Systematic review and narrative description of the outcomes of group preoperative education before elective major surgery.

Background: Group preoperative education is becoming standard care for patients preparing for surgery, alongside optimisation of exercise, diet, and wellbeing. Although patient education is essential, the effectiveness of group education programmes or 'surgery schools' as a means of delivery is unclear. This review examines whether attending group preoperative education improves patient outcomes. Methods: We systematically reviewed studies of group perioperative education before major elective surgery. Observational or intervention studies with a baseline group or control arm were included. All outcomes reported were collected and, where possible, effect estimates were summarised using random effects meta-analysis. Results: Twenty-seven studies reported on 48 different outcomes after group education. Overall, there was a 0.7 (95% confidence interval 0.27-1.13) day reduction in mean length of stay. The odds ratio for postoperative complications after abdominal surgery was 0.56 (95% confidence interval 0.36-0.85; nine studies). Patient-centred outcomes were grouped into themes. Most studies reported a benefit from group education, but only postoperative physical impairment, pain, knowledge, activation, preoperative anxiety, and some elements of quality of life were statistically significant. Conclusion: This review presents a summary of published evidence available for group preoperative education. While these data lend support for such programmes, there is a need for adequately powered prospective studies to evaluate the effectiveness of preoperative education on clinical outcomes and to evaluate whether behaviour change is sustained. Furthermore, the content, timing and mode of delivery, and evaluation measures of preoperative education require standardisation. Systematic review protocol: PROSPERO (166297).

Frailty in the over 65's undergoing elective surgery (FIT-65) - a three-day study examining the prevalence of frailty in patients presenting for elective surgery.

BACKGROUND: Frailty increases the risk of perioperative complications, length of stay, and the need for assisted-living after discharge. As the UK population ages the number of frail patients presenting for elective surgery in the UK is likely to grow. Despite the potential benefits of early diagnosis, frailty is not uniformly screened for in UK elective surgical patients and its prevalence remains unclear. The primary aim of this study was to assess the prevalence of frailty in patients aged over 65 years undergoing elective surgery. METHODS: We performed a prospective cross-sectional observational study in eight UK hospitals. Data were collected over three consecutive days with follow-up at 30 days. HRA approval was obtained (REC 20/SC/0121) and signed informed consent obtained. Participants were eligible for inclusion if they were 65 years or older and undergoing elective surgery. Pre-operative data were collected from hospital notes by anaesthetic trainees. A member of the research team blinded to the pre-operative dataset screened each participant for frailty pre-operatively using the Reported Edmonton Frail Scale (REFS). Post-operative data were collected from the notes on day of surgery and at 30 days. Participants were defined as "frail" if they scored 8 or more on the REFS. RESULTS: Two hundred twenty eight participants were recruited during the study period of whom 218 proceeded to surgery. There were 103 females and 115 males. Median age was 75 years (interquartile range 70-80). Thirty-seven participants (17.0%) were identified as frail. Frail patients were older, had a higher ASA score, were more likely to have carers and were more likely to be anaemic or present with ECG abnormalities. There were no differences in gender, BMI, place of residence or smoking status for patients identified as frail versus non-frail. There was no difference in length-of-stay between frail and non-frail patients, although those identified as frail were less likely to be discharged to their own home. CONCLUSION: We found the prevalence of frailty in a mixed population of elective surgical patients aged 65 or over to be 17.0%. Furthermore, we found the REFS to be a practical tool for pre-operative frailty screening. Frail patients presented for elective surgery with modifiable co-morbidities which could have been optimised pre-operatively. Early screening could highlight frail patients, allowing time for pre-operative planning and evidence-based optimisations of comorbidities. We therefore encourage the adoption of frailty assessment as a routine part of pre-operative assessment.

Reduced risk of myocardial infarction related to active commuting: inflammatory and haemostatic effects are potential major mediating mechanisms.

BACKGROUND: Regular physical activity is inversely associated with risk of coronary heart disease, but the precise mechanisms remain unclear. Active commuting is an environmental friendly way to achieve the recommended 30 min of daily physical activity. The aim of this study was to explore the relative contribution of markers from different potential mediating pathways on the association between active commuting and risk of myocardial infarction (MI) in a general population. DESIGN: Prospective incident nested case-control study. METHODS: Commuting habits, traditional risk factors and biomarkers were assessed at baseline and compared in 204 MI cases and 327 matched controls. RESULTS: Car commuting was significantly associated with MI risk, even after adjusting for potential confounders (odds ratio: 1.77, 95% confidence interval: 1.05-2.99). When potential mediators were included in the model, the risk was substantially attenuated. Among the traditional risk factors, apolipoprotein B/apolipoprotein A-1 ratio seemed to be the largest mediator (26.0%), followed by body mass index (18.7%). The inflammatory and haemostatic markers similarly dampened the effect, with tissue plasminogen activator/plasminogen activator inhibitor-1 complex and IL-6 explaining 33.6 and 27.6% of MI risk, respectively. Combined, the potential mediators investigated seemed to explain 40.1% of MI risk related to car commuting. CONCLUSION: Overall, the traditional, inflammatory and haemostatic markers seemed to explain a substantial proportion of the reduction in MI risk related to active commuting in this study population. The predominant effect of the inflammatory and haemostatic markers supports the hypothesis that regular physical activity may work through additional biological mechanisms to reduce coronary risk beyond traditional risk factors. However, these findings need to be confirmed in larger studies.

Long-term interleukin-6 levels and subsequent risk of coronary heart disease: two new prospective studies and a systematic review.

BACKGROUND: The relevance to coronary heart disease (CHD) of cytokines that govern inflammatory cascades, such as interleukin-6 (IL-6), may be underestimated because such mediators are short acting and prone to fluctuations. We evaluated associations of long-term circulating IL-6 levels with CHD risk (defined as nonfatal myocardial infarction [MI] or fatal CHD) in two population-based cohorts, involving serial measurements to enable correction for within-person variability. We updated a systematic review to put the new findings in context. METHODS AND FINDINGS: Measurements were made in samples obtained at baseline from 2,138 patients who had a first-ever nonfatal MI or died of CHD during follow-up, and from 4,267 controls in two cohorts comprising 24,230 participants. Correction for within-person variability was made using data from repeat measurements taken several years apart in several hundred participants. The year-to-year variability of IL-6 values within individuals was relatively high (regression dilution ratios of 0.41, 95% confidence interval [CI] 0.28-0.53, over 4 y, and 0.35, 95% CI 0.23-0.48, over 12 y). Ignoring this variability, we found an odds ratio for CHD, adjusted for several established risk factors, of 1.46 (95% CI 1.29-1.65) per 2 standard deviation (SD) increase of baseline IL-6 values, similar to that for baseline C-reactive protein. After correction for within-person variability, the odds ratio for CHD was 2.14 (95% CI 1.45-3.15) with long-term average ("usual") IL-6, similar to those for some established risk factors. Increasing IL-6 levels were associated with progressively increasing CHD risk. An updated systematic review of electronic databases and other sources identified 15 relevant previous population-based prospective studies of IL-6 and clinical coronary outcomes (i.e., MI or coronary death). Including the two current studies, the 17 available prospective studies gave a combined odds ratio of 1.61 (95% CI 1.42-1.83) per 2 SD increase in baseline IL-6 (corresponding to an odds ratio of 3.34 [95% CI 2.45-4.56] per 2 SD increase in usual [long-term average] IL-6 levels). CONCLUSIONS: Long-term IL-6 levels are associated with CHD risk about as strongly as are some major established risk factors, but causality remains uncertain. These findings highlight the potential relevance of IL-6-mediated pathways to CHD.

Increased risk of hospital-acquired foot ulcers in people with diabetes: large prospective study and implications for practice.

AIMS: Diabetes increases the risk of costly and potentially preventable hospital-acquired pressure ulceration. Given that peripheral arterial disease and neuropathy, important risk factors for foot ulceration, are more common in people with diabetes, their risk of hospital-acquired foot ulceration (HAFU) in particular may be even greater. This study aims to determine this risk. METHODS: Using data collected over 2 years from all admissions to the Ipswich Hospital NHS Trust, we conducted a prospective multilevel regression analysis of the risk of HAFU in 5043 admissions of people with diabetes versus 23 599 without diabetes. Patients over 50 years who developed HAFU at least 48 hours after admission were included in analyses. Progressive adjustment for important risk factors and subgroup analyses were conducted to compare patients with and without diabetes. RESULTS: There were significant differences between patients with and without diabetes among a range of covariates including sex, Comorbidity Score, and length of stay (p value <0.001). After progressive adjustment for age, sex, and other risk factors, there persisted a significant increase risk of HAFU in people with diabetes (OR 2.24; 95% CI 1.80 to 2.69). There were no substantial differences between clinically relevant subgroups. CONCLUSIONS: These analyses demonstrate at least a twofold increase in the risk of HAFU in patients with diabetes and suggest further work should focus on specific processes to detect those inpatients with diabetes at increased risk, in whom preventative measures may reduce the prevalence of this costly complication.

Association of apolipoprotein E genotypes with lipid levels and coronary risk.

CONTEXT: Previous reviews of associations of apolipoprotein E (apoE) genotype and coronary disease have been dominated by smaller studies that are liable to biases. OBJECTIVE: To reassess associations of apoE genotypes with circulating lipid levels and with coronary risk. DATA SOURCES: We conducted an updated meta-analysis including both published and previously unreported studies, using MEDLINE, EMBASE, BIOSIS, Science Citation Index, and the Chinese National Knowledge Infrastructure Database published between January 1970 and January 2007, reference lists of articles retrieved, and a registry of relevant studies. STUDY SELECTION: Eighty-two studies of lipid levels (86,067 healthy participants) and 121 studies of coronary outcomes (37,850 cases and 82,727 controls) were identified, with prespecified principal focus on studies with at least 1000 healthy participants for lipids and those with at least 500 coronary outcomes. DATA EXTRACTION: Information on genotype frequencies, lipid levels, coronary outcomes, and laboratory and population characteristics were recorded independently by 2 investigators and/or supplied by study investigators. RESULTS: In the most extreme comparison, people with the epsilon2/epsilon2 genotype had 1.14 mmol/L (95% confidence interval [CI], 0.87-1.40 mmol/L [44.0 mg/dL; 95% CI; 33.6-51.1 mg/dL]) or about 31% (95% CI, 23%-38%) lower mean low-density lipoprotein cholesterol (LDL-C) values than those with the epsilon4/epsilon4 genotype. There were approximately linear relationships of apoE genotypes (when ordered epsilon2/epsilon2, epsilon2/epsilon3, epsilon2/epsilon4, epsilon3/epsilon3, epsilon3/epsilon4, epsilon4/epsilon4) with LDL-C and with coronary risk. The relationship with high-density lipoprotein cholesterol was inverse and shallow and that with triglycerides was nonlinear and largely confined to the epsilon2/epsilon2 genotype. Compared with epsilon3/epsilon3, the odds ratio for coronary disease was 0.80 (95% CI, 0.70-0.90) in epsilon2 carriers and was 1.06 (95% CI, 0.99-1.13) in epsilon4 carriers. CONCLUSIONS: There are approximately linear relationships of apoE genotypes with both LDL-C levels and coronary risk. Compared with individuals with the epsilon3/epsilon3 genotype, epsilon2 carriers have a 20% lower risk of coronary heart disease and epsilon4 carriers have a slightly higher risk.

Haemostatic and inflammatory markers are independently associated with myocardial infarction in men and women.

INTRODUCTION: Previous studies have shown that plasma levels of haemostatic and inflammatory markers are associated with risk of coronary heart disease (CHD). As haemostatic markers are also acute-phase reactants, it is not clear if their association with CHD is independent of inflammatory markers and established cardiovascular risk factors. MATERIALS AND METHODS: We used a prospective incident case-control study design nested in two cohorts from Sweden. Baseline measurements of a panel of cardiovascular risk factors and eight established markers of haemostasis or inflammation were assessed in 469 first-ever myocardial infarction (MI) cases and 895 matched controls. RESULTS: After adjustment for baseline values of established risk factors, von Willebrand factor appeared to have the strongest association with MI among the haemostatic markers assayed, with an odds ratio of 2.52 (95% CI, 1.72-3.67) for a comparison of individuals in extreme thirds of baseline levels. For a similar comparison, after adjustment for established risk factors and haemostatic markers, odds ratios for IL-6 and CRP were 1.67 (95% CI, 1.08-2.60) and 1.58 (95% CI, 1.03-2.41), respectively. The relative predictive ability of the individual markers over and above established risk factors was modest according to comparisons of Area under the Receiver Operating Characteristic (AUROC) curves. However, when all eight markers were combined in a single model, the AUROC curve was significantly increased to 0.820 (95% CI, 0.795-0.846) compared to 0.762 (95% CI, 0.732-0.791) for established risk factors only. CONCLUSIONS: These findings suggest that haemostasis and inflammation have at least partially separate roles in risk of myocardial infarction.

Coronary heart disease.

Until recently, the potential relevance of genetic, biochemical and lifestyle factors to coronary heart disease have been studied in relative isolation from one another. Although this approach has yielded some major insights, it has resulted in a fragmented and incomplete understanding of the relative importance and interplay of nature and nurture in the development of coronary risk. New opportunities for more integrated, powerful and comprehensive approaches have been opened by major developments, including: establishment, collation and maturation of relevant population bioresources; emergence of technologies that enable rapid and accurate assessment of many genetic and biochemical factors, without necessitating assumptions about biological mechanisms; and advances in statistical analytical methods. This chapter provides a critical review of the strengths and limitations of established and emerging epidemiological approaches to the study of the separate and combined effects of genetic, biochemical and lifestyle factors in coronary heart disease.

A systematic review of randomised controlled trials of interventions promoting effective condom use.

BACKGROUND: Effective condom use can prevent sexually transmitted infections (STIs) and unwanted pregnancy. We conducted a systematic review and methodological appraisal of randomised controlled trials (RCTs) of interventions to promote effective condom use. METHODS: We searched for all RCTs of interventions to promote effective condom use using the Cochrane Infectious Diseases Group's trials register (Oct 2006), CENTRAL (Issue 4, 2006), MEDLINE (1966 to Oct 2006), EMBASE (1974 to Oct 2006), LILACS (1982 to Oct 2006), IBSS (1951 to Oct 2006) and Psychinfo (1996 to Oct 2006). We extracted data on allocation sequence, allocation concealment, blinding, loss to follow-up and measures of effect. Effect estimates were calculated. RESULTS: We identified 139 trials. Seven out of ten trials reported reductions in 'any STI' with five statistically significant results. Three out of four trials reported reductions in pregnancy, although none was statistically significant. Only four trials met all the quality criteria. Trials reported a median of 11 (IQR 7-17) outcome measures. Few trials used the same outcome measure. Altogether, 10 trials (7%) used the outcome 'any STI', 4 (3%) self-reported pregnancy and 22 (16%) used 'condom use at last sex'. CONCLUSIONS: The results are generally consistent with modest benefits but there is considerable potential for bias due to poor trial quality. Because of the low proportion of trials using the same outcome the potential for bias from selective reporting of outcomes is considerable. Despite the public health importance of increasing condom use there is little reliable evidence on the effectiveness of condom promotion interventions.

Association between C reactive protein and coronary heart disease: mendelian randomisation analysis based on individual participant data.

OBJECTIVE: To use genetic variants as unconfounded proxies of C reactive protein concentration to study its causal role in coronary heart disease. DESIGN: Mendelian randomisation meta-analysis of individual participant data from 47 epidemiological studies in 15 countries. PARTICIPANTS: 194 418 participants, including 46 557 patients with prevalent or incident coronary heart disease. Information was available on four CRP gene tagging single nucleotide polymorphisms (rs3093077, rs1205, rs1130864, rs1800947), concentration of C reactive protein, and levels of other risk factors. MAIN OUTCOME MEASURES: Risk ratios for coronary heart disease associated with genetically raised C reactive protein versus risk ratios with equivalent differences in C reactive protein concentration itself, adjusted for conventional risk factors and variability in risk factor levels within individuals. RESULTS: CRP variants were each associated with up to 30% per allele difference in concentration of C reactive protein (P<10(-34)) and were unrelated to other risk factors. Risk ratios for coronary heart disease per additional copy of an allele associated with raised C reactive protein were 0.93 (95% confidence interval 0.87 to 1.00) for rs3093077; 1.00 (0.98 to 1.02) for rs1205; 0.98 (0.96 to 1.00) for rs1130864; and 0.99 (0.94 to 1.03) for rs1800947. In a combined analysis, the risk ratio for coronary heart disease was 1.00 (0.90 to 1.13) per 1 SD higher genetically raised natural log (ln) concentration of C reactive protein. The genetic findings were discordant with the risk ratio observed for coronary heart disease of 1.33 (1.23 to 1.43) per 1 SD higher circulating ln concentration of C reactive protein in prospective studies (P=0.001 for difference). CONCLUSION: Human genetic data indicate that C reactive protein concentration itself is unlikely to be even a modest causal factor in coronary heart disease.