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ObjectiveTo determine whether there were inequalities in the sustained rise in infant mortality in England in recent years and the contribution of rising child poverty to these trends.DesignThis is an analysis of trends in infant mortality in local authorities grouped into five categories (quintiles) based on their level of income deprivation. Fixed-effects regression models were used to quantify the association between regional changes in child poverty and regional changes in infant mortality.Setting324 English local authorities in 9 English government office regions.ParticipantsLive-born children under 1 year of age.Main outcome measureInfant mortality rate, defined as the number of deaths in children under 1 year of age per 100 000 live births in the same year.ResultsThe sustained and unprecedented rise in infant mortality in England from 2014 to 2017 was not experienced evenly across the population. In the most deprived local authorities, the previously declining trend in infant mortality reversed and mortality rose, leading to an additional 24 infant deaths per 100 000 live births per year (95% CI 6 to 42), relative to the previous trend. There was no significant change from the pre-existing trend in the most affluent local authorities. As a result, inequalities in infant mortality increased, with the gap between the most and the least deprived local authority areas widening by 52 deaths per 100 000 births (95% CI 36 to 68). Overall from 2014 to 2017, there were a total of 572 excess infant deaths (95% CI 200 to 944) compared with what would have been expected based on historical trends. We estimated that each 1% increase in child poverty was significantly associated with an extra 5.8 infant deaths per 100 000 live births (95% CI 2.4 to 9.2). The findings suggest that about a third of the increases in infant mortality between 2014 and 2017 can be attributed to rising child poverty (172 deaths, 95% CI 74 to 266).ConclusionThis study provides evidence that the unprecedented rise in infant mortality disproportionately affected the poorest areas of the country, leaving the more affluent areas unaffected. Our analysis also linked the recent increase in infant mortality in England with rising child poverty, suggesting that about a third of the increase in infant mortality from 2014 to 2017 may be attributed to rising child poverty.

Sudden cardiac death (SCD) remains an unsolved problem in the twenty-first century. It is often due to rapid onset, ventricular arrhythmias caused by a number of different clinical conditions. A proportion of SCD patients have identifiable diseases such as cardiomyopathies, but for others, the causes are unknown. Viral myocarditis is becoming increasingly recognized as a contributor to unexplained mortality, and is thought to be a major cause of SCD in the first two decades of life. Myocardial inflammation, ion channel dysfunction, electrophysiological, and structural remodeling may play important roles in generating life-threatening arrhythmias. The aim of this review article is to examine the electrophysiology of action potential conduction and repolarization and the mechanisms by which their derangements lead to triggered and reentrant arrhythmogenesis. By synthesizing experimental evidence from pre-clinical and clinical studies, a framework of how host (inflammation), and viral (altered cellular signaling) factors can induce ion electrophysiological and structural remodeling is illustrated. Current pharmacological options are mainly supportive, which may be accompanied by mechanical circulatory support. Heart transplantation is the only curative option in the worst case scenario. Future strategies for the management of viral myocarditis are discussed.

Diabetes is a common endocrine disorder with an ever increasing prevalence globally, placing significant burdens on our healthcare systems. It is associated with significant cardiovascular morbidities. One of the mechanisms by which it causes death is increasing the risk of cardiac arrhythmias. The aim of this article is to review the cardiac (ion channel abnormalities, electrophysiological and structural remodelling) and extracardiac factors (neural pathway remodelling) responsible for cardiac arrhythmogenesis in diabetes. It is concluded by an outline of molecular targets for future antiarrhythmic therapy for the diabetic population.