aVR sign as a risk factor for life-threatening arrhythmic events in patients with Brugada syndrome

BACKGROUND: Risk stratification in Brugada syndrome (BS) is controversial, especially in asymptomatic individuals. OBJECTIVE: The aim of this study was to evaluate the significance of lead aVR in patients with BS. METHODS: Twenty-four patients with the electrocardiogram pattern of BS (24 male, mean age 32.1 +/- 13.6 years) and 24 healthy age- and gender-matched controls were studied. RESULTS: Thirteen patients were symptomatic. The R-wave amplitude or R/q ratio in lead aVR was significantly greater in patients experiencing a recurrence compared with those who did not. The aVR sign was defined as R wave >/= 0.3 mV or R/q >/= 0.75 in lead aVR. Most of the recurrences (78%) were in patients with present aVR sign; 84% of BS patients with present aVR sign had events during follow-up. In contrast, only 27% of BS patients with absent aVR sign had events during follow-up. CONCLUSION: Our study shows significant correlation between a prominent R wave in lead aVR (aVR sign) and risk for development of arrhythmic events in BS. In the presence of BS, prominent R wave in lead aVR may reflect more right ventricular conduction delay and subsequently more electrical heterogeneity, which in turn is responsible for a higher risk of arrhythmia.     

Novel pyrrolidines in the venom of the ant Monomorium indicum

New 2,5-dialkylpyrrolidines found in the venom of Monomorium indicum include trans-2-butyl-5-(4-pentenyl)pyrrolidine [1], trans-2-butyl-5-(6-heptenyl)pyrrolidine [4], trans-5-(5-hexenyl)-2-(4-pentenyl)pyrrolidine [6], trans-5-(6-heptenyl)-2-(5-hexenyl)pyrrolidine [8], and trans-5-heptyl-2-hexylpyrrolidine [16], whose structures were confirmed by synthesis. The concomitance of five previously reported trans-2,5-dialkyl-pyrrolidines along with small amounts of the cis isomers and N-methyl analogues makes the venom of M. indicum the most qualitatively diverse blend of alkaloids reported from an ant to date. The toxicities to termites of four of these alkaloids were determined.     

Expression of alpha-defensin-1 in chronic hyperplastic candidosis

BACKGROUND: Chronic hyperplastic candidosis (CHC) represents a chronic opportunistic candida infection. We clarified the presence, localization and participation of alpha-defensin-1 in host response against chronic candidal stimulus. METHODS: Immunohistochemically stained CHC biopsies (n = 10) were compared to candida negative idiopathic leukoplakia (n = 10). RESULTS: In CHC alpha-defensin-1 was detected in neutrophils intravascularly, in lamina propria and in the epithelium, in part in intraepithelial microabscesses. Staining intensity of individual neutrophils varied and was associated with peri- and extracellular staining, in particular in the superficial epithelial cell layers. In controls only very few homogeneously staining neutrophils were detected intravascularly without any extracellular alpha-defensin-1 deposition. CONCLUSIONS: Neutrophils form microabscesses and respond to Candida by activation and release of alpha-defensin-1 to peri- and extracellular matrix. This together with the epithelial cell migration from the basal layer to epithelial surface leads to alpha-defensin-1 rich protective shield in the most superficial epithelial cell layers.     

Further evidence of dopamine transporter dysregulation in ADHD: a controlled PET imaging study using altropane.

BACKGROUND: The dopamine transporter (DAT) is known to be a key regulator of dopamine, and recent studies of genetics, treatment, and imaging have highlighted the role of DAT in attention-deficit/hyperactivity disorder (ADHD). The findings of in vivo neuroimaging of DAT in ADHD have been somewhat discrepant, however. METHOD: Dopamine transporter binding was measured using a highly selective ligand (C-11 altropane) and positron emission tomography (PET). The sample consisted of 47 well-characterized, treatment-na?ve, nonsmoking, non-comorbid adults with and without ADHD. Additionally, control subjects had few symptoms of ADHD. RESULTS: Results showed significantly increased DAT binding in the right caudate in adults with ADHD compared with matched control subjects without this disorder. CONCLUSIONS: These results confirm abnormal DAT binding in the striatum of adults with ADHD and provide further support that dysregulation of DAT may be an important component of the pathophysiology of ADHD.     

Fontan completion without surgery.

OBJECTIVE: There are several modifications introduced in the preparation for a subsequent non-surgical transcatheter completion of the Fontan procedure. We report our experience with one type of the modification and the short-term results following its implementation. METHODS: During bidirectional cavopulmonary connection (BCPC) an intra-atrial lateral tunnel is additionally created, as intended for a Fontan procedure but fenestrated with a 10-14 mm aperture. The cardiac end of the superior vena cava (SVC) is then patched to maintain the physiology of BCPC. During the interventional transcatheter completion procedure, the SVC patch is perforated using radio-frequency (RF) energy, balloon-dilated, and stented as well. The aperture is closed with a device when required. Paired t-test was used to compare data before and after the Fontan completion. RESULTS: From June 2003 to February 2006, 16 patients (9 boys and 7 girls, mean age 12 months) underwent the surgical procedure described. The mean bypass time was 137 min and the mean ischemic time was 77 min. There were no operative deaths. One patient with bilateral SVC required a take down due to recurrent effusions. Ten months later, nine patients underwent completion (mean age 20 months, mean weight 10.6 kg). The stents were dilated to a mean diameter of 14.4mm. All except one aperture was closed with a device. The mean fluoroscopy time was 41 min. Oxygen saturation increased from 85 to 94% (p=0.001). Pulmonary artery pressures remained normal (16 mmHg before and 19 mmHg after, p=0.12). No patients required mechanical ventilation and none developed pleural effusions or arrhythmias. All were discharged from hospital within 6 days of the Fontan completion. Twenty-two months after Fontan, all were well. Echocardiography revealed no gradients across the stents. Two patients had minor leaks across the aperture. One underwent further stent dilatation a year later. CONCLUSIONS: Fontan completion without surgery is suitable in patients with single ventricles with lower mortality and morbidity, avoids multiple surgical interventions while maintaining the staged approach and allows for successive dilatation of the Fontan pathway to accommodate for growth.     

Comparison of survival by allocation to medical therapy, surgery, or heart transplantation for ischemic advanced heart failure.

BACKGROUND: To ascertain survival of ischemic advanced heart failure patients by treatment allocation, we examined the outcome of transplant assessment patients allocated to medical therapy, high-risk conventional surgery, or transplantation. METHODS: Patients were identified from the Papworth transplant database and excluded if primary etiology was not ischemic. Grouping was undertaken according to treatment allocation at initial assessment, and analysis was performed by intention to treat. Survival was computed from the time of assessment and Cox regression used to stratify patients according risk with the Heart Failure Survival Score. RESULTS: From May 1993 to September 2001, a total of 755 patients were admitted for transplant assessment, with 348 (46.1%) identified as having heart failure of ischemic origin. Variables required for calculation of the Heart Failure Survival Score was available in 273 patients (78.4%), and 20 patients (7.3%) were lost to follow-up. Of the remaining 253 patients, 89 (35.2%) were allocated to medical therapy, 32 (12.6%) to surgery, and 132 (52.2%) to transplantation. The relative risk (95% confidence limit) of death compared with medical therapy was 0.62 (0.28, 1.40) for surgery and 0.38 (0.24, 0.61) for transplantation in medium- to high-risk patients. For low-risk patients, the relative risks for death compared with medical therapy were 1.87 (0.63, 5.60) for surgery and 1.97 (0.79, 4.96) for transplantation. CONCLUSIONS: Transplantation improved survival of medium- and high-risk patients compared with medical therapy. In the low-risk group, this was not evident. However, repeated assessment of risk is required because the hazard for death rises steadily after the third year in these patients.     

Xanthogranulomatous orchitis: Review of the published work and report of one case

Xanthogranulomatous orchitis is an extremely rare inflammatory non-neoplastic destructive lesion of the testis. We report a 44-year-old man who presented with right scrotal swelling and two discharging sinuses. Testicular tumor markers were normal. Scrotal ultrasound showed heterogeneous testicular areas and irregular margin of the tunica. Surgical exploration revealed infected, unhealthy testicular tissue with necrosis and tumor-like lesion. Orchidectomy was done and histopathology showed xanthogranulomatous orchitis.     

NOS1 polymorphism is associated with atopy but not exhaled nitric oxide levels in healthy children

Exhaled nitric oxide (FE_NO) is raised in atopy. The mechanism for this is unclear. The aim of this study was to investigate whether the number of AAT repeats in intron 20 of the NOS1 gene, recently associated with variations in FE_NO in adults with asthma and cystic fibrosis, was associated with the raised FE_NO in healthy atopic children. Eighty-seven healthy children (44 girls, 42 atopic, age range 6–18 years) underwent measurements of FE_NO, spirometry, airway responsiveness and skin prick testing. Genotyping was carried out to determine the number of AAT repeats. There was no association between the number of AAT repeats and FE_NO in either the whole sample of healthy children (n = 87) or in the subsample of healthy atopics (n = 42). However, a greater number of atopic children had two high repeat alleles compared with non-atopic children (33.3% vs. 13.6%, respectively, p = 0.03). This suggests that variations in the NOS1 gene may contribute to atopy without this relationship being reflected by FE_NO.