Action for cities : the Thatcher government and inner city policy

This article reintroduces the issue of the inner city into the project of understanding the Thatcher government. Through exploring how the Thatcher government formed urban policy in the 1980s, I want to make a contribution to the debate of whether 1979 saw a definite break with past approaches, or whether it is better seen as a continuation of the period of confusion and retreat which characterises much of the 1970s. Furthermore, I want to ask how much new policy ideas really did amount to a particularly Thatcherite, or indeed a neoliberal, urbanism, or whether it was more a case of returning to the admixture of dirigisme and deregulation that had long been at the heart of Tory approaches –albeit dressed up with new terminologies and often in new neo-vernacular styling. These questions are important for a broader issue of how we periodise the changes to cities in the post-war period

Surface fragmented QRS in a patient with hypertrophic cardiomyopathy and malignant arrhythmias: Is there an association?

An 18- year old woman with hypertrophic cardiomyopathy, aborted sudden cardiac death and implanted with an implantable cardioverter defibrillator (ICD), developed progressive fragmentation of her surface 12-lead electrocardiogram (ECG). During the follow-up, she presented with multiple appropriate ICD discharges. Here, we discuss the possible association between surface fragmented ECG and the risk of ventricular arrhythmias in patients with hypertrophic cardiomyopathy

Regarding the editorial by Sau and Ng. 'Hypertrophic cardiomyopathy risk stratification based on clinical or dynamic electrophysiological features: two sides of the same coin'

This Letter to the Editor refers to article ‘Hypertrophic cardiomyopathy risk stratification based on clinical or dynamic electrophysiological features: two sides of the same coin’ by Sau A, Ng, FS https://doi.org/10.1093/europace/euad072. ‘Response to the letter to the editor EUPC-D-23-00362 of Richard Saumarez’, by Arunashis Sau and Fu Siong Ng, https://doi.org/10.1093/europace/euad174

The ventricular ectopic QRS interval (VEQSI): A potential marker for ventricular arrhythmia in ischaemic heart disease

Objectives The purpose of this study was to determine the potential value of a novel marker for the severity of structural heart disease and the risk of arrhythmia. Background The ventricular ectopic QRS interval (VEQSI) has been shown to identify structural heart disease and predict mortality in an unselected population. In ischemic heart disease (IHD), risk stratification for sudden death is imperfect. We hypothesized that VEQSI would identify patients with prior myocardial infarction (MI) compared with healthy subjects and distinguish IHD patients who have suffered life-threatening events from those without prior significant ventricular arrhythmia. Methods The 12-lead Holter recordings from 189 patients with previous MI were analyzed: 38 with prior ventricular tachycardia/ventricular fibrillation (MI-VT/VF) (66 ± 9 years; 92% male); 151 without prior significant ventricular arrhythmia (MI-no VT/VF) (64 ± 11 years; 74% male). These were compared with 60 healthy controls (62 ± 7 years; 70% male). All ventricular ectopic beats were reviewed and maximal VEQSI duration (VESQI max) was recorded as the duration of the longest ventricular ectopic beat. Results VEQSI max was longer in post-MI patients compared with normal controls (185 ± 26 ms vs. 164 ± 16 ms; p 198 ms had 86% sensitivity, 85% specificity, 62% positive predictive value, and 96% negative predictive value for identifying patients with prior life-threatening events (odds ratio: 37.4; 95% confidence interval: 13.0 to 107.5). Conclusions VEQSI max >198 ms distinguishes post-MI patients with prior life-threatening events from those without prior significant ventricular arrhythmia. This may be a useful additional index for risk stratification in IHD

Should lethal arrhythmias in hypertrophic cardiomyopathy be predicted using non-electrophysiological methods?

While sudden cardiac death (SCD) in hypertrophic cardiomyopathy (HCM) is due to arrhythmias, the guidelines for prediction of SCD are based solely on non-electrophysiological methods. This study aims to stimulate thinking about whether the interests of patients with HCM are better served by using current, 'risk factor', methods of prediction or by further development of electrophysiological methods to determine arrhythmic risk. Five published predictive studies of SCD in HCM, which contain sufficient data to permit analysis, were analysed to compute receiver operating characteristics together with their confidence bounds to compare their formal prediction either by bootstrapping or Monte Carlo analysis. Four are based on clinical risk factors, one with additional MRI analysis, and were regarded as exemplars of the risk factor approach. The other used an electrophysiological method and directly compared this method to risk factors in the same patients. Prediction methods that use conventional clinical risk factors and MRI have low predictive capacities that will only detect 50-60% of patients at risk with a 15-30% false positive rate [area under the curve (AUC) = ∼0.7], while the electrophysiological method detects 90% of events with a 20% false positive rate (AUC = ∼0.89). Given improved understanding of complex arrhythmogenesis, arrhythmic SCD is likely to be more accurately predictable using electrophysiologically based approaches as opposed to current guidelines and should drive further development of electrophysiologically based methods

Ruled by records: The expropriation of land and the misappropriation of lists in Islamabad

In this article, I investigate the ongoing battle between villagers on the outskirts of Islamabad, Pakistan, and the state development agency attempting to expropriate their land. This battle has been waged through the medium of documents, particularly lists, which villagers and colluding officials have used to defraud the Pakistani government of the equivalent of millions of dollars. Through this case study, I develop an approach to contemporary state governance as material practice, showing how government discourse is shaped by the material forms it takes and highlighting the issue of reference and predication (or how words relate to things). [ governance, documents, state, semiotics, technology, materiality, South Asia, Pakistan ]Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/75363/1/j.1548-1425.2008.00095.x.pd

Atrial arrhythmogenesis in wild-type and Scn5a+/Δ murine hearts modelling LQT3 syndrome

Long QT(3) (LQT3) syndrome is associated with abnormal repolarisation kinetics, prolonged action potential durations (APD) and QT intervals and may lead to life-threatening ventricular arrhythmias. However, there have been few physiological studies of its effects on atrial electrophysiology. Programmed electrical stimulation and burst pacing induced atrial arrhythmic episodes in 16 out of 16 (16/16) wild-type (WT) and 7/16 genetically modified Scn5a+/Δ (KPQ) Langendorff-perfused murine hearts modelling LQT3 (P < 0.001 for both), and in 14/16 WT and 1/16 KPQ hearts (P < 0.001 for both; Fisher’s exact test), respectively. The arrhythmogenic WT hearts had significantly larger positive critical intervals (CI), given by the difference between atrial effective refractory periods (AERPs) and action potential durations at 90% recovery (APD90), compared to KPQ hearts (8.1 and 3.2 ms, respectively, P < 0.001). Flecainide prevented atrial arrhythmias in all arrhythmogenic WT (P < 0.001) and KPQ hearts (P < 0.05). It prolonged the AERP to a larger extent than it did the APD90 in both WT and KPQ groups, giving negative CIs. Quinidine similarly exerted anti-arrhythmic effects, prolonged AERP over corresponding APD90 in both WT and KPQ groups. These findings, thus, demonstrate, for the first time, inhibitory effects of the KPQ mutation on atrial arrhythmogenesis and its modification by flecainide and quinidine. They attribute these findings to differences in the CI between WT and mutant hearts, in the presence or absence of these drugs. Thus, prolongation of APD90 over AERP gave positive CI values and increased atrial arrhythmogenicity whereas lengthening of AERP over APD90 reduced such CI values and produced the opposite effect

Arrhythmogenic actions of the Ca2+ channel agonist FPL-64716 in Langendorff-perfused murine hearts

The experiments explored the extent to which alterations in L-type Ca2+ channel-mediated Ca2+ entry triggers Ca2+-mediated arrhythmogenesis in Langendorff-perfused murine hearts through use of the specific L-type Ca2+ channel modulator FPL-64716 (FPL). Introduction of FPL (1 μm) resulted in a gradual development (>10 min) of diastolic electrical events and alternans in spontaneously beating hearts from which monophasic action potentials were recorded. In regularly paced hearts, they additionally led to non-sustained and sustained ventricular tachycardia (nsVT and sVT). Programmed electrical stimulation (PES) resulted in nsVT and sVT after 5–10 and >10 min perfusion, respectively. Pretreatments with nifedipine, diltiazem and cyclopiazonic acid abolished arrhythmogenic tendency induced by subsequent introduction of FPL, consistent with its dependence upon both extracellular Ca2+ entry and the degree of filling of the sarcoplasmic reticular Ca2+ store. Values for action potential duration at 90% repolarization when any of these agents were applied to FPL-treated hearts became indistinguishable from those shown by untreated control hearts, in contrast to earlier reports of their altering in long QT syndrome type 3 and hypokalaemic murine models for re-entrant arrhythmogenesis. These arrhythmic effects instead correlated with alterations in Ca2+ homeostasis at the single-cell level found in investigations of the effects of both FPL and the same agents in regularly stimulated fluo−3 loaded myocytes. These findings are compatible with a prolonged extracellular Ca2+ entry that potentially results in an intracellular Ca2+ overload and produces the cardiac arrhythmogenecity following addition of FPL

Museums and the ‘new museology’ : theory, practice and organisational change

The widening of roles and expectations within cultural policy discourses has been a challenge to museum workers throughout Great Britain. There has been an expectation that museums are changing from an ‘old’ to a ‘new museology’ that has shaped museum functions and roles. This paper outlines the limitations of this perceived transition as museum services confront multiple exogenous and endogenous expectations, opportunities, pressures and threats. Findings from 23 publically funded museum services across England, Scotland and Wales are presented to explore the roles of professional and hierarchical differentiation, and how there were organisational and managerial limitations to the practical application of the ‘new museology’. The ambiguity surrounding policy, roles and practice also highlighted that museum workers were key agents in interpreting, using and understanding wide-ranging policy expectations. The practical implementation of the ‘new museology’ is linked to the values held by museum workers themselves and how they relate it to their activities at the ground level