Epicardial Mapping: Ventricular Epicardial Activation is Unaffected by Heart Position

Epicardial ventricular mapping was performed in five dogs during sinus rhythm with a sock array containing 41 bipolar electrodes. Maps were generated with a computer-assisted mapping system when the heart was in situ and when the heart was lifted by 44 degrees out of the chest. Times of earliest and latest epicardial activation in these two states did not differ. Despite a different frontal plane QRS axis, location of earliest activation was not affected by lifting the heart. In two of the five animals, the site of latest epicardial activation was minimally different from the heart in situ, but the general pattern of epicardial activation was unchanged. Therefore, the change in frontal plane QRS axis with lifting the heart was due to a change in heart position rather than a general change of heart activation.     

Prevalence of cytomegalovirus antibody in hemophiliacs and homosexuals infected with human immunodeficiency virus type 1

We determined the prevalence of antibody to cytomegalovirus (CMV) in the sera of non-homosexual hemophilia patients and homosexual men infected with the human immunodeficiency virus type 1 (HIV-1). CMV antibody testing by latex agglutination revealed 33 of 58 HIV-1 infected hemophiliacs (57%) were antibody-positive compared with 54 of 54 HIV-1 infected asymptomatic non-hemophiliac homosexuals (100%) (p less than .001). Nine of 15 hemophiliacs (60%) with symptomatic HIV-1 infection were CMV antibody-positive. We also tested 22 HIV-1 antibody-negative hemophiliacs who had received non-heat treated factor concentrates. 14 of these 22 (64%) were CMV antibody-positive compared with 57% of HIV-1 antibody-positive hemophiliacs. We conclude 1) there is little correlation between transmission of HIV-1 and CMV by factor concentrates, 2) the presence of CMV antibody does not appear to be associated with clinical stage of HIV-1 infection in hemophiliacs, and 3) there may be a significant number of CMV antibody-negative hemophiliacs with HIV-1 infection at risk for primary infection and subsequent disease if CMV seronegative blood products are not provided for future transfusions.     

藻酸钠复合自体软骨细胞修复猪关节软骨缺损的近期效果

目的:采用藻酸钠自体软骨细胞混合物修复猪的关节软骨缺损,观察近期成骨效应。方法:实验于2004-03/2005-04在中山大学附属第二医院实验中心完成。3个月龄的小型猪8只,取其关节软骨进行细胞原代培养,获取原代细胞后,分别进行免疫组织化学法检测细胞Ⅱ型胶原表达。然后对8只小型猪的32个关节进行动物关节缺损的模型建立,每个关节共造3个人工缺损,选择关节左右随机对照。将已经培养好的软骨细胞与已经配制好并消毒的藻酸钠混合,移植到猪的关节软骨缺损处。每只猪关节内注射3个实验点,1个用藻酸钠/细胞混合液为实验组,1个单纯支架材料为单纯材料对照组,1个缺损做空白对照组,模型中缺损区均为关节负重区,胶原纤维绿色(亮绿复染)。修复所用细胞为自体软骨体外培养后,进行移植修复,采用3代体外培养软骨细胞,均匀混和藻酸钠后,行自体移植。8周后取实验关节进行大体观察、苏木精-伊红染色、Masson染色、免疫组织化学法染色观察及O’driscoll组织学评分。结果:纳入小型猪8只,除其中1例因手术切断伸直肌腱而使猪关节活动障碍,其余均未见手术后关节活动障碍,所有手术无术后感染,无关节内感染,无动物死亡。移植的软骨细胞在藻酸钠载体中生长良好,形成透明软骨。根据O’driscoll组织学评分标准,实验组32个猪关节缺损修复的组织学评分为(20.25±1.64)分,高于单纯材料对照组的(7.46±1.29)分及空白对照组的(6.00±2.09)分。免疫组织化学染色可见修复软骨以表达Ⅱ型胶原为主,无Ⅰ型胶原。结论:藻酸钠复合自体软骨细胞作为软骨移植的替代物是可行的,远期效果还有待进一步研究。     

Bradycardia and Syncope in Children Not Controlled by Pacing: Beta-Adrenergic Hypersensitivity

Cardiac pacing is frequently employed in the therapy of children with syncope and documented bradycardia. This report describes two children, ages 7 and 9 years, who underwent placement of demand ventricular pacing systems for documented bradycardia and syncope. Cardiac catheterization and intracardiac electrophysiological studies failed to show evidence of structural abnormalities, sinus node or conduction system disease, inducible arrhythmias, or VA conduction in each patient. Both patients had persistent symptoms after pacemaker implantation. Autonomic function testing with continuous heart rate and blood pressure monitoring revealed exaggerated beta-adrenergic responses to simple standing and small doses of isoproterenol. Symptoms were completely eliminated with atenolol. In these two children, cardiac pacing alone was not adequate for relief of symptoms. Autonomic mechanisms of bradycardia and hypotension should be considered prior to implantation of permanent pacing systems in children.     

A study of the SCN5A gene in a cohort of 76 patients with Brugada syndrome

We aim to study the SCN5A gene in a cohort of Brugada syndrome (BS) patients and evaluate the genotype–phenotype correlation. BS is caused by mutations in up to 10 different genes, SCN5A being the most frequently involved. Large genomic rearrangements in SCN5A have been associated with conduction disease, but its prevalence in BS is unknown. Seventy‐six non‐related patients with BS were studied. Clinical characteristics and family risk profile were recorded. Direct sequencing and multiplex ligation‐dependent probe amplification (MLPA) of the SCN5A gene for identification of mutations and larger rearrangements were performed, respectively. Eight patients (10.5%) had point mutations (R27H, E901K, G1743R (detected in three families), V728I, N1443S and E1152X). Patients with mutations had a trend toward a higher proportion of spontaneous type I Brugada electrocardiogram (ECG) (87.5% vs 52.9%, p = 0.06) and had evidence of familial disease (62.5%, vs 23.5%, p = 0.03). The symptoms and risk profile of the carriers were not different from wild‐type probands. There were non‐significant differences in the prevalence of type I ECG, syncope and history of arrhythmia in carriers of selected polymorphisms. None of the patients had any deletion/duplication in the SCN5A gene. In conclusion, 10.5% of our patients had mutations in the SCN5A gene. Patients with mutations seemed to have more spontaneous type I ECG, but no differences in syncope or arrhythmic events compared with patients without mutations. Larger studies are needed to evaluate the role of polymorphisms in the SCN5A in the expression of the phenotype and prognosis. Large rearrangements were not identified in the SCN5A gene using the MLPA technique.