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Summary Background Vitamin E (α-tocopherol) is thought to have a role in prevention of atherosclerosis, through inhibition of oxidation of low-density lipoprotein. Some epidemiological studies have shown an association between high dietary intake or high serum concentrations of α-tocopherol and lower rates of ischaemic heart disease. We tested the hypothesis that treatment with a high dose of α-tocopherol would reduce subsequent risk of myocardial infarction (MI) and cardiovascular death in patients with established ischaemic heart disease. Methods In this double-blind, placebo-controlled study with stratified randomisation, 2002 patients with angiographically proven coronary atherosclerosis were enrolled and followed up for a median of 510 days (range 3-981). 1035 patients were assigned α-tocopherol (capsules containing 800 IU daily for first 546 patients; 400 IU daily for remainder); 967 received identical placebo capsules. The primary endpoints were a combination of cardiovascular death and non-fatal MI as well as non-fatal Ml alone. Findings Plasma α-tocopherol concentrations (measured in subsets of patients) rose in the actively treated group (from baseline mean 34·2 μmol/L to 51·1 μmol/L with 400 IU daily and 64·5 μmol/L with 800 IU daily) but did not change in the placebo group. α-tocopherol treatment significantly reduced the risk of the primary trial endpoint of cardiovascular death and non-fatal Ml (41 vs 64 events; relative risk 0·53 [95% Cl 0·34-0·83; p=0·005). The beneficial effects on this composite endpoint were due to a significant reduction in the risk of non-fatal Ml (14 vs 41; 0·23 [0·11-0·47]; p=0·005); however, there was a non-significant excess of cardiovascular deaths in the α-tocopherol group (27 vs 23; 1·18 [0·62-2·27]; p=0·61). All-cause mortality was 36 of 1035 α-tocopherol-treated patients and 27 of 967 placebo recipients. Interpretation We conclude that in patients with angiographically proven symptomatic coronary atherosclerosis, α-tocopherol treatment substantially reduces the rate of non-fatal MI, with beneficial effects apparent after 1 year of treatment. The effect of α-tocopherol treatment on cardiovascular deaths requires further study.

The International Liaison Committee on Resuscitation has called for a randomised trial of delivery to a cardiac arrest centre. We aimed to assess whether expedited delivery to a cardiac arrest centre compared with current standard of care following resuscitated cardiac arrest reduces deaths. ARREST is a prospective, parallel, multicentre, open-label, randomised superiority trial. Patients (aged ≥18 years) with return of spontaneous circulation following out-of-hospital cardiac arrest without ST elevation were randomly assigned (1:1) at the scene of their cardiac arrest by London Ambulance Service staff using a secure online randomisation system to expedited delivery to the cardiac catheter laboratory at one of seven cardiac arrest centres or standard of care with delivery to the geographically closest emergency department at one of 32 hospitals in London, UK. Masking of the ambulance staff who delivered the interventions and those reporting treatment outcomes in hospital was not possible. The primary outcome was all-cause mortality at 30 days, analysed in the intention-to-treat (ITT) population excluding those with unknown mortality status. Safety outcomes were analysed in the ITT population. The trial was prospectively registered with the International Standard Randomised Controlled Trials Registry, 96585404. Between Jan 15, 2018, and Dec 1, 2022, 862 patients were enrolled, of whom 431 (50%) were randomly assigned to a cardiac arrest centre and 431 (50%) to standard care. 20 participants withdrew from the cardiac arrest centre group and 19 from the standard care group, due to lack of consent or unknown mortality status, leaving 411 participants in the cardiac arrest centre group and 412 in the standard care group for the primary analysis. Of 822 participants for whom data were available, 560 (68%) were male and 262 (32%) were female. The primary endpoint of 30-day mortality occurred in 258 (63%) of 411 participants in the cardiac arrest centre group and in 258 (63%) of 412 in the standard care group (unadjusted risk ratio for survival 1·00, 95% CI 0·90–1·11; p=0·96). Eight (2%) of 414 patients in the cardiac arrest centre group and three (1%) of 413 in the standard care group had serious adverse events, none of which were deemed related to the trial intervention. In adult patients without ST elevation, transfer to a cardiac arrest centre following resuscitated cardiac arrest in the community did not reduce deaths. British Heart Foundation.

Results of the CHAOS trial of alpha-tocopherol showed a 75% decrease in non-fatal myocardial infarction in the alpha-tocopherol group, but apparently no effect on mortality. Mitchinson et al discuss more accurate study of deaths and of compliance.

Research on the use of vitamin E in therapy for ischemic heart disease provides conflicting results, but there is good reason to believe that a high dose of vitamin E may prevent myocardial infarction in patients with coronary atherosclerosis.

This study reports the cardiac structure and function of a lifelong male endurance athlete, who has run over 148 000 miles, who presented with symptoms of chest discomfort, dyspnoea and loss of competitive running performance. Importantly, the athlete documented several periods of regular intensive endurance activity while suffering with flu-like symptoms. Cardiovascular MRI demonstrated a pattern of late gadolinium enhancement, which indicated myocardial scarring as a result of previous myocarditis.Myocarditis is a non-ischaemic inflammatory disease of the myocardium associated with cardiac dysfunction and arrhythmogenic substrate. The clinical course of viral myocarditis is mostly insidious with limited cardiac inflammation and dysfunction. However, as in the present case, overwhelming inflammation may occur in a subset of patients leading to myocardial fibrosis due to recurrent inflammation.

Collapse after prolonged endurance exercise is common and usually benign. This case study reports a triathlete who suffered a vaso-vagal associated collapsed after exercise. Misdiagnosis of myocardial injury in the presence of elevated cardiac troponins and ECG anomalies led to inappropriate management and highlights the difficulty in treating the collapsed athlete following arduous exercise.

Mortgage Securitization in Canada: The Context Institutional background The federal government supports housing finance in Canada through mortgage insurance and public securitization programs.3 Federally regulated lenders are required to obtain mortgage insurance on loans in which the homebuyer has made a down payment of less than 20 per cent of the purchase price.4 Mortgage insurance is provided by the Canada Mortgage and Flousing Corporation (CMFIC) and private insurers; insurance from both sources is guaranteed by the government, although not to the same degree.5 In Table 1, we illustrate the interaction between mortgage insurance and securitization in Canada. To reduce taxpayer exposure and encourage development of private mortgage markets, the government announced its intention to prohibit the use of insured mortgages as collateral in non-CMHC securitization vehicles.6 To date, private-label securitization of uninsured mortgages primarily consists of short-term asset-backed commercial paper (ABCP)7 and some longer-term residential mortgage-backed securities (RMBS).

Collapse after prolonged endurance exercise is common and usually benign. This case study reports a triathlete who suffered a vaso-vagal associated collapsed after exercise. Misdiagnosis of myocardial injury in the presence of elevated cardiac troponins and ECG anomalies led to inappropriate management and highlights the difficulty in treating the collapsed athlete following arduous exercise.

This study reports the cardiac structure and function of a lifelong male endurance athlete, who has run over 148 000 miles, who presented with symptoms of chest discomfort, dyspnoea and loss of competitive running performance. Importantly, the athlete documented several periods of regular intensive endurance activity while suffering with flu-like symptoms. Cardiovascular MRI demonstrated a pattern of late gadolinium enhancement, which indicated myocardial scarring as a result of previous myocarditis. Myocarditis is a non-ischaemic inflammatory disease of the myocardium associated with cardiac dysfunction and arrhythmogenic substrate. The clinical course of viral myocarditis is mostly insidious with limited cardiac inflammation and dysfunction. However, as in the present case, overwhelming inflammation may occur in a subset of patients leading to myocardial fibrosis due to recurrent inflammation.

This article describes the ARM Scalable Vector Extension (SVE). Several goals guided the design of the architecture. First was the need to extend the vector processing capability associated with the ARM AArch64 execution state to better address the computational requirements in domains such as high-performance computing, data analytics, computer vision, and machine learning. Second was the desire to introduce an extension that can scale across multiple implementations, both now and into the future, allowing CPU designers to choose the vector length most suitable for their power, performance, and area targets. Finally, the architecture should avoid imposing a software development cost as the vector length changes and where possible reduce it by improving the reach of compiler auto-vectorization technologies. SVE achieves these goals. It allows implementations to choose a vector register length between 128 and 2,048 bits. It supports a vector-length agnostic programming model that lets code run and scale automatically across all vector lengths without recompilation. Finally, it introduces several innovative features that begin to overcome some of the traditional barriers to autovectorization.