Search

Background Unstable functional reentrant circuits known as rotors have been consistently observed in atrial fibrillation and are mechanistically believed critical to the maintenance of the arrhythmia. Recently, using a Poisson renewal theory‐based quantitative framework, we have demonstrated that rotor formation (λf) and destruction rates (λd) can be measured using in vivo electrophysiologic data. However, the association of λf and λd with clinical, electrical, and structural markers of atrial fibrillation phenotype is unknown. Methods RENEWAL‐AF is a multicenter prospective cross‐sectional study recruiting adult patients with paroxysmal or persistent atrial fibrillation undergoing clinically indicated catheter ablation. Patients will undergo intraprocedural electrophysiologic atrial fibrillation mapping, with λf and λd to be determined from 2‐minute unipolar electrogram recordings acquired before ablation. The primary objective will be to determine the association of λf and λd as markers of fibrillatory dynamics with clinical, electrical, and structural markers of atrial fibrillation clinical phenotype, measured by preablation transthoracic echocardiogram and cardiac magnetic resonance imaging. An exploratory objective is the noninvasive assessment of λf and λd using surface ECG characteristics via a machine learning approach. Results Not applicable. Conclusion This pilot study will provide insight into the correlation between λf/λd with clinical, electrophysiological, and structural markers of atrial fibrillation phenotype and provide a foundation for the development of noninvasive assessment of λf/λd using surface ECG characteristics will help expand the use of λf/λd in clinical practice., Using a Poisson renewal theory‐based quantitative framework, we have recently demonstrated that rotor formation and destruction rates in atrial fibrillation can be objectively quantified using in vino electrophysiological data. RENEWAL‐AF is a pilot prospective cross‐sectional study investigating the association between the rates of rotor formation and destruction with clinical, electrical and structural markers of AF phenotype.

Objectives: This study sought to determine the long-term prognostic value of myocardial deformation imaging by echocardiography in risk stratification of sudden cardiac death (SCD) and malignant ventricular arrhythmias (VAs) in a large consecutive cohort of patients with left ventricular (LV) systolic impairment, irrespective of its etiology. Background: Left ventricular ejection fraction (LVEF) is limited for prediction of SCD. Echocardiographic strain-derived mechanical dispersion (MD) and global longitudinal strain (GLS) has been linked to VA and SCD. However, due to low event rates, the role of these parameters has not been fully elucidated. Methods: Consecutive clinically stable patients who underwent echocardiographic study performed in an outpatient setting from 2008 to 2014 with a Simpson left ventricular ejection fraction (LVEF) ≤45% were included in the study. Strain analysis was performed in which the LV was separated into 16 segments for regional analysis. Mechanical dispersion (MD) was calculated as the SD of the time to peak of each of the 16 regions. Outcome data were obtained from medical records. Results: A total of 939 patients were included in the study, with median LVEF of 37% (interquartile range 30% to 42%). At follow-up (91.4 ± 23.4 months), 96 VA events had occurred. Multivariate analysis demonstrated that only MD ≥75 ms (hazard ratio: 9.45; 95% confidence interval: 4.75 to 18.81; p < 0.0001) was predictive of VA events. Low MD predicted a low event rate, irrespective of LVEF. Conclusions: Using LVEF alone is inferior for prediction of VA and SCD, particularly in patients with moderately reduced LVEF. MD is easily obtained from standard echocardiographic images and can be used to improve risk prognosis, particularly in patients who are currently excluded from cardiac defibrillator insertion based on LVEF. usc Refereed/Peer-reviewed

Pharmacological management of rheumatoid arthritis (RA) includes synthetic and biological disease-modifying antirheumatic drugs (DMARDs). Biological DMARDs, also referred to as “biologics,” rapidly retard progression of the joint damage seen in RA. Rituximab is a well-established biologic for the management of RA with several biosimilar versions available. This document presents the consensus statements on the usage of rituximab for the management of RA developed by a group of 14 experienced rheumatologists from India. This expert panel identified areas of interests, collated and summarized relevant literature, developed, debated and refined and revised the statements which were voted upon at relevant stages. Subsequently, a wider consultative process including voting on the draft statements involved 18 more rheumatologists from across India. The approved final version has 28 consensus statements related to the following seven areas of rituximab therapy in RA, namely, contraindication, pretreatment screening, treatment schedule, evaluation of response, safety, and research agenda for future. It is envisaged that these consensus statements would help in optimizing the usage of rituximab in RA not only in India but also in other countries and benefit all stakeholders.

Atrial fibrillation (AF) is an established independent risk factor for stroke. Current guidelines regard AF as binary; either present or absent, with the decision for anti-coagulation driven by clinical variables alone. However, there are increasing data to support a biological gradient of AF burden and stroke risk, both in clinical and non-clinical AF phenotypes. As such, this raises the concept of combining AF burden assessment with a clinical risk score to refine and individualize the assessment of stroke risk in AF—the CHA2DS2VASc-AFBurden score. We review the published data supporting a biological gradient to try and construct a putative schema of risk attributable to AF burden.

Spondyloarthritis (SpA) is a family of systemic inflammatory rheumatic diseases that have been extensively reported and studied from India over the last >4 decades. The epidemiological studies estimate the prevalence of SpA to be 7–9 per 10,000 persons. There are a number of studies describing the clinical features of the different subsets of SpA showing the presence of all the clinical subtypes of SpA. Long-term follow-up studies are also available showing the variable progression of these subtypes. HLA-B27 and its subtypes are reported from India; its frequency in the Indian population is ~6% but >90% in ankylosing spondylitis (AS) with decreasing frequencies in other subtypes of SpA. The association of B*27:05 and B*27:04 with AS and SpA family of diseases has been confirmed in several studies. There have been several publications related to the immunopathogenesis of SpA showing evidence of sensitization to antigen fragments of enterobacteria leading to the perturbations in the innate and acquired immune system causing the diseases. “Slipped disc” and “tuberculosis” are the two most common misdiagnoses made by nonrheumatologists. An important observation was a steady decrease in the male: female ratio from 16 to 18:1 reported in the 1980s and 1990s down to 3:1 in most recent reports. This is likely to be due to increasing awareness and recognition of female SpA. An important observation has been a significantly higher proportion of peripheral arthritis reported among Indian axial SpA (axSpA) patients. It could be due to environmental exposure causing reactive arthritis type of onset that evolves into clinically recognizable SpA over time. In recent years, the reports on nonradiographic and radiographic axSpA categories have also appeared with similarities to that reported from the Western countries. This category showed the lowest male:female ratio (1.2:1) indicative of a much higher proportion of females in the nonradiographic axSpA category. The specific features related to the management were the widespread use of sulfasalazine for axSpA and much less use of biologicals, most likely due to financial reasons, in India.

Background: Abfraction is a loss of tooth structure along the gingival margin and manifests with different clinical appearances. It has multifactorial etiology and may occur due to normal and abnormal tooth function and may also be accompanied by pathological wear, such as abrasion and erosion. The theory behind the abfraction is that the tooth flexure in the cervical area is caused due to occlusal compressive forces and tensile stresses. This results in the fractures in the hydroxyapatite (HA) crystals. It is also caused by the low packing density of the Hunter–Schreger band (HSB) at the cervical area. Unfortunately, there is a lack of evidence regarding the outcome of abfraction with or without intervention. The aim of this review is to collect clinical information from the literature and discuss the etiology, pathogenesis, clinical representation, and management. Also, search databases for clinical studies that describe the role of sclerotic dentine in non-carious cervical lesions (NCCLs) are becoming a clinical challenge. Methods: The literature was searched that described the etiology, pathogenesis, clinical representation, and management of the abfraction lesions. Also, a specific question regarding the formation of sclerotic dentin in the NCCL lesion was described and searched for evidence that challenges etching, bonding, and successfully restoring NCCLs. The databases PUBMED, SCOPUS, MEDLINE, WEB of SCIENCE, and EMBASE were searched using the key terms. The inclusion criteria were the randomized controlled clinical trial, cohort studies, and cross-sectional studies that aimed at determining the role of sclerotic dentine in NCCLs and its effect on etching, bonding. Results: One clinical study was retrieved according to the PRISMA flowchart and PICO format. The longer etching time, total-etch adhesive system, and EDTA pre-treatment of the sclerotic dentin of cervical wedge-shaped defects could improve the bonding strength in lesions like NCCL's. Conclusion: In conclusion, clinical challenges that occur due to NCCLs are better managed by a proper understanding of factors like etiopathogenesis, ultra-structure of enamel, and dentine and their effect on the bonding of restorations of the tooth.

Background Ventricular fibrillation (VF) is characterized by multiple wavelets and rotors. No equation to predict the number of rotors and wavelets observed during fibrillation has been validated in human VF. Objective The purpose of this study was to test the hypothesis that a single equation derived from a Markov M/M/∞ birth-death process could predict the number of rotors and wavelets occurring in human clinical VF. Methods Epicardial induced VF (256-electrode) recordings obtained from patients undergoing cardiac surgery were studied (12 patients; 62 epochs). Rate constants for phase singularity (PS) (which occur at the pivot points of rotors) and wavefront (WF) formation and destruction were derived by fitting distributions to PS and WF interformation and lifetimes. These rate constants were combined in an M/M/∞ governing equation to predict the number of PS and WF in VF episodes. Observed distributions were compared to those predicted by the M/M/∞ equation. Results The M/M/∞ equation accurately predicted average PS and WF number and population distribution, demonstrated in all epochs. Self-terminating episodes of VF were distinguished from VF episodes requiring termination by a trend toward slower PS destruction, slower rates of PS formation, and a slower mixing rate of the VF process, indicated by larger values of the second largest eigenvalue modulus of the M/M/∞ birth-death matrix. The longest-lasting PS (associated with rotors) had shorter interactivation time intervals compared to shorter-lasting PS lasting Conclusion The M/M/∞ equation explains the number of wavelets and rotors observed, supporting a paradigm of VF based on statistical fibrillatory dynamics.

Embolic stroke results in a necrotic core of cells destined to die, but also a peri-ischemic, watershed penumbral region of potentially salvageable brain tissue. Approaches to effectively differentiate between the ischemic and peri-ischemic zones is critical for novel therapeutic discovery to improve outcomes in survivors of stroke. MicroRNAs are a class of small non-coding RNAs regulating gene translation that have region- and cell-specific expression and responses to ischemia. We have previously reported that global inhibition of cerebral microRNA200c after experimental stroke in mice is protective, however delineating the post-stroke sub-regional and celltype specific patterns of post-stroke miR-200c expression are necessary to minimize off-target effects and advance translational application. Here, we detail a novel protocol to visualize regional miR-200c expression after experimental stroke, complexed with visualization of regional ischemia and markers of oxidative stress in an experimental stroke model in mice. In the present study we demonstrate that the fluorescent hypoxia indicator pimonidazole hydrochloride, the reactive-oxygen-species marker 8-hydroxy-deoxyguanosine, neuronal marker MAP2 and NeuN, and the reactive astrocyte marker GFAP can be effectively complexed to determine regional differences in ischemic injury as early as 30 min post-reperfusion after experimental stroke, and can be effectively used to distinguish ischemic core from surrounding penumbral and unaffected regions for targeted therapy. This multi-dimensional post-stroke immunofluorescent imaging protocol enables a greater degree of subregional mechanistic investigation, with the ultimate goal of developing more effective post-stroke pharmaceutical therapy.

Hypertrophic cardiomyopathy (HCM) is an inherited cardiac disorder affecting one in 500 of the general population. Atrial fibrillation (AF) is the most common arrhythmia in patients with HCM. We sought to characterize the atrial electrophysiological and structural substrate in young and aging Gly203Ser cardiac troponin-I transgenic (HCM) mice. At 30 weeks and 50 weeks of age (n = 6 per strain each group), the left atrium was excised and placed on a multi-electrode array (MEA) for electrophysiological study, subsequent histological analyses and plasma samples were analyzed for biomarkers of extracellular matrix remodeling and cell adhesion and inflammation. Wild-type mice of matched ages were included as controls. Young HCM mice demonstrated significantly shortened atrial action potential duration (APD), increased conduction heterogeneity index (CHI), increased myocyte size, and increased interstitial fibrosis without changes in effective refractory periods (ERP), conduction velocity (CV), inflammatory infiltrates, or circulating markers of extracellular matrix remodeling and inflammation. Aging HCM mice demonstrated aggravated changes in atria electrophysiology and structural remodeling as well as increased circulating matrix metalloproteinases (MMP)-2, MMP-3, and VCAM-1 levels. This model of HCM demonstrates an underlying atrial substrate that progresses with age and may in part be responsible for the greater propensity for AF in HCM.

Background The beneficial effects of cardiac resynchronization therapy (CRT) in heart failure are largely considered to be due to improved mechanical contractility. The contributory role of electrical remodelling is less clear. We sought to evaluate the impact of electrical remodelling in these patients. Methods 33 patients with conventional indications for CRT and with ischemic (ICM) (n = 17) and non-ischemic (NICM) (n = 16) aetiologies for heart failure were prospectively recruited. Functional parameters of peak exercise oxygen consumption (VO2max) and Minnesota quality of life (QOL) score, echocardiographic measures of LV functions and parameters of electrical remodelling, e.g. intrinsic QRS duration (iQRSD), intracardiac conduction times of LV pacing to RV electrocardiogram (LVp-RVegm), were measured at CRT implant and after 6 months. Results Only two electrical parameters predicted functional or symptomatic improvement. LVp-RVegm reduction significantly correlated with improvement in VO2max (r = −0.42, p = 0.03 while reduction in iQRSD significantly correlated with improvement in QOL score (r = 0.39, p = 0.04). The extent of changes in LVp-RVegm and iQRSD was significantly greater in NICM than in ICM patients (p = 0.017 and p = 0.042 for heterogeneity). There was also significant differential impact on QOL score in the NICM relative to the ICM group (p = 0.003) but none with VO2max. On multivariate analysis, only non-ischemic aetiology was a significant determinant of reduction in iQRSD. Conclusion CRT induces potentially beneficial reduction in LVp-RVegm and iQRSD, which are seen selectively in NICM rather than ICM patients. The extent of improvement in these markers is associated with some functional and symptomatic measures of CRT efficacy.

Background Little is known about the utilisation and safety of catheter ablation of atrial fibrillation (AF) among public and private sector hospitals. Aims To examine the uptake of AF ablations and compare procedural safety between the sectors. Method: Hospitalisation data from all public and private hospitals in four large Australian states (NSW, QLD, VIC and WA) were used to identify patients undergoing AF ablation from 2012 to 17. The primary endpoint was any procedure-related complications up to 30-days post-discharge. Logistic regression was used to evaluate the association between treatment at a public hospital and risk of complications adjusting for covariates. Results Private hospitals performed most of the 21,654 AF ablations identified (n = 16,992, 78.5 %), on patients who were older (63.5 vs. 59.9y) but had lower rates of heart failure (7.9 % vs. 10.4 %), diabetes (10.2 % vs. 14.1 %), and chronic kidney diseases (2.4 % vs. 5.2 %) (all p p Conclusions Private hospitals performed most of AF ablations in Australia with a lower rate of complications when compared with public hospitals. Further investigations are needed to identify the precise mechanisms of this observed difference.

Aims Population studies that provide unbiased estimates of gender differences in risk of complications following catheter ablation of atrial fibrillation (AF) are sparse. We sought to evaluate the association of female gender and risk of complications following AF ablation in a nationwide cohort. Methods and results We identified 35 211 patients (29.5% females) undergoing AF ablations from 2008 to 2017 using national hospitalization data from Australia and New Zealand. The primary outcome was any procedural complication occurring up to 30-days after discharge. Logistic regression was used to adjust for differences in baseline characteristics between sexes. Compared with males, females were older (mean age 64.9 vs. 61.2 years), had higher rates of hypertension (14.0% vs. 11.6%) and haematological disorders (5.3% vs. 3.8%) and experienced a higher rate of procedural complications (6.96% vs. 5.41%) (all P Conclusion Females undergoing AF ablations experienced a 25% higher risk of procedural complications compared with males, a disparity that has persisted over time despite a falling complication rate. Efforts to reduce this gender disparity should focus on reducing the incidence of pericardial effusion, pericarditis, vascular injury, and bleeding.

Atrial fibrillation (AF) is the most commonly encountered cardiac arrhythmia in clinical practice. However, current therapeutic interventions for atrial fibrillation have limited clinical efficacy as a consequence of major knowledge gaps in the mechanisms sustaining atrial fibrillation. From a mechanistic perspective, there is increasing evidence that atrial fibrosis plays a central role in the maintenance and perpetuation of atrial fibrillation. Electrophysiologically, atrial fibrosis results in alterations in conduction velocity, cellular refractoriness, and produces conduction block promoting meandering, unstable wavelets and micro-reentrant circuits. Clinically, atrial fibrosis has also linked to poor clinical outcomes including AF-related thromboembolic complications and arrhythmia recurrences post catheter ablation. In this article, we review the pathophysiology behind the formation of fibrosis as AF progresses, the role of fibrosis in arrhythmogenesis, surrogate markers for detection of fibrosis using cardiac magnetic resonance imaging, echocardiography and electroanatomic mapping, along with their respective limitations. We then proceed to review the current evidence behind therapeutic interventions targeting atrial fibrosis, including drugs and substrate-based catheter ablation therapies followed by the potential future use of electro phenotyping for AF characterization to overcome the limitations of contemporary substrate-based methodologies. Refereed/Peer-reviewed

Background Comparing outcomes of care between public and private hospitals is critical to inform patients and improve care quality. Purpose To compare complication rates following catheter ablation of atrial fibrillation (AF) up to 30-days post discharge between public and private hospitals. Methods We included patients ≥18 years who underwent AF ablation in the Australian states of New South Wales, Queensland, Victoria, and Western Australia from 2010–2015. The primary outcome was the occurrence of any complication up to 30-days after discharge. The association between provider type and the risk of complications was examined using logistic regression with inverse probability of treatment weighting (IPTW) propensity scores to account for differences in measured confounders. The minimum strength of association required for an unmeasured confounder to nullify any observed association was estimated using the E value. Results We identified 18,074 AF ablations during the study period (mean age 62.3±11.4y, 28.8% female, 78.4% performed in private hospitals). Patients ablated at public hospitals were younger (59.3 vs. 63.1y, p Conclusion AF ablation at a public hospital was associated with a 46% higher risk of complications compared with ablation at a private hospital, mainly driven by a higher risk of complications requiring cardiac surgery, acute kidney injury, cardiorespiratory failure, infections, and bleeding. The disparity could be due to differences in care quality between two sectors or explained by unmeasured confounders such as higher procedural complexity in public hospitals. Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): The National Heart Foundation of Australia

Background Recent studies from the United States report rising rates of in-hospital complications and mortality following catheter ablation of atrial fibrillation (AF) but whether such a trend is observed in other populations is uncertain. Purpose To examine the trends in complications and mortality following AF ablations up to 30 days after discharge in Australia and New Zealand (ANZ) using nationwide data. Methods All patients ≥18y undergoing catheter ablation of AF from 2010–2015 were identified using hospitalisation data from all public and most private hospitals in ANZ. The primary endpoint was one or more procedural complications during the hospital stay or within 30 days of discharge. The secondary endpoints were mortality and other specific complications. Unadjusted trend was evaluated using Cochran-Armitage test while that of complications, adjusting for differences in other characteristics, was evaluated using multivariate logistic regression with the year of ablation modelled as a continuous variable. Results are reported as odd ratios (OR) and 95% confidence intervals (CI). Results A total of 22,582 AF ablations were included (mean age 62.2±11.6y, 29.1% female, 94.4% elective procedures). The number of ablations increased by 26.4% during the study period (3,097 in 2010 to 3,915 in 2015). Rates of heart failure (8.98% to 10.09%, p for trend=0.010), diabetes (4.52% to 12.46%, p Conclusions Though more patients with heart failure, diabetes and chronic kidney disease underwent catheter ablation of AF over time in ANZ, the overall complication rate was unchanged with a significant decrease in the incidences of major bleeding and venous thromboembolism. However, rate of acute kidney injury nearly doubled, and this could be a potential target for efforts to further improve procedural safety. Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): The National Heart Foundation of Australia

A 19-year-old Australian Indigenous woman presented after suffering a ventricular fibrillation cardiac arrest whilst swimming, leading to near drowning, in a remote Aboriginal community of South Au...

What you need to know Assessing non-melanocytic skin lesions is a routine part of general practice. The key concern for patient and doctor is often whether the lesion may be a basal cell carcinoma or squamous cell carcinoma, collectively termed non-melanoma skin cancer (NMSC). This article aims to help primary care clinicians, who may not routinely have access to dermoscopy and biopsy, to identify possible NMSC lesions, which require further specialist assessment or monitoring. ### How this article was made We searched for relevant journal articles in the British Journal of Dermatology , BMJ , and British Association of Dermatology guidelines. A secondary literature search was conducted using Google Scholar with the key words “basal cell carcinoma,” “squamous cell carcinoma,” “non-melanoma skin cancer” associated with “risk factors,” “treatment,” “management,” “follow-up.” Non-melanoma skin cancer is more commonly diagnosed than all other malignancies combined,1 and the incidence of skin cancer is rising, with rates of NMSC predicted to reach almost 400 000 per year in the UK by 2025.2 This is thought to be due to a combination of people living longer, increased exposure to ultraviolet (UV) light, and improved data collection and diagnostic tools.34 Risk factors are summarised in table 1, with the key environmental risk being UV exposure from tan-seeking behaviour and outdoor activities without adequate sun protection.12 Both basal cell carcinomas and cutaneous squamous cell carcinomas are more common with increasing age, with incidence of cutaneous squamous cell carcinomas peaking at 66 years of age. View this table: Table 1 Risk factors for non-melanoma skin cancer Box 1 summarises the procedure …

Case Presentation A 44-year-old woman was referred for evaluation of dyspnea on exertion and multiple nodular opacities on a chest CT scan. She had a medical history of autoimmune encephalitis, diabetes mellitus, hypertension, migraines, and allergic rhinitis. Ten years earlier, the patient was admitted to an outside institution with symptoms of shortness of breath. She was found to have multiple pulmonary nodules and was diagnosed empirically with and treated for sarcoidosis. She was told that her pulmonary nodules had improved on follow up. However, she continued to have symptoms of dyspnea. Due to progressive symptoms of shortness of breath, she was referred to pulmonology. She reported a weight gain of 80 pounds over the last year. She denied fever, chills, hemoptysis, night sweats, joint swelling, or skin rash. She is a former cigarette smoker with a 15 pack-year smoking history, quit smoking in 2005. She denied alcohol or drug use. She resided in Arkansas and Texas over the past decade. She previously worked as a teacher and is currently unemployed. She had no other relevant exposures. She denied a family history of autoimmune diseases or malignancies.

Background: Despite a century of research, no clear quantitative framework exists to model the fundamental processes responsible for the continuous formation and destruction of phase singularities (PS) in cardiac fibrillation. We hypothesized PS formation/destruction in fibrillation could be modeled as self-regenerating Poisson renewal processes, producing exponential distributions of interevent times governed by constant rate parameters defined by the prevailing properties of each system. Methods: PS formation/destruction were studied in 5 systems: (1) human persistent atrial fibrillation (n=20), (2) tachypaced sheep atrial fibrillation (n=5), (3) rat atrial fibrillation (n=4), (5) rat ventricular fibrillation (n=11), and (5) computer-simulated fibrillation. PS time-to-event data were fitted by exponential probability distribution functions computed using maximum entropy theory, and rates of PS formation and destruction (λ f /λ d ) determined. A systematic review was conducted to cross-validate with source data from literature. Results: In all systems, PS lifetime and interformation times were consistent with underlying Poisson renewal processes (human: λ f , 4.2%/ms±1.1 [95% CI, 4.0–5.0], λ d , 4.6%/ms±1.5 [95% CI, 4.3–4.9]; sheep: λ f , 4.4%/ms [95% CI, 4.1–4.7], λ d , 4.6%/ms±1.4 [95% CI, 4.3–4.8]; rat atrial fibrillation: λ f , 33%/ms±8.8 [95% CI, 11–55], λ d , 38%/ms [95% CI, 22–55]; rat ventricular fibrillation: λ f , 38%/ms±24 [95% CI, 22–55], λ f , 46%/ms±21 [95% CI, 31–60]; simulated fibrillation λ d , 6.6–8.97%/ms [95% CI, 4.1–6.7]; R 2 ≥0.90 in all cases). All PS distributions identified through systematic review were also consistent with an underlying Poisson renewal process. Conclusions: Poisson renewal theory provides an evolutionarily preserved universal framework to quantify formation and destruction of rotational events in cardiac fibrillation.

Review question:The question of this review is: what is the adherence to the use of activity monitoring devices or applications to improve physical activity in adults with cardiovascular disease?Specifically, the review objectives are:To quantify the extent of adherence (as specified by the

Aim To test the validity of an augmented tuberculosis skin test (a-TST) combined with Quantiferon TB-gold® (QFTG) test for the screening of latent tuberculosis infection (LTBI) in patients with rheumatoid arthritis (RA) being considered for treatment with biologic disease-modifying anti-rheumatic drugs or targeted synthetic disease-modifying anti-rheumatic drugs. Method Standard TST using 1 tuberculin unit (TU) of purified protein derivative (PPD, RT23 strain) was carried out. If the positivity was less as compared to the general population, then a-TST using 10 TU PPD was employed. Simultaneously, QFTG test was also performed. Results Using standard TST, 6/44 (13.6%), patients were positive compared to the reported figures of ~ 40% of the general population; 38 of the remaining TST-negative patients were then given an a-TST with 10 TU PPD; eight of them dropped out. Of the remaining 30 patients, eight (26.6%) were positive. Another 70 patients tested directly with a-TST; 22 (31.4%) were found positive. Thus, of a total of 100 patients tested with a-TST, 30 (30%) were positive. In 54 a-TST negative patients, QFTG was done; seven (13%) were positive. Thus, in combined a-TST with QFTG, 43% of the RA patients were found positive, suggestive of the presence of LTBI. Conclusion Combined a-TST with QFTG testing gave 43% positivity among RA patients, which is close to the reported ~ 40% Mantoux positivity in the general population. Therefore, this method for the screening of LTBI in Indian patients with RA being considered for tumor necrosis factor alpha treatment could be satisfactory for offsetting TB flare. It may apply to other high-burden TB countries around the world.

In a landmark breakthrough in 1976, Reichlin and Mattioli discovered the first myositis-specific antibody (MSA) called anti-Mi2 antibody that identified a specific clinical phenotype characterized by pathognomonic skin rash of dermatomyositis, typical proximal muscle weakness, good response to treatment, and the absence of interstitial lung disease and cancer. The discovery firmly placed inflammatory muscle diseases among the group of systemic rheumatic autoimmune diseases. Over the next four decades, a large number of additional MSAs have been discovered in this group of patients called “idiopathic inflammatory myopathy” (IIM). It is becoming clear that the increasing numbers of autoantibodies being discovered may necessitate a name change to “autoimmune myositis” (AIM), as recently suggested by a French-Canadian group. In the light of these discoveries, it was evident that a new classification system based on the combination of clinical phenotypes and the associated autoantibodies would soon be propounded. Preliminary report on such a classification was published in 2016 by the Swedish Group from Karolinska Institute led by Prof. Ingrid Lundberg. In October 2017, the European League Against Rheumatism and the American College of Rheumatology published the provisional classification criteria for IIM with the aim to categorize patients in uniform subgroups of clinical phenotype for meaningful drug trials. These are exciting times for clinicians, for research scientists, and for the patients with inflammatory myositis with reasons to be optimistic about a bright future. This short review provides a summary of the present knowledge with emphasis on its clinical implications.

Background: Nonsteroidal anti-inflammatory drugs (NSAIDs) are considered the first-line drugs for axial spondyloarthritis because of their high efficacy in controlling symptoms. However, the review of the literature shows that among Caucasian patients, only ~ 1/3rd with recent disease onset and only ~10% with the long-standing disease achieved partial or complete remission. The present study was, therefore, aimed at finding out how many Indian axSpA patients achieved low-disease activity state or remission over a short period of 12 weeks. Methods: This was a retrospective study including 35 patients, both nonradiographic and radiographic axSpA, classified according to the Assessment of Spondyloarthritis International Society criteria (2009). Information was extracted from the electronic medical records for patients who had only received NSAIDs without any disease-modifying anti-rheumatic drugs or biologicals. The primary objective was to analyze the effect of continuous use of NSAIDs on their disease activity status as measured by the Ankylosing Spondylitis Disease Activity Score (ASDAS)-C-reactive protein (CRP) cutoff values at the baseline as compared to that after 3 months. Results: A total of 31/35 patients continuously treated with NSAIDs for 12 weeks showed statistically significant improvement in their disease activity status as measured by ASDAS-CRP (P < 0.05). A total of 19/35 and 12/35 patients achieved remission (i.e., ASDAS-CRP < 1.3) and low disease state (i.e., ASDAS-CRP

Objective: The objective of the study was to study the effectiveness of a recommended screening strategy for latent tuberculosis infection (LTBI) in patients with systemic inflammatory rheumatic diseases (SIRDs) treated with biological disease-modifying antirheumatic drugs (bDMARDs). Methods: The study included patients being considered for bDMARD treatment. Screening strategy included screening with “4S symptom complex (current cough, fever, weight loss, and night sweats) for TB,” augmented Mantoux test using ten tuberculin unit (TU) strength simultaneously with QuantiFERON®-TB Gold (QFTG) test. Those with a Mantoux test reading of ≥10 mm induration at 48–72 h and/or with a positive QFTG test, were given TB prophylaxis before initiating bDMARDs. They were followed and monitored for any features of tuberculosis flare. Results: A total of 730 patients (265 rheumatoid arthritis, 400 axial spondyloarthritis [axSpA], 34 psoriatic arthritis, and 31 others) were considered for bDMARDs. Two hundred and sixty-seven (36.6%) were positive for LTBI. They were treated either with isoniazid monotherapy for 6 months or with rifampicin + isoniazid for 4 months. bDMARDs were started 1 month after initiating chemoprophylaxis. Five (0.68%) patients developed active TB disease in the follow-up. In a total of 2930 “control” patients with the same diseases but never having taken bDMARDs, 18 (0.61%) developed active TB disease. The proportion of patients developing active TBI during the same period of follow-up did not differ between those who were and those who were not treated with bDMARDs. None of the study participants had “4S” symptoms. Conclusion: The strategy of clinical screening for active TBI with “4S complex,” standard chest radiograph, and an augmented Mantoux testing (10 TU purified protein derivative, [PPD]) simultaneously with QFTG test for the screening of LTBI, was successful in identifying active TBI in patients treated with bDMARDs.

Protected channels of surviving myocytes in late postinfarction ventricular scar predispose to ventricular tachycardia (VT). However, only a few patients develop VT spontaneously. We studied differences in electric remodeling and protected channels in late postinfarction patients with and without spontaneous VT. Patients with ischemic cardiomyopathy (ICM) with recurrent sustained monomorphic VT (n = 22) were compared with stable ICM patients without spontaneous VT (control group; n = 5). Left ventricular mapping was performed with a 20-pole catheter. Detailed pace mapping was used to identify channels of protected conduction, and confirmed, when feasible, by entrainment. Anatomical and electrophysiological properties of VT channels and non-VT channels in VT patients and channels in controls were evaluated. Seventy-three (median 3) VTs were inducible in VT patients compared to two (median 0) in controls. The VT channels in VT patients (n = 57, 3 ± 1 per patient) were lengthier (mean ± SEM 53 ± 5 vs. 33 ± 4 vs. 24 ± 8 mm), had longer S-QRS (73 ± 4 vs. 63 ± 3 vs. 44 ± 8 ms), longer conduction time (103 ± 13 vs. 33 ± 4 vs. 24 ± 8 ms), and slower conduction velocity (CV) (0.85 ± 0.21 vs. 1.39 ± 0.20 vs. 1.31 ± 0.41 m/s) than non-VT channels in VT patients (n = 183, 8 ± 6 per patient) (p ≤ 0.01) and channels in controls (n = 46, 9 ± 8 per patient) (p ≤ 0.01). Additionally, non-VT channels in VT patients had longer S-QRS (p = 0.02); however, they were similar in length, conduction time, and CV compared to channels in controls. Channels supporting VT are lengthier, with longer conduction times and slower CV compared to channels in patients without spontaneous VT. These observations may explain why some ICM patients have spontaneous VT and others do not.

Haemonchus contortus resistant to multiple anthelmintics threaten the viability of the small ruminant industry in areas where this parasite is prevalent. In response to this situation, the FAMACHA© system was developed and validated for use with small ruminants as a way to detect clinical anemia associated with haemonchosis. Given that H. contortus and multiple anthelmintic resistance is a similar problem in camelids, the FAMACHA© system might also provide the same benefits. To address this need, a validation study of the FAMACHA© system was conducted on 21 alpaca and llama farms over a 2-year period. H. contortus was the predominant nematode parasite on 17 of the 21 farms (10 alpaca and 7 llama farms) enrolled in the study, based on fecal culture results. The FAMACHA© card was used to score the color of the lower palpebral (lower eye lid) conjunctiva on a 1-5 scale. Packed cell volume (PCV) values were measured and compared to FAMACHA© scores using FAMACHA© score cutoffs of ≥3 or ≥4 and with anemia defined as a PCV ≤15%, ≤17%, or≤20%. PCV was significantly associated with FAMACHA© score, fecal egg count (FEC), and body condition score (BCS), regardless of the FAMACHA© cutoff score or the PCV% chosen to define clinical anemia (p

The objective of this study was to characterise the peripheral arthritis of spondyloarthritis (pSpA) excluding psoriatic-, inflammatory enteropathy-related, post-infectious reactive-SpA and arthritis associated with axial SpA/ankylosing spondylitis (axSpA/AS). Patients presenting with the clinical features of the broad spectrum of SpA were screened for the presence of peripheral arthritis using the Assessment of SpondyloArthritis International Society (ASAS) criteria. The other conditions that could cause pSpA, e.g. psoriasis, inflammatory enteropathy, reactive arthritis and axSpA/AS, were excluded. Their assessment included clinical, laboratory and imaging features. Of a total of 405 patients seen within the spectrum of SpA, 25 (6.2%) patients were identified as pSpA with none of the conditions that could be attributed to their disease. The male to female ratio was 2.6:1; the pattern of involvement was predominantly lower extremity asymmetrical large joint oligoarthritis in persons below the age of 40 years (60% were

The SPAST gene, which produces two isoforms of the microtubule-severing protein spastin, is the chief gene mutated in hereditary spastic paraplegia. Truncated M1 spastin proteins are toxic and have the potential to accumulate in these patients., The SPAST gene, which produces two isoforms (M1 and M87) of the microtubule-severing protein spastin, is the chief gene mutated in hereditary spastic paraplegia. Haploinsufficiency is a popular explanation for the disease, in part because most of the >200 pathogenic mutations of the gene are truncating and expected to produce only vanishingly small amounts of shortened proteins. Here we studied two such mutations, N184X and S245X, and our results suggest another possibility. We found that the truncated M1 proteins can accumulate to notably higher levels than their truncated M87 or wild-type counterparts. Reminiscent of our earlier studies on a pathogenic mutation that generates full-length M1 and M87 proteins, truncated M1 was notably more detrimental to neurite outgrowth than truncated M87, and this was true for both N184X and S245X. The greater toxicity and tendency to accumulate suggest that, over time, truncated M1 could damage the corticospinal tracts of human patients. Curiously, the N184X mutation triggers the reinitiation of translation at a third start codon in SPAST, resulting in synthesis of a novel M187 spastin isoform that is able to sever microtubules. Thus microtubule severing may not be as reduced as previously assumed in the case of that mutation.

Since 1984 the diagnosis of ankylosing spondylitis (AS) has been based upon the modified New York (mNY) criteria with mandatory presence of radiographic sacroiliitis, without which the diagnosis is not tenable. However, it may take years or decades for radiographic sacroiliitis to develop delaying the diagnosis for long periods. It did not matter in the past because no effective treatment was available. However, with the availability of a highly effective treatment, namely, tumour necrosis factor-α inhibitors (TNFi), the issue of early diagnosis of AS acquired an urgency. The Assessment of SpondyloArthritis International Society (ASAS) classification criteria published in 2009 was a significant step towards this goal. These criteria described an early stage of the disease where sacroiliitis was demonstrable only on MRI but not on standard radiograph. Therefore, this stage of the disease was labelled “nonradiographic axial SpA” (nr-axSpA). But questions have been raised if, in search of early diagnosis, specificity was compromised. The Federal Drug Administration (FDA, USA) withheld approval for the use of TNFi in patients with nr-axSpA because of issues related to the specificity of these criteria. This review attempts to clarify some of these aspects of the nr-axSpA-AS relationship and also tries to answer the question whether ASAS classifiable radiographic axial spondyloarthritis (r-axSpA) term can be interchangeably used with the term AS.

Perinatal testicular torsion is a rare condition with an incidence of 1 in 7500 live births. 70% are prenatal and 30% postnatal. Postnatal torsion presents as an acute scrotum, whereas prenatal torsion may be usually missed as it is a non-tender hard mass. Management of prenatal torsion is controversial. We are reporting three such case series presenting within a period of 1 year. Prenatal testicular torsion is usually missed as it is asymptomatic and later presents as cryptorchid. Careful postnatal physical examination and documentation is essential, as a missed case can later present as cryptorchid and may lead to medicolegal issues. In torsion in the immediate perinatal period, the testis may be salvaged if promptly operated.

Purpose of review Asthma and chronic obstructive pulmonary disease are both commonly encountered respiratory conditions. The term asthma--COPD overlap (ACO) has been used to identify patients presenting with features of both conditions. Controversy exists regarding its definition, approach to diagnosis and management. In this publication, recent evidence has been reviewed that provides insight into diagnosis and management of this condition. Recent findings Previously, multiple criteria were used to define Asthma--COPD overlap. In this publication, the most recent guidelines to identify this condition have been reviewed. This publication provides a summary of the recent evidence with regard to the role of various diagnostic modalities including the use of biomarkers, such as exhaled nitric oxide, serum IgE and provides updated evidence on available treatment choices for this condition. Summary ACO is a commonly encountered clinical condition with patients experiencing frequent exacerbations and resulting in increased healthcare resource utilization. Recent interest in ACO has led to development of a framework towards diagnosis and management of this condition. Therapeutic choices for ACO range from bronchodilator therapy to immunomodulatory therapy, highlighting the heterogeneity of this condition. Additional research is required to improve understanding of pathogenesis and improve outcomes in ACO.

Background It is important to investigate complications of catheter ablation for atrial fibrillation (AF) - an increasingly common procedure - to inform patients and guide efforts to improve procedural quality. However, clinical trials and registries are limited by selection bias, while existing population-based studies either lack nation-wide data, or fail to report post-discharge complications. The timing and impact of these complications are also poorly understood. Purpose To obtain unbiased and comprehensive estimates of complications of AF ablations using national data from Australia and New Zealand. We also evaluated the impact of in-hospital complications on the length of stay and assessed the timing of post-discharge complications. Methods We included patients aged ≥18 years undergoing catheter ablation with a primary diagnosis of AF between 2010–2015 in all public and most private hospitals in Australia and New Zealand. The primary outcome was the occurrence of major complications in-hospital or up to 30-days after discharge. We identified major complications based on a literature review and expert clinical opinion and defined these using International Classification of Diseases – 10th revision, Australian Modification diagnoses codes and Australian Classification of Health Interventions procedure codes. We determined the impact of in-hospital complications on the length of stay, adjusting for other covariates, by using negative binomial regression, and reported results as incident rate ratio (IRR) and 95% confidence intervals (CI). Time to first post-discharge complication was evaluated using Kaplan Meier survival analysis. Results A total of 20,057 AF ablations were included (mean age 62.1±11.6 y, 56.7% ≤65 years old; 29.2% female; median length of stay 1 day). Of these, major complications occurred in 6.3% procedures (4.6% occurring in-hospital and a further 2.0% occurring in the 30-day post discharge). The most common complications were bleeding or haematoma formation and perforation (primarily pericardial effusion), which accounted to 60.3% and 14.3% of all complications, respectively. Rate of procedure-related deaths was 0.1%. Occurrence of an in-hospital complication more than doubled the length of stay (IRR: 2.3, 95% CI 2.2–2.4) with complications requiring cardiac surgery (IRR 4.5, 95% CI 3.2–6.4) and vascular injuries (IRR 3.9, 95% CI 3.1–4.9) having the length of stay prolonged the most (Figure 1A). In the first-week, 67.3% of post-discharge complications had occurred, and this number reached 95% within three-weeks (Figure 1B). Conclusions Major complications after AF ablation were common. In-hospital complications doubled the length of stay. Approximately 30% of complications occurred after discharge with the risk highest in the first seven days. Efforts to reduce complications should focus on reducing the incidence of bleeding and pericardial effusions which counted for more than 75% of all complications. Acknowledgement/Funding National Heart Foundation of Australia, The Hospital Research Foundation

Background: Myocardial infarction is among the leading causes of morbidity and mortality in young adults around the world. Objectives: In the YOUTH (Young Myocardial Infarction Study of the Western Indians) registry, we aimed to evaluate risk factor profile and angiographic outcomes of reperfusion therapies of infarct-related artery in young western Indians (≤40 years) having ST-segment elevation myocardial infarction. Methods: A total of 1,179 consecutive patients aged ≤40 years who presented with ischemic heart disease from June 2012 to December 2014 were enrolled in the YOUTH registry. A total of 787 patients with ST-segment elevation myocardial infarction were further evaluated. Categorical data was assessed using chi-square test, whereas continuous data was assessed using Student’s t test. Regression analysis was performed to investigate the strength of association. Results: In the YOUTH registry, the study population was predominantly male (93%) with tobacco consumption as major prevalent risk factor (49.7%). Of 787 patients, 451 (57.31%) were thrombolyzed, 326 (41.42%) did not receive any reperfusion therapy, and 10 patients (1.27%) underwent primary angioplasty. Younger age, window period n= 235) being thrombolyzed in a window period of n= 3), whereas bleeding complication was noted only in 1 patient. Highlights MI has been reported to be a major cause of morbidity and mortality in young adults around the world with greater incidences in developing countries. Better understanding of the disease-related features might lead to further improvements in the management of this patient population. With this YOUTH registry, we aimed to evaluate risk factor profile, mode of reperfusion therapy, and angiographic assessment for patency of IRA in young western Indians having STEMI. We based on our findings, recommend pharmacological mode of reperfusion to achieve patency of IRA in young STEMI patients based on the observations of YOUTH registry. The findings of this study have clinical implications as identification of risk factors of myocardial infarction in young adults contributes significantly in its timely clinical management.

Role of cancer stem cells in the esophageal carcinogenesis is not clear.To assess the expression of CD44 and CD133 cancer stem cell markers in esophageal squamous cell carcinoma (ESCC) and its predisposing lesions by immunohistochemistry.Prospective study as a part of an intramural research project.Tissues samples were obtained with endoscopic biopsy and from surgically resected esophageal specimens. Fifty cases each of histopathologically diagnosed cases of esophageal squamous cell carcinoma and its predisposing lesions (mild, moderate, and severe dysplasia and esophagitis) were evaluated for stem cell marker CD44 and C133 by immunohistochemistry using a scoring system.Chi-square test, analysis of variance (ANOVA), post-hoc tests (Tukey-HSD) were used as appropriate for data analysis. Two sided P0.05 was considered as significant.CD44 expression was significantly higher in ESCC as compared to dysplasia and esophagitis (mean IS 7.92 ± 1.45 vs. 6.34 ± 0.80 vs 5.15 ± 0.86 respectively, P0.001). CD133 expression was also significantly higher in ESCC as compared to dysplasia (mean IS 6.82 ± 1.57 vs. 1.00 ± 0.00 respectively, P0.001) while esophagitis showed no expression. CD44 and CD133 expressions were significantly higher in poorly differentiated ESCC than moderately differentiated and well differentiated lesions (CD44 mean IS 6.94 ± 1.44 vs 8.17 ± 1.38 vs. 8.63 ± 1.02 respectively, P0.001 and CD 133 mean IRS 5.63 ± 0.81 vs 6.00 ± 00 vs. 9.0 ± 00 respectively, P0.001).Significantly higher expression of CD44 and CD133 cancer stem cell markers in ESCC as compared to its predisposing lesions (esophagitis and dysplasia) suggests its role in esophageal carcinogenesis.

Background: Inflammatory polyarthritis is seen in ~80% of patients with systemic lupus erythematosus (SLE); yet, there is no validated “instrument” for its assessment. The commonly used measures of disease activity, namely SLE Disease Activity Index 2000 (SLEDAI2K) and British Isles Lupus Assessment Group are complex and impractical for routine use in busy outpatient clinics. This “proof of concept” study's primary aim was to test clinical disease activity index (CDAI) as a possible instrument for measuring the joint disease in SLE that may have a face value and sensitivity to change. The secondary aim was to determine the efficacy of low-dose methotrexate in the SLE joint disease. Materials and Methods: This open-label study included the Systemic Lupus International Collaborating Clinics criteria classifiable thirty patients with SLE with inflammatory polyarthritis as the main manifestation. SLE disease activity and the joint disease activity were assessed using SLEDAI2K and CDAI, respectively, at the baseline and in the follow-up. The CDAI and the SLEDAI2K scores were compared between the first and the last visit, as well as compared with each other, using a nonparametric test (Wilcoxon signed-rank test). Results: CDAI scores improved significantly on treatment from a mean of 19.30 to 1.58 and in SLEDAI2K from 7.83 to 0.6, respectively; the pre- and the postintervention scores were statistically highly significant (P 0.05), indicating similarity in their sensitivity to change. A significant number of patients achieved low disease activity status or remission in their joint disease. Conclusion: CDAI appears to be sensitive to change with treatment. Therefore, it could be used as a tool for assessing inflammatory arthritis in SLE.

Methotrexate (MTX) was synthesised as a folate antagonist for use in treating childhood leukaemia in 1940s. Gubner and colleagues in 1953 used several log-order lower doses of MTX that mimicked the anti-inflammatory properties of cortisone. They used it successfully in treating rheumatoid arthritis (RA). Their work was however overlooked because the Nobel Prize winning drug cortisone held sway in those days. With increasing awareness of the adverse effects of cortisone, interest was rekindled in discovering 'steroid-sparing' drugs. Hoffmeister and Willkens used low-dose MTX (LD-MTX) in treating RA patients in 1960s with impressive results. Pivotal trials in 1984-5 established the efficacy and safety of LD-MTX in treating RA that gained FDA approval in 1988. LD-MTX at doses

The aim of this study was to investigate the effect of caffeine on the symptoms of methotrexate (MTX) intolerance in patients with RA. The follow-up patients with RA seen over a period of 11 months were included in this work. The degree of MTX intolerance, if present, was classified as 'moderate' and 'severe'. Those with intolerance were advised caffeine (coffee or dark chocolate) synchronised with the MTX dose. The effect was assessed as 'very good', 'good' or 'none'. Among 855 patients seen during this period, 313 (36.6 %) did not have any MTX intolerance, 542 (63.4 %) patients had some degree of MTX intolerance, 422 (77.8 %; 49.3 % of the total patients) had 'minimal' intolerance not requiring any intervention. The remaining 120 (22.1 %) of the 542 (14 % of the total 855) patients had 'moderate' or 'severe' MTX intolerance. Among these, 55 % had complete relief of symptoms and were able to continue taking the advised dose of MTX; 13.3 % had partial improvement and continued taking MTX but only with antiemetics; 7.5 % were minimally better but were somehow managing; 10 % were complete caffeine failure without any relief; 14.2 % did not like caffeine (coffee or dark chocolate) and did not want to take it. Caffeine relieved the symptoms of MTX intolerance in 55 % and partial relief in 13 % of the patients. A significant number of patients did not like to take caffeine (coffee or dark chocolate). It is of note that northern part of India is primarily a tea-drinking population where coffee is not a favourite drink.

Neurons are terminally differentiated cells that use their microtubule arrays not for cell division but rather as architectural elements required for the elaboration of elongated axons and dendrites. In addition to acting as compression-bearing struts that provide for the shape of the neuron, microtubules also act as directional railways for organelle transport. The stability properties of neuronal microtubules are commonly discussed in the biomedical literature as crucial to the development and maintenance of the nervous system, and have recently gained attention as central to the etiology of neurodegenerative diseases. Drugs that affect microtubule stability are currently under investigation as potential therapies for disease and injury of the nervous system. There is often a lack of consistency, however, in how the issue of microtubule stability is discussed in the literature, and this can affect the design and interpretation of experiments as well as potential therapeutic regimens. Neuronal microtubules are considered to be more stable than microtubules in dividing cells. On average, this is true, but in addition to an abundant stable microtubule fraction in neurons, there is also an abundant labile microtubule fraction. Both are functionally important. Individual microtubules consist of domains that differ in their stability properties, and these domains can also differ markedly in their composition as well as how they interact with various microtubule-related proteins in the neuron. Myriad proteins and pathways have been discussed as potential contributors to microtubule stability in neurons. © 2016 Wiley Periodicals, Inc.

Aims Thromboembolic risk stratification schemes and clinical guidelines for atrial fibrillation (AF) regard risk as independent of classification into paroxysmal (PAF) and non-paroxysmal atrial fibrillation (NPAF). The aim of the current study was to conduct a systematic review evaluating the impact of AF type on thromboembolism, bleeding, and mortality. Methods and results PubMed was searched through 27 November 2014 for randomized controlled trials, cohort studies, and case series reporting prospectively collected clinical outcomes stratified by AF type. The incidence of thromboembolism, mortality, and bleeding was extracted. Atrial fibrillation clinical outcome data were extracted from 12 studies containing 99 996 patients. The unadjusted risk ratio (RR) for thromboembolism in NPAF vs. PAF was 1.355 (95% CI: 1.169–1.571, P < 0.001). In the study subset off oral anticoagulation, unadjusted RR was 1.689 (95% CI: 1.151–2.480, P = 0.007). The overall multivariable adjusted hazard ratio (HR) for thromboembolism was 1.384 (95% CI: 1.191–1.608, P < 0.001). The overall unadjusted RR for all-cause mortality was 1.462 (95% CI: 1.255–1.703, P < 0.001). Multivariable adjusted HR for all-cause mortality was 1.217 (95% CI: 1.085–1.365, P < 0.001). Rates of bleeding were similar, with unadjusted RR 1.00 (95% CI: 0.919–1.087, P = 0.994) and adjusted HR 1.025 (95% CI: 0.898–1.170, P = 0.715). Conclusion Non-paroxysmal atrial fibrillation is associated with a highly significant increase in thromboembolism and death. These data suggest the need for new therapies to prevent AF progression and further studies to explore the integration of AF type into models of thromboembolic risk.

Atrial fibrillation (AF) is the most common cardiac arrhythmia in humans, with an estimated lifetime prevalence of 25%. It is characterized by irregular and disorganized electrical activation of the atria. In the past decade, catheter ablation, i.e., focally burning targeted areas of cardiac muscle, has emerged as a potentially curative therapy for AF. Accompanying this development there has been an increasing interest in quantitative intraprocedural signal analysis to guide the selection of ablation targets. In this review, we provide an overview of quantitative signal processing approaches for mapping and ablation of AF.

Background:Systemic sclerosis (SSc) is an autoimmune the disease of the connective tissue that is clinically characterized by the involvement of skin (fibrosis, contractures of the finger joints), microvascular abnormalities (Raynaud’s phenomenon and complications), gastrointestinal involvement (gastroesophageal reflux disease - GERD, the lower GI tract involvement), musculoskeletal involvement (polyarthralgia, muscle disease), and involvement of internal organs (especially lungs, heart, and kidneys). Lifestyle modification techniques could have significant impact on various aspects of the disease including early disease control, increased drug adherence, positive attitude towards life, decreased financial burden of treatment, maintaining mobility and joints range of motion, minimizing or delaying joint contractures and decreased dependency with regular physical therapy. Counselling explaining the benefits of lifestyle modification related to these aspects of daily living may make a major difference in the quality of life of the patients with SSc.Objectives:To assess the benefits of lifestyle modification technique in improving the quality of life in patients with SSc.Methods:Patients with SSc attending the Rheumatology clinic of this institution, willing to participate in the survey, were enrolled in this study. All the information including the follow-up details were recorded in a pre-designed form. Their demographic information (age, gender) and disease characteristics (diagnosis, duration, treatment) were recorded, All the patients were explained the lifestyle modifications and their benefits, reinforced at each follow-up visit using posters (visual), written lifestyle modification techniques (using printed material) to raise their awareness of how to improve several of the above manifestations of SSc.Results:One hundred fifty (n=150) consecutive SSc patients were included in the study. It was observed that with repeated counselling 125 (83.3 %) patients adopted the lifestyle modification technique according to the advice imparted and felt a positive benefit in their daily life. However, 25 (16.6%) could not or did not follow the imparted lifestyle change advice on a regular basis. Those who were able to modify the life-style as counselled showed the following results:80 % were able to avoid exposure to cold by adopting the following measures: Wearing gloves and extra woolen socks, using mittens most of the time, wearing woollen undergarments to keep the central regions of the body region warm. These patients noted 55% decrease in the episodes of Raynaud’s phenomenon.Early evening meals and raising the head-end of the bed: 60% decrease in gastrointestinal symptoms.Regular physiotherapy: 65 % decrease dependency on others; 55% could maintain flexibility with physical exercises.Regular application and rubbing of the skin with lanoline-containing skin moisturizers 60 % improve your skin’s health80% were able to avoid active and passive tobacco use.Conclusion:The lifestyle modification techniques are important to control disease and its complications. Thus, after intense and regular counselling by the specialist rheumatology nurses on the lifestyle modification technique (83.3%) adapted the advised lifestyle modifications. The study showed the important role specialist rheumatology nurses can play in educating patients and helping them improving their quality of life.References:[1] Hudson M, Thombs BD, Steele R. at ell. Canadian Scleroderma Research G. QOL in patients with systemic sclerosis compared to the general population and patients with other chronic conditions. J Rheumatol. 2009;36(4):768–72.Disclosure of Interests:None declared