Persistent left superior vena cava is rare but important congenital vascular anomaly. It results when the left superior cardinal vein caudal to the innominate vein fails to regress. It is most commonly observed in isolation but can be associated with other cardiovascular abnormalities including atrial septal defect, bicuspid aortic valve, coarctation of aorta, coronary sinus ostial atresia, and cor triatriatum. The presence of PLSVC can render access to the right side of heart challenging via the left subclavian approach, which is a common site of access utilized when placing pacemakers and Swan-Ganz catheters. Incidental notation of a dilated coronary sinus on echocardiography should raise the suspicion of PLSVC. The diagnosis should be confirmed by saline contrast echocardiography.

The epithelial-mesenchymal transition (EMT) contributes to cancer metastasis. Two ZEB family members, ZEB1 and ZEB2(SIP1), inhibit transcription of the E-cadherin gene and induce EMT in vitro. However, their relevance to human cancer is insufficiently studied. Here, we performed a comparative study of SIP1 and ZEB1 proteins in cancer cell lines and in one form of human malignancy, carcinoma of the bladder. Whereas ZEB1 protein was expressed in all E-cadherin-negative carcinoma cell lines, being in part responsible for the high motility of bladder cancer cells, SIP1 was hardly ever detectable in carcinoma cells in culture. However, SIP1 represented an independent factor of poor prognosis (P ‫؍‬ 0.005) in a series of bladder cancer specimens obtained from patients treated with radiotherapy. In contrast, ZEB1 was rarely expressed in tumor tissues; and E-cadherin status did not correlate with the patients' survival. SIP1 protected cells from UV-and cisplatin-induced apoptosis in vitro but had no effect on the level of DNA damage. The anti-apoptotic effect of SIP1 was independent of either cell cycle arrest or loss of cell-cell adhesion and was associated with reduced phosphorylation of ATM/ATR targets in UV-treated cells. The prognostic value of SIP1 and its role in DNA damage response establish a link between genetic instability and metastasis and suggest a potential importance for this protein as a therapeutic target. In addition, we conclude that the nature of an EMT pathway rather than the deregulation of E-cadherin per se is critical for the progression of the disease and patients' survival. E pithelial mesenchymal transition (EMT) is a genetic program controlling cell migration during embryonic development and in wound healing (1, 2). Aberrant activation of EMT programs occurs in cells of epithelial tumors and contributes to the formation of cancer stem cells and metastasis (1-4). EMT is characterized by the loss of epithelial and the acquisition of mesenchymal features. EMT programs are controlled by several master regulators including TWIST, SNAIL (SNAI1 and SNAI2), and ZEB (ZEB1/␦EF1/TCF8 and SIP1/ZEB2) protein family members. These proteins act downstream in EMTinducing signal transduction pathways activated by growth factors, integrin engagement and hypoxia (1-3). Their expression is tightly regulated at the posttranscriptional level. Recent reports highlighted the importance of miR-200 microRNA family in the regulation of ZEB1 and SIP1 protein expression (5). ZEB proteins bind proximal E-boxes within the E-cadherin gene (cdh1) promoter and repress transcription by recruiting corepressor complexes (6). Likewise, they directly repress numerous genes encoding components of the epithelial junctional complex and cell polarity factors (7,8). The relevance of ZEB proteins to tumor progression has been studied in several forms of human cancer. Expression of ZEB1 correlated with the aggressive phenotype in various histological types of endometrial carcinoma and was detected in sarcomatous compartment of endometri...

Atrial fibrillation (AF) is more common in those with obstructive sleep apnea (OSA) than in unaffected individuals and recurs more frequently in the presence of severe OSA after electrical cardioversion and AF ablation. However, it is unknown whether severity of OSA influences the efficacy of anti-arrhythmic drug (AAD) therapy in patients with OSA and AF. This study examined the impact of OSA severity on treatment of symptomatic AF with AADs. We studied 61 patients (62 ± 15 years; 21 women) treated with AADs for symptomatic AF who had overnight polysomnography. Rhythm control was prospectively defined as successful if a patient remained on the same AAD therapy for a minimum of 6 months with ≥75% reduction in symptomatic AF burden. Twenty-four patients (40%) had severe OSA. Thirty patients (49%) were rhythm controlled with AADs. Non-responders to AADs were more likely to have severe OSA than milder disease (52% vs 23%; p < 0.05); those with severe OSA were less likely to respond to AADs than participants with non-severe OSA (39% vs 70%; p = 0.02). Non-responders had higher apnea-hypopnea indices than responders (34 ± 25 vs 22 ± 18 events/hour; p = 0.05), but there were no differences between these groups in minimum oxygen saturation or % time spent in REM sleep. In conclusion, patients with severe OSA are less likely to respond to AAD therapy for AF than those with milder forms of OSA.

Background Common single nucleotide polymorphisms (SNPs) at chromosomes 4q25 (rs2200733, rs10033464 near PITX2), 1q21 (rs13376333 in KCNN3), and 16q22 (rs7193343 in ZFHX3) have consistently been associated with the risk of atrial fibrillation (AF). Single-center studies have shown that 4q25 risk alleles predict recurrence of AF after catheter ablation of AF. Here, we performed a meta-analysis to test the hypothesis that these 4 AF susceptibility SNPs modulate response to AF ablation. Methods and Results Patients underwent de novo AF ablation between 2008 and 2012 at Vanderbilt University, the Heart Center Leipzig, and Massachusetts General Hospital. The primary outcome was 12-month recurrence, defined as an episode of AF, atrial flutter, or atrial tachycardia lasting >30 seconds after a 3-month blanking period. Multivariable analysis of the individual cohorts using a Cox proportional hazards model was performed. Summary statistics from the 3 centers were analyzed using fixed effects meta-analysis. A total of 991 patients were included (Vanderbilt University, 245; Heart Center Leipzig, 659; and Massachusetts General Hospital, 87). The overall single procedure 12-month recurrence rate was 42%. The overall risk allele frequency for these SNPs ranged from 12% to 35%. Using a dominant genetic model, the 4q25 SNP, rs2200733, predicted a 1.4-fold increased risk of recurrence (adjusted hazard ratio, 1.3 [95% confidence intervals, 1.1–1.6]; P=0.011). The remaining SNPs, rs10033464 (4q25), rs13376333 (1q21), and rs7193343 (16q22) were not significantly associated with recurrence. Conclusions Among the 3 genetic loci most strongly associated with AF, the chromosome 4q25 SNP rs2200733 is significantly associated with recurrence of atrial arrhythmias after catheter ablation for AF.

Coronary artery fistula (CAF) is an anomalous connection between a coronary artery and a major vessel or cardiac chamber. Most of the coronary fistulas are discovered incidentally during angiographic evaluation for coronary vascular disorder. The management of CAF is complicated and recommendations are based on anecdotal cases or very small retrospective series. We present three cases of CAF, two of which were symptomatic due to hemodynamically significant coronary steal phenomenon. They underwent successful transcatheter coil embolization, leading to resolution of their symptoms. Percutaneous closure offers a safe and effective way for the management of symptomatic patients. CAFs are rare cardiac anomalies but can give rise to a variety of symptoms because of their hemodynamic consequences or complications. They should be part of cardiac differential diagnosis particularly in patients without other risk factors. Correction of CAF is indicated if the patients are symptomatic or if other secondary complications develop.

Context:The prevalence of psychiatric illness in correctional settings is significantly elevated, with higher than community rates reported for most mental disorders.Aims:(1) To examine the socio-demographic profile of convicted prisoners. (2) To evaluate the prevalence of psychiatric disorders in convicted prisoners.Materials and Methods:500 convicts were assessed for psychiatric morbidity with the help of (a) Socio-demographic proforma, (b) Pareek Udai and Trivedi G's socio-economic status scale (rural) (household schedule), (c) Kuppuswamy's economic status scale (urban) and (d) Present State Examination (PSE).Results:23.8% of the convicted prisoners were suffering from psychiatric illness excluding substance abuse. 56.4% of the prisoners had history of substance abuse / dependence prior to incarceration.Conclusions:The results suggest that a substantial burden of psychiatric morbidity exists in the prison population of India and the burden of psychiatric illness in this vulnerable and marginalized population poses a serious challenge to psychiatrists.

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Background-The mechanisms of atrial fibrillation (AF) induced by obstructive sleep apnea (OSA) are not completely understood. This study investigated the roles of the intrinsic and extrinsic cardiac autonomic nervous system in OSA-induced AF and provided noninvasive autonomic nervous modulation for the suppression of OSA-induced AF by using low-level transcutaneous electrical stimulation (LL-TS) of the auricular branch of the vagus nerve at the tragus.