Higher anticholinergic burden from medications is associated with significant increase in markers of inflammation in the EPIC-Norfolk prospective population-based cohort study

BackgroundHigher medication anticholinergic burden is associated with increased risk of cardiovascular disease and cognitive decline. A mechanistic pathway has not been established. We aimed to determine whether inflammation may mediate these associations.MethodsParticipants were drawn from the European Prospective Investigation into Cancer, Norfolk cohort (40-79 years at baseline). Anticholinergic burden score (ACB) was calculated at first (1HC) (1993/97) and second (2HC) (1998/2000) health checks. Fibrinogen and C-reactive protein (CRP) were measured during 1HC and Tumour Necrosis Factor alpha (TNF-a) and interleukin 6 (IL-6) during 2HC. Cross-sectional associations between ACB and inflammatory markers were examined for both health checks. Prospective associations were also examined between 1HC ACB and 2HC inflammatory markers. Models were adjusted for age, sex, lifestyle factors, co-morbidities and medications.Results17,678 and 22,051 participants were included in cross-sectional analyses for CRP, and fibrinogen, respectively. 5,101 participants with data on TNF-a and IL-6 were included in the prospective analyses. Cross-sectionally, compared to ACB=0, ACB =4 was associated with higher fibrinogen, beta (95% confidence interval)=0.134 g/l (0.070, 0.199), CRP 1.175 mg/l (0.715, 1.634), IL-6 0.593 pg/ml (0.254, 0.932) and TNF-a 0.137 pg/ml (0.033, 0.241). Furthermore, a point increase in ACB was associated with a higher levels of all markers. Prospectively, compared to ACB=0, ACB =4 was associated with higher IL-6(pg/ml): 0.019 (-0.323, 0.361) and TNF-a (pg/ml): 0.202% (0.81, 0.323). In addition, a unit increase in ACB was associated with a significantly higher TNF-a and IL-6.ConclusionHigher ACB was associated with higher inflammatory markers. Inflammation may mediate the relationship between anticholinergic medications and adverse outcomes

Long‑term risk of stroke following percutaneous coronary intervention : can we predict the future and can we change it?

Peer reviewedPublisher PD

Association between osteoarthritis and cardiovascular disease: systematic review and meta-analysis

Background: To examine for a possible relationship between osteoarthritis and cardiovascular disease (CVD). Design: A systematic review and meta-analysis Methods: Published and unpublished literature from: MEDLINE, EMBASE, CINAHL, the Cochrane Library, OpenGrey and clinical trial registers. Search to 22nd November 2014. Cohort, case-control, randomised and non-randomised controlled trial papers reporting the prevalence of CVD in osteoarthritis were included. Results: Fifteen studies with 32,278,744 individuals were eligible. Pooled prevalence for overall CVD pathology in people with osteoarthritis was 38.4% (95% Confidence interval (CI): 37.2% to 39.6%). Individuals with osteoarthritis were almost three times as likely to have heart failure (Relative Risk (RR): 2.80; 95% CI: 2.25 to 3.49) or ischaemic heart disease (RR: 1.78; 95% CI: 1.18 to 2.69) compared to matched non-osteoarthritis cohorts. No significant difference was detected between the two groups for the risk of experiencing myocardial infarction or stroke. There was a three-fold decrease in the risk of experiencing a transient ischaemic attack in the osteoarthritis cohort compared to the non-osteoarthritis group. Conclusions: Prevalence of CVD in patients with OA is significant. There was an observed increased risk of incident heart failure and ischaemic heart disease in people with OA compared to matched controls. However the relationship between OA and CVD is not straight-forward and there is a need to better understand the potential common pathways linking pathophysiological mechanisms

Substantial decline in hospital admissions for heart failure accompanied by increased community mortality during COVID-19 pandemic

Aims We hypothesized that a decline in admissions with heart failure during COVID-19 pandemic would lead to a reciprocal rise in mortality for patients with heart failure in the community.Methods and results We used National Heart Failure Audit data to identify 36 974 adults who had a hospital admission with a primary diagnosis of heart failure between February and May in either 2018, 2019, or 2020. Hospital admissions for heart failure in 2018/19 averaged 160/day but were much lower in 2020, reaching a nadir of 64/day on 27 March 2020 [incidence rate ratio (IRR): 0.40, 95% confidence interval (CI): 0.38-0.42]. The proportion discharged on guideline-recommended pharmacotherapies was similar in 2018/19 compared to the same period in 2020. Between 1 February-2020 and 31 May 2020, there was a 29% decrease in hospital deaths related to heart failure (IRR: 0.71, 95% CI: 0.67-0.75; estimated decline of 448 deaths), a 31% increase in heart failure deaths at home (IRR: 1.31, 95% CI: 1.24-1.39; estimated excess 539), and a 28% increase in heart failure deaths in care homes and hospices (IRR: 1.28, 95% CI: 1.18-1.40; estimated excess 189). All-cause, inpatient death was similar in the COVID-19 and pre-COVID-19 periods [odds ratio (OR): 1.02, 95% CI: 0.94-1.10]. After hospital discharge, 30-day mortality was higher in 2020 compared to 2018/19 (OR: 1.57, 95% CI: 1.38-1.78).Conclusion Compared with the rolling daily average in 2018/19, there was a substantial decline in admissions for heart failure but an increase in deaths from heart failure in the community. Despite similar rates of prescription of guideline-recommended therapy, mortality 30 days from discharge was higher during the COVID-19 pandemic period

Prognosis of Acute Ischaemic Stroke Patients with Cancer : A National Inpatient Sample Study

Acknowledgments: We thank Jesus Perdomo-Lampignano, MB ChB for his assistance with the figures. We also acknowledge the HCUP Data Partners (https://www.hcup-s.ahrq.gov/db/hcupdatapartners. jsp—accessed on 30 January 2021)Peer reviewedPublisher PD

Excess mortality in England and Wales during the first wave of the COVID-19 pandemic

Background Deaths during the COVID-19 pandemic result directly from infection and exacerbation of other diseases and indirectly from deferment of care for other conditions, and are socially and geographically patterned. We quantified excess mortality in regions of England and Wales during the pandemic, for all causes and for non-COVID-19-associated deaths. Methods Weekly mortality data for 1 January 2010 to 1 May 2020 for England and Wales were obtained from the Office of National Statistics. Mean-dispersion negative binomial regressions were used to model death counts based on pre-pandemic trends and exponentiated linear predictions were subtracted from: (i) all-cause deaths and (ii) all-cause deaths minus COVID-19 related deaths for the pandemic period (week starting 7 March, to week ending 8 May). Findings Between7Marchand8May2020,therewere 47 243 (95% CI: 46 671 to 47 815) excess deaths in England and Wales, of which 9948 (95% CI: 9376 to 10 520) were not associated with COVID-19. Overall excess mortality rates varied from 49 per 100 000 (95% CI: 49 to 50) in the South West to 102 per 100 000 (95% CI: 102 to 103) in London. Non-COVID-19 associated excess mortality rates ranged from −1 per 100 000 (95% CI: −1 to 0) in Wales (ie, mortality rates were no higher than expected) to 26 per 100 000 (95% CI: 25 to 26) in the West Midlands. Interpretation The COVID-19 pandemic has had markedly different impacts on the regions of England and Wales, both for deaths directly attributable to COVID-19 infection and for deaths resulting from the national public health response

Effect of age on the prognostic value of left ventricular function in patients with acute coronary syndrome:a prospective registry study

Objective: This study aims to study the prognostic impact of LV function on mortality and examine the effect of age on the prognostic value of left ventricular function.  Methods: We examined the Myocardial Ischaemia National Audit Project (MINAP) registry (2006-2010) data with a mean follow up of 2.1 years. LV function was categorized into good (ejection fraction (EF) ≥50%), moderate (EF 30-49%) and poor (EF <30%) categories. Cox-proportional hazards models were constructed to examine the prognostic significance of LV function in different age groups (<65, 65-74, 75-84 and ≥85 years) on all-cause mortality adjusting for baseline variables.  Results: Of 424,848 patients, LV function data available for 123,609. Multiple imputations were used to impute missing values of LV function and the final sample for analyses were drawn from 414,305. After controlling for confounders, 339,887 participants were included in the regression models. For any age group, mortality was higher with worsening degree of LV impairment. Increased age reduced the adverse prognosis associated with reduced LV function (hazard ratios (HRs) of death comparing poor LV function to good LV function were 2.11 95%CI 1.88-2.37 for age <65 years and 1.28 95%CI 1.20-1.36 for age ≥85 years. Older patients had a high mortality risk even in those with good LV function. HRs of mortality for ≥85 compared to <65 years (HR=1.00) within good, moderate and poor ejection fractions groups were 5.89, 4.86 and 3.43, respectively.  Conclusions: In patients with ACS, clinicians should interpret the prognostic value of LV function taking into account patient’s age

Outcomes in patients with acute and stable coronary syndromes: insights from the prospective NOBORI-2 study

BACKGROUND: Contemporary data remains limited regarding mortality and major adverse cardiac events (MACE) outcomes in patients undergoing PCI for different manifestations of coronary artery disease. OBJECTIVES: We evaluated mortality and MACE outcomes in patients treated with PCI for STEMI (ST-elevation myocardial infarction), NSTEMI (non ST-elevation myocardial infarction) and stable angina through analysis of data derived from the Nobori-2 study. METHODS: Clinical endpoints were cardiac mortality and MACE (a composite of cardiac death, myocardial infarction and target vessel revascularization). RESULTS: 1909 patients who underwent PCI were studied; 1332 with stable angina, 248 with STEMI and 329 with NSTEMI. Age-adjusted Charlson co-morbidity index was greatest in the NSTEMI cohort (3.78±1.91) and lowest in the stable angina cohort (3.00±1.69); P<0.0001. Following Cox multivariate analysis cardiac mortality was independently worse in the NSTEMI vs the stable angina cohort (HR 2.31 (1.10-4.87), p = 0.028) but not significantly different for STEMI vs stable angina cohort (HR 0.72 (0.16-3.19), p = 0.67). Similar observations were recorded for MACE (<180 days) (NSTEMI vs stable angina: HR 2.34 (1.21-4.55), p = 0.012; STEMI vs stable angina: HR 2.19 (0.97-4.98), p = 0.061. CONCLUSIONS: The longer-term Cardiac mortality and MACE were significantly worse for patients following PCI for NSTEMI even after adjustment of clinical demographics and Charlson co-morbidity index whilst the longer-term prognosis of patients following PCI STEMI was favorable, with similar outcomes as those patients with stable angina following PCI

A review of interventions to improve clinical outcomes following hospitalisation for heart failure

Heart failure (HF) is a leading cause of hospitalisation and death among older adults in high-income countries. HF is often accompanied by comorbid conditions, and patients hospitalised for HF commonly die or are readmitted in the weeks follow- ing hospital discharge. The objectives of this paper are to discuss the burden of HF hospitalisations in healthcare systems and to review strategies that reduce hospitalisations and death in this condition

In-hospital Outcomes of Acute Ischaemic Stroke Patients with Atrial Septal Defect. : A National Inpatient Sample Study.

Acknowledgements We would like to acknowledge the HCUP Data Partners (https://www.hcup10 us.ahrq.gov/db/hcupdatapartners.jsp). Sources of Funding FC received the Leslie Wilson Endowed Scholarship as a part of the Aberdeen Summer Research Scholarship Programme of the Aberdeen Clinical Academic Training (ACAT) Pathways. The Leslie Wilson Endowed Scholarship is funded by Department of Medicine for the Elderly, NHS Grampian.Peer reviewedPostprin