No abstract

n 1992, Brugada et al described 8 cases of aborted sudden death in patients without demonstrable structural heart disease, but with a peculiar electrocardiogram (ECG) pattern consisting of right bundle-branch block (RBBB) and ST-segment elevation in leads V1 to V3. 1 Three of 8 patients in this report were children, and familial occurrence was recognized. Since then, a few case reports have been published on this syndrome in young populations. [2][3][4] Brugada syndrome may cause sudden death in children, even in the first few months of life where it may be misdiagnosed as sudden infant death syndrome. The Brugada-type ECG is not rare in the adult Japanese population (0.14 to 0.70%). [5][6][7] However, the prevalence of this type of ECG in schoolchildren remains unclear. We evaluated the prevalence of Brugada-type ECG, incomplete RBBB (IRBBB) and complete RBBB (CRBBB) in Japanese schoolchildren stratified according to age. Circulation Journal Vol.68, April 2004 Methods ECG DefinitionsAll ECGs were recorded at standard gain (1 mV/10 mm) and paper speed (25 mm/s). An ECG was considered to be Brugada-type when the 12-lead ECG fully met the criteria for the Brugada syndrome as recently published in a consensus report. 8 To compare the prevalence with previous reports of healthy populations, we defined "Brugada-like" ECG as follows. The 12-lead ECG showed RBBB (rsR' or Rsr' pattern in V1 lead) and ST-segment elevation in the right precordial leads. The ST-segment elevation was defined as an elevation of the J point of ≥0.1 mV in leads V1 through V3. According to the configuration, ST-segment elevations were designated as either coved or saddle-back.Complete RBBB was defined as a QRS duration ≥0.12 s, with an RsR' configuration and IRBBB was defined as a QRS duration <0.12 s, with an rSr' configuration in the right precordial leads.The ECG records of all study subjects were reviewed by Yamakawa, without any information about the subjects including age, sex, or family history of sudden death. Ishikawa and Sumita reviewed those records on which judgments had been made, and they concurred with the judgments. Study SubjectsThe study population consisted of 20,387 young 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). ConclusionThe pre...

Objective-Low-density lipoprotein (LDL) apheresis is a potential therapy for conventional therapy-resistant peripheral artery disease. In the present study, we examined the chronic effects of LDL apheresis on clinical parameters in vivo and endothelial cell functions in vitro in hemodialysis patients who had the complication of peripheral artery disease. Methods and Results-Twenty-five patients were enrolled, and the responses of 19 patients to LDL apheresis were analyzed. Patients were classified into 2 groups according to change in ankle-brachial pressure index (ABI) after treatment: patients with improved ABI (responders, nϭ10) and patients with worsened ABI (nonresponders, nϭ9). In the responders, apheresis resulted in a long-term reduction of circulating levels of oxidized LDL, C-reactive protein, and fibrinogen. In human umbilical vein endothelial cells (HUVECs), the serum from the responders increased expression of activated endothelial nitric oxide synthase protein and proliferative activity. Key Words: atherosclerosis Ⅲ endothelium Ⅲ nitric oxide synthase Ⅲ oxidized lipids Ⅲ peripheral arterial disease Ⅲ lipoproteins Ⅲ oxidative stress C ardiovascular disease is the primary cause of death in patients with end-stage renal disease. Patients on dialysis are reported to have a 10 -20-fold greater risk of cardiovascular disease-associated mortality than the general population after stratification for age, gender, race, and the presence or absence of diabetes. Patients undergoing dialysis have many of the risk factors for atherosclerosis, such as hypertension, dyslipidemia, and disturbed calcium-phosphate metabolism, and, indeed, they commonly experience severe atherosclerosis, including peripheral artery disease (PAD). Low-density lipoprotein (LDL) apheresis is a potentially useful treatment for conventional therapy-resistant hypercholesterolemic patients with coronary artery disease and PAD. 1,2 Previously, it was shown that a single LDL apheresis session enhanced the peripheral microcirculation, probably by increasing the production of nitric oxide (NO) and bradykinin, 3 reducing blood viscosity and adhesion molecules, 4 and inducing endothelium-dependent vasodilatation. 5 However, the precise molecular mechanism of the long-term effects of LDL apheresis on the improvement of the peripheral circulation remains unclear and warrants further investigation.We undertook the present study to investigate the shortand long-term effects of LDL apheresis on clinical and laboratory parameters in vivo and vascular endothelial cell function in vitro, in hemodialysis patients with PAD, and to identify factors related to the improvement of the peripheral circulation by LDL apheresis. Methods Patients and Study DesignThe study protocol was approved by the Human Ethics Committee of Yokohama City University Hospital. A total of 25 consecutive hemodialysis patients with leg impairments and ankle-

A 40-year-old man was referred to our hospital because of an abnormal shadow on the left cardiac border on the chest roentgenogram at the regular medical health examination without any symptoms. A giant coronary artery aneurysm of left anterior descending artery with a maximum diameter of approximately 50 mm was detected with computed tomography and coronary angiography. The patient was treated and followed up medically. Four years later, the size of the coronary artery aneurysm became larger. Then resection of the coronary artery aneurysm and coronary artery bypass grafting were successfully performed. Coronary artery aneurysms are rare in adults and are usually found in association with Kawasaki disease, coronary atherosclerosis, and so on. We also review the literature of giant coronary artery aneurysms exceeding 50 mm in diameter.

To investigate the relation between the angiotensin-converting enzyme (ACE) gene polymorphism and acute coronary syndromes with respect to environmental factors, we analyzed the association of genotype with the coronary angiographic findings of patients with acute myocardial infarction or unstable angina pectoris, and we examined the linkage of each genotype with established risk factors for coronary artery disease. We determined the ACE genotype in 152 Japanese patients with acute coronary syndromes and 399 healthy individuals. The genotype distributions were not different between the two groups ( P =.74, χ 2 test). In the former group, coronary angiograms were evaluated by criteria based on the number of diseased vessels, the number of stenotic lesions (≥50%), and the relative abnormal arterial portion (extent index). Although the number of stenotic lesions was higher in patients with the DD genotype than in those with the ID or II genotype ( P =.006), there were no differences in the number of diseased vessels or the extent index. When only smokers were analyzed, the number of diseased vessels ( P =.032), number of stenotic lesions ( P =.003), and extent index ( P =.019) were all higher in patients with the DD genotype than in those with the ID or II genotype. In contrast, these differences in the respective parameters did not exist in nonsmokers. The results indicate smoking-associated effects of the ACE genotype on the severity of coronary atherosclerosis.