Left atrial diameter in estimating success rates of radio-frequency ablation treating atrial fibrillation.

Background: Ablation devices are being utilized in surgical procedures treating atrial fibrillation. Few studies seek to define a cut-off value for left atrial diameter size beyond which risks of procedure outweigh chance of sinus recovery. This study aims to identify a cut-off value for pre-operative left atrial diameter to assess the efficacy of surgical radio-frequency ablation for treatment of chronic atrial fibrillation in patients undergoing mitral valve surgery. Methods: A prospective 6-month follow-up cohort study was done, in which 40 patients were recruited during the period from May 2016 till April 2018. All patients had rheumatic mitral valve disease and permanent atrial fibrillation. Receiver operator characteristic (ROC) curves were used to calculate the area under the curve and cut-off value for left atrial diameter. The efficacy of the overall survival time was estimated using the Kaplan‐Meier method. Results: Pre-operatively left atrial diameter of 59 mm was significantly associated with decrease in the possibility of reverting to sinus rhythm after surgery (OR 0.292, p-value = 0.001). The cut-off value for left atrial diameter was 59mm (sensitivity = 93.3%, specificity = 96.1%). Kaplan-Meier survival estimates were 175.07 days (156.3 - 193.9) for patients with left atrial diameter < 59mm and 62.64 days (26.6-98.7) for patients with left atrial diameter > 59mm. Conclusion: In patients undergoing mitral valve, higher degrees of success are associated with smaller left atrial diameter in terms of conservation of the sinus rhythm post operatively

2. Role of ascorbic acid & statin in reduction of the incidence of the atrial fibrillation in patients under B-blocker and undergoing coronary artery bypass graft operation in early post-operative period

Atrial fibrillation (AF) is the most common sustained arrhythmia that is associated with significant morbidity and mortality. Current available therapies remain inadequate in symptom control and secondary prevention and are often associated with significant side effects. The mechanisms underlying the pathogenesis of AF are poorly understood, although electrophysiological remodeling has been described as an important initiating step. Recently, increasing evidence implicates oxidative stress and inflammation in the pathogenesis of AF. We searched the literature for evidence to support the use of antioxidant vitamins C and anti-inflammatory statin combined with B-blocker in the prevention of AF post CABG. Antioxidant vitamin C, through its reactive-oxygen-species- (ROS-) scavenging effect, have shown a role in AF prevention post CABG. Methods: A prospective controlled randomized study will include(three hundred patients aged from 40 to 65 years of both sexes. They will be divided into three groups of patients: Group I: A hundred (CABG) patients commenced on only B-blocker for at least one week pre-operatively. Group II: A hundred (CABG) patients commenced on B-blocker & ascorbic acid for at least one week pre-operatively. Group III: A hundred (CABG) patients commenced on B-blocker & statin for at least one week pre-operatively. Results: 24 patients out of 100 patients developed atrial fibrillation in 1st group, compared with 6 patients out of 100 patients in 2nd group, and 7 patients out of 100 patients in 3rd group developed atrial fibrillation. Conclusion: Combination of B-blocker with ascorbic acid & statin is better than B-blocker alone in reduction of atrial fibrillation after CABG in early post operative period

Subclinical venous thromboembolism after pulmonary resection for lung cancer: an observational study

Abstract Background Subclinical venous thromboembolism is a hidden pathology which may present with catastrophic consequences if not diagnosed at an early stage. This study was undertaken to estimate the occurrence and associated risk factors of subclinical deep vein thrombosis after lung resection for lung cancer patients. A prospective observational cohort study was performed in a tertiary cardiothoracic surgery center. One hundred fifty patients who underwent different types of lung resection for lung cancer were enrolled. Caprini’s risk score was assessed in all patients. All patients received prophylactic stockings and anticoagulants. On the 5th postoperative day, a duplex venous ultrasound of bilateral lower limbs was performed on every asymptomatic patient. Results Out of 150 patients enrolled in the study, 147 patients completed the study. Four patients (2.72%) developed subclinical deep vein thrombosis. The patients were divided into 2 groups: group 1 (n = 143) post-lung resection and no DVT and group 2 (n = 4) with post-lung resection subclinical DVT. No patient developed postoperative clinical DVT. The incidence was found to be highest in the group of individuals who had a longer stay in the ICU (odds ratio 37.9) (p = 0.04). Among the various pathologies, the incidence was higher in patients who received preoperative chemotherapy (odds ratio 21.9) (p = 0.001). One patient in the subclinical DVT group (25%) died, while no mortality was observed in the no DVT group. Conclusions The incidence of subclinical deep vein thrombosis is low in the postoperative period among patients undergoing lung resection for lung cancer if appropriate prophylactic measures are applied. However, patients receiving preoperative chemotherapy and those with longer periods of immobilization are at a higher risk of developing postoperative DVT despite anticoagulant prophylaxis. Due to the sample size and design limitations, the mentioned risk factors could be associated with DVT not a cause of DVT. It might be justified to screen these high-risk groups to detect subclinical DVT to allow for post-discharge prophylaxis

Sulforaphane Downregulates Hepatic Fibroblast Growth Factor 21 (FGF21) of Diet Induced Obese Mice

Background: Fibroblast growth factor 21 is a hormone-like protein that plays a critical role as an energy regulator. Sulforaphane (SFN) is expected to have potential therapeutic effects in treating obesity. This study aims to investigate the effect of SFN treatment on hepatic gene expression of FGF-21 of diet induced obese mice. Methods: CD1 male mice and two groups of lean and diet induced obesity (DIO) model after feeding a high fat diet were used. Afterward, both lean and DIO mice were treated for four weeks with either SFN (5mg/kg BW) (n=10) or Vehicle (n=10). After that, blood and liver samples were collected and analyzed. Hepatic FGF-21 gene expression was measured using qRT-PCR. Results: Treatment of DIO mice with SFN causes a significant reduction in body weight gain (15.42%) compared to DIO-vehicle group, which showed a weight gain by (3.86%), p-value<0.0001. In addition, SFN treatment to lean group did not affect body weight. DIO-SFN treated mice showed a significant reduction in fasting glucose, leptin, and insulin levels compared to DIO-vehicle treated group, p-value<0.05. Hepatic FGF-21 gene expression was significantly upregulated in DIO-vehicle compared to lean-vehicle mice with ˜ 3 folds, p-value<0.05. Treatment of DIO with SFN causes a significant downregulation of FGF-21 gene expression by ˜9 folds compared with DIO-vehicle treated group, p-value<0.05. Conclusions: Treatment of DIO mice with SFN causes downregulation of hepatic FGF21 expression in obese mice. The effects of SFN on FGF21 gene expression could be a direct effect or secondary to weight loss, which warrants further studies.QNRF, NPRP 9 -351-3-07

Sulforaphane reduces obesity by reversing leptin resistance.

The ascending prevalence of obesity in recent decades is commonly associated with soaring morbidity and mortality rates, resulting in increased health-care costs and decreased quality of life. A systemic state of stress characterized by low-grade inflammation and pathological formation of reactive oxygen species (ROS) usually manifests in obesity. The transcription factor nuclear factor erythroid-derived 2-like 2 (NRF2) is the master regulator of the redox homeostasis and plays a critical role in the resolution of inflammation. Here, we show that the natural isothiocyanate and potent NRF2 activator sulforaphane reverses diet-induced obesity through a predominantly, but not exclusively, NRF2-dependent mechanism that requires a functional leptin receptor signaling and hyperleptinemia. Sulforaphane does not reduce the body weight or food intake of lean mice but induces an anorectic response when coadministered with exogenous leptin. Leptin-deficient mice and leptin receptor mutant mice display resistance to the weight-reducing effect of sulforaphane, supporting the conclusion that the antiobesity effect of sulforaphane requires functional leptin receptor signaling. Furthermore, our results suggest the skeletal muscle as the most notable site of action of sulforaphane whose peripheral NRF2 action signals to alleviate leptin resistance. Transcriptional profiling of six major metabolically relevant tissues highlights that sulforaphane suppresses fatty acid synthesis while promoting ribosome biogenesis, reducing ROS accumulation, and resolving inflammation, therefore representing a unique transcriptional program that leads to protection from obesity. Our findings argue for clinical evaluation of sulforaphane for weight loss and obesity-associated metabolic disorders.Qatar National Research Fund (NPRP9-351-3-075