Proximal Sessile Serrated Adenomas Are More Prevalent in Caucasians, and Gastroenterologists Are Better Than Nongastroenterologists at Their Detection

Background and Aim. Proximal sessile serrated adenomas (PSSA) leading to colorectal cancer (CRC) represent an alternate pathway for CRC development. In this study, we aim to determine the prevalence of PSSAs and the impact of patient, colonoscopy, and endoscopist-related factors on PSSA detection. Methods. Patients ≥ 50 years of age undergoing a screening colonoscopy between 2012 and 2014 were included. Detection rates based on patient gender, race, colonoscopy timing, fellow participation, bowel preparation quality, and specialty of the endoscopist were calculated. t-tests were used to compare detection rates and a multivariate-adjusted analysis was performed. Results. 140 PSSAs were detected from 4151 colonoscopies, with a prevalence of 3.4%. Detection rate was higher in Caucasians compared to African-Americans (AA) (3.7 ± 4.1 versus 0.96 ± 3.5; p<0.001). Gastroenterologists detected more PSSAs compared to nongastroenterologists (3.9 ± 3.5 versus 2.2 ± 3.0; p=0.028). These findings were still significant after adjusted multivariate analysis. The rest of the factors did not make significant difference in PSSA detection rate. Conclusions. PSSAs are more prevalent in Caucasians compared to AAs. Racial difference in prevalence of PSSAs is intriguing and warrants further investigation. Gastroenterologists have a significantly higher PSSADR compared to nongastroenterologists. Educational measures should be implemented in nongastroenterologists to improve their PSSA detection rates

Mapping 123 million neonatal, infant and child deaths between 2000 and 2017

Since 2000, many countries have achieved considerable success in improving child survival, but localized progress remains unclear. To inform efforts towards United Nations Sustainable Development Goal 3.2—to end preventable child deaths by 2030—we need consistently estimated data at the subnational level regarding child mortality rates and trends. Here we quantified, for the period 2000–2017, the subnational variation in mortality rates and number of deaths of neonates, infants and children under 5 years of age within 99 low- and middle-income countries using a geostatistical survival model. We estimated that 32% of children under 5 in these countries lived in districts that had attained rates of 25 or fewer child deaths per 1,000 live births by 2017, and that 58% of child deaths between 2000 and 2017 in these countries could have been averted in the absence of geographical inequality. This study enables the identification of high-mortality clusters, patterns of progress and geographical inequalities to inform appropriate investments and implementations that will help to improve the health of all populations

Global, regional, and national burden of neurological disorders, 1990–2016 : a systematic analysis for the Global Burden of Disease Study 2016

Background: Neurological disorders are increasingly recognised as major causes of death and disability worldwide. The aim of this analysis from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2016 is to provide the most comprehensive and up-to-date estimates of the global, regional, and national burden from neurological disorders. Methods: We estimated prevalence, incidence, deaths, and disability-adjusted life-years (DALYs; the sum of years of life lost [YLLs] and years lived with disability [YLDs]) by age and sex for 15 neurological disorder categories (tetanus, meningitis, encephalitis, stroke, brain and other CNS cancers, traumatic brain injury, spinal cord injury, Alzheimer's disease and other dementias, Parkinson's disease, multiple sclerosis, motor neuron diseases, idiopathic epilepsy, migraine, tension-type headache, and a residual category for other less common neurological disorders) in 195 countries from 1990 to 2016. DisMod-MR 2.1, a Bayesian meta-regression tool, was the main method of estimation of prevalence and incidence, and the Cause of Death Ensemble model (CODEm) was used for mortality estimation. We quantified the contribution of 84 risks and combinations of risk to the disease estimates for the 15 neurological disorder categories using the GBD comparative risk assessment approach. Findings: Globally, in 2016, neurological disorders were the leading cause of DALYs (276 million [95% UI 247–308]) and second leading cause of deaths (9·0 million [8·8–9·4]). The absolute number of deaths and DALYs from all neurological disorders combined increased (deaths by 39% [34–44] and DALYs by 15% [9–21]) whereas their age-standardised rates decreased (deaths by 28% [26–30] and DALYs by 27% [24–31]) between 1990 and 2016. The only neurological disorders that had a decrease in rates and absolute numbers of deaths and DALYs were tetanus, meningitis, and encephalitis. The four largest contributors of neurological DALYs were stroke (42·2% [38·6–46·1]), migraine (16·3% [11·7–20·8]), Alzheimer's and other dementias (10·4% [9·0–12·1]), and meningitis (7·9% [6·6–10·4]). For the combined neurological disorders, age-standardised DALY rates were significantly higher in males than in females (male-to-female ratio 1·12 [1·05–1·20]), but migraine, multiple sclerosis, and tension-type headache were more common and caused more burden in females, with male-to-female ratios of less than 0·7. The 84 risks quantified in GBD explain less than 10% of neurological disorder DALY burdens, except stroke, for which 88·8% (86·5–90·9) of DALYs are attributable to risk factors, and to a lesser extent Alzheimer's disease and other dementias (22·3% [11·8–35·1] of DALYs are risk attributable) and idiopathic epilepsy (14·1% [10·8–17·5] of DALYs are risk attributable). Interpretation: Globally, the burden of neurological disorders, as measured by the absolute number of DALYs, continues to increase. As populations are growing and ageing, and the prevalence of major disabling neurological disorders steeply increases with age, governments will face increasing demand for treatment, rehabilitation, and support services for neurological disorders. The scarcity of established modifiable risks for most of the neurological burden demonstrates that new knowledge is required to develop effective prevention and treatment strategies. Funding: Bill & Melinda Gates Foundation

Acute-Onset Heart Failure Secondary to Biventricular Non-Compaction Cardiomyopathy and Atrial Septal Defect in a Woman Presenting in the Seventh Decade

We present a case of a previously asymptomatic 63-year-old woman who presented with worsening dyspnoea for 3 weeks. Initial transthoracic and later transoesophageal echocardiography confirmed biventricular non-compaction cardiomyopathy and a large secundum atrial septal defect (ASD) measuring 1.4 cm. Additionally, there was a haemodynamically significant left to right shunt causing acute decompensated systolic heart failure. She eventually underwent closure of the septal defect using a AMPLATZER Septal Occluder device. Decision to close the defect was made as the left to right shunt was causing severe pulmonary hypertension and acute heart failure. Since most heart failure treatments involve lowering of the LV afterload there was consideration that this could cause right to left shunting and could cause an Eisenmenger physiology. Hence the AMPLATZER Septal Occluder device was placed to eliminate the shunt through the ASD. The ASD combined with the non-compaction posed significant treatment challenge in this case

Devices and interventions for the prevention of adverse outcomes of tachycardia on heart failure

Heart failure (HF) is the leading cause of hospitalization in the USA. Despite advances in pharmacologic management, the incidence of HF is on the rise and survivability is persistently reduced. Sympathetic overdrive is implicated in the pathophysiology of HF, particularly HF with reduced ejection fraction (HFrEF). Tachycardia can be particularly deleterious and thus has spurred significant investigation to mitigate its effects. Various modalities including vagus nerve stimulation, baroreceptor activation therapy, spinal cord stimulation, renal sympathetic nerve denervation, left cardiac sympathetic denervation, and carotid body removal will be discussed. However, the effects of these modalities on tachycardia and its outcomes in HFrEF have not been well-studied. Further studies to characterize this are necessary in the future