Effects of social participation and physical activity on all-cause mortality among older adults in Norfolk, England: an investigation of the EPIC-Norfolk study.

OBJECTIVES: There is growing evidence of an association between social participation and improved physical and mental health among older individuals. The aims of this study were to explore the relationship between self-reported participation in groups, clubs, or organizations and all-cause mortality among older adults and examine the role of physical activity as a potential modifier of the health effects of social participation. STUDY DESIGN: EPIC-Norfolk is a prospective cohort study that recruited 25,639 individuals between the ages of 40 and 79 in Norfolk County, England. This study involved a retrospective analysis of 8623 participants who had returned for the third health check between 2004 and 2011. METHODS: Participants were categorized into those who reported participating socially and those who did not and were stratified by involvement in 0, 1, or 2 or more groups. Cox Proportional Hazards models were constructed to compare all-cause mortality between the groups. Stratum-specific hazard ratios were calculated by physical activity level to assess for effect modification. RESULTS: Of the participants, 861 (9.98%) died during the follow-up period. After adjustment for confounding, social participation was associated with lower all-cause mortality (HR 0.84, 95% CI 0.73-0.97). Involvement in 2 or more groups was associated with lower all-cause mortality (hazard ratio [HR] 0.83, 95% confidence interval [CI] 0.70-0.97), but the association was not statistically significant for people involved in only 1 group (HR 0.86, 95% CI 0.73-1.03). Physical activity appeared to modify the effect of social participation on mortality. CONCLUSIONS: This study's findings provide evidence of an association between social participation and lower all-cause mortality for older adults. They also suggest that the effect of social participation on health is greater for people who are more physically active. Population-level interventions to facilitate social participation may contribute to improving health and wellbeing among older individuals.

Understanding the future research needs in Postural Orthostatic Tachycardia Syndrome (POTS): Evidence mapping the POTS adult literature.

POTS is under diagnosed with an estimated prevalence of 0.2%. North American and Australian researchers, as well as patient groups have called for more research into POTS. However, there has been no comprehensive appraisal of the current POTS evidence base. AIM: To map the POTS evidence base. METHODS: Two reviewers systematically searched 12 databases until July 1st 2019 using the search term "Postural Tachycardia Syndrome" (n = 7280) and categorised the literature. Inclusion criteria included all adult published literature with no language restrictions. 779 papers are analysed and mapped. RESULTS: Seven themes were identified: symptomology and quality of life 16.8% (n = 132), biomedical topics 16.5% (n = 130), co-morbidities 10.3% (n = 81), non-pharmacological management 9.8% (n = 77), aetiologies 6.9% (n = 53), pharmacological management 6.7% (n = 53), and clinical management 6.6% (n = 52). There 45 subthemes. Quality appraisal of the research studies (n = 233) evaluated design, sample size, outcome measures, data analysis and research biases. 74.8% (n = 175) were observational designs and 25.2% (n = 59) were experimental designs (16 using a randomised controlled design, 11 of which had a sample size greater than 21). 47.4% (n = 111) of studies only measured duration of effect for <1 day. 11.5% (n = 27) of studies reported outcomes using an unvalidated subjective measurement tool. CONCLUSION: The volume of adult POTS literature is small and the validity and reliability of the research lacks rigour. The evidence map methodology provides POTS researchers with a benchmark for research thus far. This paper adds an in-depth research appraisal to the broad calls for action, highlighting the pressing need for multicentre, good quality research in POTS, to support guidelines and consensus development in the future.

Effects of left bundle-branch block on cardiac structure, function, perfusion, and perfusion reserve: implications for myocardial contrast echocardiography versus radionuclide perfusion imaging for the detection of coronary artery disease.

BACKGROUND: We aimed to investigate the cardiac effects of left bundle-branch block (LBBB) using myocardial contrast echocardiography (MCE) to ascertain the value of MCE for detecting coronary artery disease (CAD) and to uncover the mechanism that affects the accuracy of single-photon emission computed tomography (SPECT) in these patients. METHODS AND RESULTS: Sixty-three symptomatic LBBB patients (group A), 10 left ventricular ejection fraction-matched control subjects without LBBB and no CAD (group B), and 10 normal control subjects (group C) underwent resting echocardiography. Rest and vasodilator MCE and SPECT were undertaken in LBBB patients. Septal (SW) and posterior wall (PW) thickness, thickening, quantitative myocardial blood flow (MBF), and MBF reserve were measured. SW/PW thickness and percentage thickening ratios were lower (P<0.01 and P<0.05, respectively) in group A compared with both groups B and C, but resting SW/PW MBF and MBF reserve ratios were similar in all 3 groups. MBF reserve but not MBF was reduced in groups A and B (2.2+/-0.7 versus 2.2+/-0.2; P=0.98) compared with group C (3.1+/-0.5; P<0.01). SW thickness was an independent predictor (P=0.006) of SPECT perfusion defects in LBBB patients without CAD. MCE (92%) had a sensitivity similar to SPECT (92%); however, the specificity of MCE (95%) was superior (P<0.0001) to SPECT (47%) for the detection of CAD. CONCLUSIONS: Despite asymmetrical reduction in SW thickness and function, MBF is preserved and MBF reserve is homogeneously reduced in LBBB patients with left ventricular systolic dysfunction. Because of partial volume effects, the accuracy of SPECT for detecting CAD was significantly compromised compared with MCE in this patient cohort.

Diabetes, Obesity and Atrial Fibrillation: Epidemiology, Mechanisms and Interventions.

Body mass index (BMI) is a powerful predictor of death, type 2 diabetes (T2DM) and cardiovascular (CV) morbidity and mortality. Over the last few decades, we have witnessed a global rise in adult obesity of epidemic proportions. Similarly, there has been a parallel increase in the incidence of atrial fibrillation (AF), itself a significant cause of cardiovascular morbidity and mortality. This may be partly attributable to advances in the treatment of coronary heart disease (CHD) and heart failure (HF) improving life expectancy, however, epidemiological studies have demonstrated an independent association between obesity, diabetes and AF, suggesting possible common pathophysiological mechanisms and risk factors. Indeed, cardiac remodeling, haemodynamic alterations, autonomic dysfunction, and diastolic dysfunction have been reported in obese and diabetic cohorts. Moreover, diabetic cardiomyopathy is characterized by an adverse structural and functional cardiac phenotype, which may predispose to the development of AF. In this review, we discuss the pathophysiological and mechanistic relationships between obesity, diabetes and AF, and some of the challenges posed in the management of this high-risk group of individuals.

Obesity, diabetes and atrial fibrillation; epidemiology, mechanisms and interventions.

The last few decades have witnessed a global rise in adult obesity of epidemic proportions. The potential impact of this is emphasized when one considers that body mass index (BMI) is a powerful predictor of death, type 2 diabetes (T2DM) and cardiovascular (CV) morbidity and mortality [1, 2]. Similarly we have witnessed a parallel rise in the incidence of atrial fibrillation (AF), the commonest sustained cardiac arrhythmia, which is also a significant cause of cardiovascular morbidity and mortality. Part of this increase is attributable to advances in the treatment of coronary heart disease (CHD) and heart failure (HF) improving life expectancy and consequently the prevalence of AF. However, epidemiological studies have demonstrated an independent association between obesity and AF, possibly reflecting common pathophysiology and risk factors for both conditions. Indeed, weight gain and obesity are associated with structural and functional changes of the cardiovascular system including left atrial and ventricular remodeling, haemodynamic alterations, autonomic dysfunction, and diastolic dysfunction. Moreover, diabetic cardiomyopathy is characterized by an adverse structural and functional cardiac phenotype which may predispose to the development of AF [3]. In this review, we discuss the pathophysiological and mechanistic relationships between obesity, diabetes and AF, and the challenges posed in the management of this high-risk group of individuals.

Clinico-pathological features of postural hypotension in diabetic autonomic neuropathy.

We report the clinico-pathological features and management of a 49-year-old male with a 30-year history of Type 1 diabetes mellitus who had nephropathy (proteinuria 1.81 g/24 h, creatinine 136 micromol/l), proliferative retinopathy and severe somatic and autonomic neuropathy. A sural nerve biopsy demonstrated marked myelinated fibre loss with unmyelinated fibre degeneration and regeneration combined with extensive endoneurial microangiopathy. The management of the patient's blood pressure problems (supine hypertension) and symptomatic postural hypotension is discussed.