ObjectivesTo investigate the use of oral anticoagulants (AC) and antiplatelet agents (AP) in the management of atrial fibrillation (AF) among patients in primary care in England.DesignEpidemiological study.Setting1857 general practices in England representing a practice population of 13.1 million registered patients.Patients231 833 patients with a history of AF.Main outcome measuresThe primary outcome was AC and AP use by CHADS2 score and age groups <30 years, 30–49 years, 50–64 years, 65–79 years and >79 years.Results231 833 patients with a history of AF were identified, giving a prevalence among uploading practices of 1.76%. Prevalence of AF varied markedly between practices, related to differing practice age profiles. The total number of patients with AF in a practice was strongly predicted by the number of patients aged 65 years and over in the practice. 57.0% of the AF population had a CHADS2 score ≥2 and 83.7%≥1. 114 212 (49.3%) patients received AC therapy. AC uptake increased with increasing CHADS2 score up to a score of 3, but thereafter reached a plateau. Among 132 099 patients with a CHADS2 score ≥2, 72 211 (54.7%) received an AC, 14 987(11.3%) were recorded as having a contraindication or having declined AC therapy, leaving 44 901 (34.0%) not on AC therapy and without a recorded contraindication or recorded refusal. Among patients not prescribed an AC, 79.9% were prescribed an AP. The use of AC declined in the elderly (for CHADS2≥2, 47.4% of patients ≥80 years, compared with 64.5% for patients aged <80 years, p<0.001). By contrast, AP uptake was more prevalent among elderly patients.ConclusionsOver one-third of patients with AF and known risk factors who are eligible for AC do not receive them. There is a high use of AP among patients not receiving AC. Uptake of AC is particularly poor among patients aged 80 years and over.

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The long QT syndrome (LQTS) is a condition characterized by abnormal prolongation of the QT interval with an associated risk of ventricular arrhythmias and sudden cardiac death. Congenital forms of LQTS arise due to rare and highly penetrant mutations that segregate in a Mendelian fashion. Over the years, multiple mutations in genes encoding ion channels and ion channel binding proteins have been reported to underlie congenital LQTS. Drugs are by far the most common cause of acquired forms of LQTS. Emerging evidence suggests that drug-induced LQTS also has a significant heritable component. However, the genetic substrate underlying drug-induced LQTS is presently largely unknown. In recent years, advances in next-generation sequencing technology and molecular biology techniques have significantly enhanced our ability to identify genetic variants underlying both monogenic diseases and more complex traits. In this review, we discuss the genetic basis of congenital and drug-induced LQTS and focus on future avenues of research in the field. Ultimately, a detailed characterization of the genetic substrate underlying congenital and drug-induced LQTS will enhance risk stratification and potentially result in the development of tailored genotype-based therapies.

Whilst the decision regarding defibrillator implantation in a patient with a familial sudden cardiac death syndrome is likely to be most significant for any particular individual, the clinical decision-making process itself is complex and requires interpretation and extrapolation of information from a number of different sources. This document provides recommendations for adult patients with the congenital Long QT syndromes, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia, hypertrophic cardiomyopathy, and arrhythmogenic right ventricular cardiomyopathy. Although these specific conditions differ in terms of clinical features and prognosis, it is possible and logical to take an approach to determining a threshold for implantable cardioveter-defibrillator implantation that is common to all of the familial sudden cardiac death syndromes based on estimates of absolute risk of sudden death.

This study assessed the efficacy of a new dose reduction regime in fluoroscopically guided electrophysiology (EP) procedures, which included diagnostic electrophysiological investigations, radiofrequency ablation, and biventricular pacing. A modified dose regime for fluoroscopy was implemented in one of our cardiac electrophysiology laboratories. The x-ray system was programmed with a hierarchy of three fluoroscopy doses, and therefore image quality and settings. The default (lowest) dose mode was not expected to be suitable for all patient sizes or for the entirety of all procedures. Staff raised the dose level in a stepped manner as and when required to optimize the imaging requirements of the procedure. Phantom studies indicated that the low dose mode provided adequate image quality for visualizing EP catheters, while significantly lowering patient skin dose. In 52 clinical cases, questionnaires were used to assess the subjective clinical image quality. The mean image quality score for the low dose setting was rated between "adequate" and "good." The fluoroscopy dose level was raised from the lowest level for 6% of the total fluoroscopy time. Procedural Dose Area Product (DAP) meter readings were analyzed for patients prior to (n = 85) and after (n = 150) the implementation of the low dose regime and showed an overall reduction in DAP rate of 74%. The hierarchical dose regime proved to be acceptable in routine clinical practice for EP procedures, leading to significant reductions in patient doses.