images were obtained immediately and 4 h after infusion. Left ventriculography (LVG) was performed within 3 weeks and at 6 months when follow-up ²⁰¹Tl SPECT was also performed. From 20 SPECT segments, both the summed defect score (RDS) and the number of defect segments (ES) were calculated. The infarcted area was defined as ^99mTc-PYP uptake segments. Wall motion was estimated in 7 LVG segments. The ES of R-²⁰¹Tl (5.5±2.8), immediate GIK-²⁰¹Tl (4.0±2.3), and 4-h GIK-²⁰¹Tl (5.6±2.7) were lower than that of ^99mTc-PYP (7.5 ±4.1) (p<0.05), and the ES had significantly declined 6 months later on ²⁰¹Tl (3.5±2.8) (p<0.05). Although the RDS of R-²⁰¹Tl (11.3±7.9) and 4-h GIK-²⁰¹Tl (11.2±6.3) were greater than at the 6-month ²⁰¹Tl (7.1±6.5), immediate GIK-²⁰¹Tl (7.4±6.5) was equivalent to follow-up ²⁰¹Tl. The sensitivity of immediate GIK-²⁰¹Tl was highest among the imaging methods. Conclusion To detect myocardial viability after AMI, early imaging with GIK-²⁰¹Tl is more useful than resting ²⁰¹Tl imaging. (Circ J 2004; 68: 348 - 354)

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Background Some patients with hypertrophic cardiomyopathy (HCM) develop left ventricular (LV) wall thinning associated with LV dilatation and systolic dysfunction. Recently, matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs (TIMPs) were reported to be involved in ventricular remodeling, however, little is known about MMPs and TIMPs in patients with HCM. Methods and Results Enzyme-linked immunoassays were used to measure the plasma concentrations of MMP-2, MMP-3, MMP-9, TIMP-1, and TIMP-2 in 11 patients with HCM accompanied by systolic dysfunction (fractional shortening (FS) <25%, group A), 17 patients with HCM who had preserved systolic function (FS ≥25%, group B), and 50 age-matched clinically healthy control subjects (mean age: 57 years). The concentration of MMP-2 in group A was significantly higher than in group B and the control subjects (1,124±84, 792±49, 809±26 ng/ml, respectively), whereas there was no significant difference between group B and the control subjects. MMP-2 concentrations significantly increased as the New York Heart Association functional class increased in patients with HCM. TIMP-2 was also significantly higher in group A patients than in group B and the control subjects (45.3±4.7, 34.6±2.2, 33.7±1.8 ng/ml, respectively), but there was no difference between group B and control subjects. TIMP-1 was significantly higher in HCM patients than in control subjects. MMP-3 and MMP-9 concentrations did not differ among the 3 groups. Both MMP-2 and TIMP-2 correlated significantly with FS and LV dimension, negatively and positively, respectively. Conclusions These results suggest that changes in the release and activity of MMP-2 and TIMP-2 may be associated with the mechanisms responsible for cardiac remodeling in patients with HCM. (Circ J 2004; 68: 355 - 360)

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Background The present multicenter study investigated whether the combination of angiotensin-converting enzyme inhibitor (ACEI) and angiotensin II receptor blocker (ARB) is more beneficial for preventing left ventricular remodeling and suppressing neurohumoral factors than either ACEI or ARB alone. Methods and Results One hundred and six patients with mild-to-moderate congestive heart failure treated in 26 Japanese institutes were randomly assigned to the combination therapy or monotherapy. Changes in physical activity (New York Heart Association functional classes, Specific Activity Scale (SAS)), concentrations of neurohumoral factors (plasma renin activity, angiotensin II, aldosterone, and brain natriuretic peptide (BNP)), and cardiac function for 6 months were compared between the 2 groups. It was found that the combination therapy, which was administered at doses standard in Japan, increased the SAS score (4.5±1.5 to 4.9±1.5, p<0.05) and decreased the plasma BNP concentration (183±163 to 135±118 pg/ml, p<0.05). In contrast, there were no changes in SAS score (4.5±1.4 to 4.6±1.4, NS) or BNP concentration (156±157 to 151±185 pg/ml, NS) in the patients receiving monotherapy. Conclusions The results of the study demonstrate that the combination therapy, even at the standard doses for Japan, improves physical activity and plasma BNP concentration more than the monotherapy. A larger study is required to assess the effects of the combination therapy on major clinical outcomes. (Circ J 2004; 68: 361 - 366)

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Background Connective tissue disease, which is an inflammatory condition represented by C-reactive protein (CRP), is a risk factor for ischemic heart disease. The aim of the present study was to examine if there is a relationship between connective tissue disease and coronary spastic angina, and whether the inflammatory condition was associated with ischemic heart disease, even in patients with connective tissue disease. Methods and Results The study group comprised 73 consecutive patients with connective tissue disease who were admitted to the Department of Cardiovascular Medicine between April 2000 and March 2003. Of the 73 patients, 38 (19 men, 19 women) were diagnosed as having an ischemic heart disease (7 patients acute coronary syndrome, 19 patients coronary spastic angina, 12 patients stable exertional angina). In the present study, 19 (50.0%) of the 38 patients of ischemic heart disease were diagnosed as having coronary spastic angina. In the same study period, 151 (38.7%) of 390 patients with ischemic heart disease (without connective tissue disease) were diagnosed as having coronary spastic angina. The frequency of the patients with coronary spastic angina tended to be higher in patients with connective tissue disease than in patients without connective tissue disease. Among the study patients, serum CRP concentrations (mg/dl) were higher in patients with acute coronary syndrome (1.50±1.19, n=7) and those with coronary spastic angina (1.06±1.78, n=19) than in those with non-ischemia (0.35±0.40, n=35, p<0.05). Conclusions Coronary spastic angina is a frequent complication in patients with connective tissue disease and the inflammatory condition is associated with coronary spastic angina and unstable angina in patients with connective tissue disease. (Circ J 2004; 68: 367 - 370)

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Background Animal models are indispensable in order to investigate the mechanism of various diseases and to explore the counter measures for those disease states. Although there are several animal models of ischemic heart diseases, surgical interventions required to create myocardial ischemia sometimes give rise to a problem in the yield of model. This study describes a new technique for inducing myocardial ischemia in rats. Methods and Results A 0.014-inch guidewire was introduced via the carotid artery and selectively advanced into the coronary arteries under fluoroscopy. Transmural myocardial ischemia was confirmed by ST-segment elevation and by the appearance of left ventricular wall motion abnormalities on the echocardiogram. Reversibility of the wire-induced myocardial ischemia was demonstrated by complete resolution of both ST-segment elevation and wall motion abnormalities after removing the wire. Conclusion Wire-induced myocardial ischemia was reproducible and is less invasive than conventional ischemic models in rats. This method is a powerful and useful tool for the investigation of ischemic heart disease in small animals. (Circ J 2004; 68: 371 - 375)

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Background Because the effects of an aldosterone receptor antagonist on transcriptional factors and mRNA expression have not been fully examined in myocardial infarction (MI), the present study examined the effects of spironolactone (SPIRO) and candesartan cilexitil (CAN) on activation of activator protein-1 (AP-1), nuclear factor-κB (NF-κB) and mRNA expression in the non-ischemic myocardium after MI. Methods and Results MI was induced by ligation of the coronary artery in Wistar rats, which were separated into (1) vehicle-treated group, (2) CAN-treated group (10 mg/kg per day), (3) SPIRO-treated group (100 mg/kg per day) and (4) CAN + SPIRO-treated group. The activity of both AP-1 and NF-κB was significantly increased at 4 weeks after MI. CAN or SPIRO significantly prevented the cardiac remodeling and activity of AP-1 and NF-κB. Furthermore, CAN + SPIRO prevented the cardiac remodeling and activation of AP-1 and NF-κB, compared with CAN or SPIRO alone. Myocardial atrial natriuretic peptide, brain natriuretic peptide, collagen I and III mRNAs were enhanced by MI, and CAN or SPIRO alone significantly reduced the mRNAs. CAN + SPIRO significantly prevented these mRNAs, compared with CAN or SPIRO alone. Conclusions Both aldosterone and angiotensin II are involved in the myocardial transcriptional activation of AP-1, NF-κB and the cardiac remodeling-related mRNAs. The combination of CAN and SPIRO may be a potent therapeutic strategy for preventing cardiac remodeling after MI. (Circ J 2004; 68: 376 - 382)

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Ventricular assist devices (VADs) have been used as a bridge to cardiac transplantation in patients with end-stage congestive heart failure. Despite adequate anticoagulation, thromboembolism is a major complication and in particular, a left ventricular (LV) thrombus associated with VADs has been reported as an important cause of thromboembolic complications. The frequency of LV thrombus formation in the patients with VAD support using LV apical cannulation is reported to be low. A 61-year-old woman supported with VAD with LV apical cannulation had a mobile LV thrombus adjacent to the inflow cannula diagnosed by transesophageal echocardiography. (Circ J 2004; 68: 383 - 384)

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A 44-year-old man was referred to hospital for the evaluation of atypical chest pain. His chest X-ray showed leftward displacement of the heart. During echocardiography, the apical window displaced laterally in the usual left lateral position and characteristic motions of the interventricular septum and left ventricular posterior wall were recognized with postural alterations. We presumed a complete absence of the left pericardium. Magnetic resonance imaging (MRI), however, demonstrated a partial left-sided pericardium. The diagnosis was corrected to partial absence of the left pericardium and we have carefully followed up this case without surgical prophylactic intervention. It is very important to differentiate partial from complete absence of the pericardium, because only in patients with partial absence of the pericardium is there a risk of fatal myocardial strangulation. The features of the chest X-ray and echocardiography of this case, which strongly suggested complete absence of the left pericardium, are possibly not always reliable signs. In cases with these abnormal imaging features, MRI may provide additional useful information, as in this case. (Circ J 2004; 68: 385 - 388)

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Percutaneous coronary intervention (PCI) was performed for chronic total occlusion of the proximal right coronary artery in a 70-year-old male with unstable angina. The forceful manipulation of the guide catheter led to an aortocoronary dissection involving the right Valsalva sinus and the ascending aorta. Intracoronary ultrasound (ICUS) showed the important characteristics of the dissection, enabling successful coronary stenting under ICUS guidance. (Circ J 2004; 68: 389 - 391)

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Pulmonary artery obstruction is a rare complication of acute thoracic aortic dissection. A 74-year-old woman was admitted to hospital with respiratory distress. Computed tomography scan showed right pulmonary artery occlusion and a thoracic aortic dissection of the Stanford A type. Lung perfusion scan revealed a defect in the entire right lung field. These findings mimicked acute pulmonary thromboembolism accompanying aortic dissection. On the other hand, pulmonary angiography revealed a round smooth defect of the right pulmonary artery, indicating an extrinsic compression. The patient finally died of cardiac tamponade. Autopsy disclosed that the right pulmonary artery was compressed by a hematoma in the adventitial space around the pulmonary artery. Such a mechanism of pulmonary artery obstruction caused by acute aortic dissection is unique, and is distinct from that caused by chronic non-dissecting aortic aneurysms, which themselves compress the pulmonary arteries. This complication inevitably follows aortic rupture; therefore, emergency operation to repair the dissected aorta must be performed to avoid the following catastrophic event. (Circ J 2004; 68: 392 - 395)

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The expression of TWEAK (TNFSF12) and TweakR/Fn14 was detected in regions rich in macrophage/foam cells in atherosclerotic plaques. The role of TWEAK in monocytes in relation to atherogenesis was investigated by analyzing the cellular events induced by TWEAK in a human macrophage-like cell line, THP-1. TWEAK induced various molecular mediators of atherogenesis, such as IL-6, MCP-1, IL-8 and MMP-9, and the induction was augmented by interferon-γ. TWEAK-induced activation of MMP-9 was mediated by activation of NF-κB. These results suggest that TWEAK is involved in atherosclerosis by inducing pro-inflammatory cytokines and extracellular matrix degrading enzymes, which reduce plaque stability. (Circ J 2004; 68: 396 - 399)

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