Objective-To determine whether a low ankle brachial pressure index is associated with an increased risk of cardiovascular events and death, and whether the prediction of such events could be improved by including this index.Design-Cohort study. Setting-11 practices in Edinburgh, Scotland. Subjects-1592 men and women aged 55-74 years selected at random from the age-sex registers of 11 general practices and followed up for 5 years.Main outcome measures-Incidence of fatal and non-fatal cardiovascular events and all cause mortality.Results-At baseline 90 (5.7%) of subjects had an ankle brachial pressure index <0.7, 288 (18.2%) had an index 's0.9, and 566 (35.6%) < 1.0. After five years subjects with an index <0.9 at baseline had an increased risk of non-fatal myocardial infarction (relative risk 1.38, 95% confidence interval 0.88 to 2.16), stroke (1.98, 1.05 to 3.77), cardiovascular death (1.85, 1.15 to 2.97), and all cause mortality (1.58, 1.14 to 2.18) after adjustment for age, sex, coronary disease, and diabetes at baseline. The ability to predict subsequent events was greatly increased by combining the index with other risk factors-for example, hypertensive smokers with normal cholesterol concentrations had a positive predictive value of 25.0%, increasing to 43.8% in subjects with a low index and decreasing to 15.6% in those with a normal index.Conclusion-The ankle brachial pressure index is a good predictor of subsequent cardiovascular events, and improves on predictions by conventional risk factors alone. It is simple and accurate and could be included in routine screening of cardiovascular status. IntroductionCoronary heart disease is the main cause of death and disability in elderly people,' and numerous primary and secondary prevention trials have attempted to reduce its impact.2 Important risk factors include hypercholesterolaemia, hypertension, and cigarette smoking,3 and attempts have been made to target those at greatest risk by using scoring systems such as the Dundee method4 or by identifying subjects with early

Background Exercise programmes are a relatively inexpensive, low-risk option compared with other, more invasive therapies for treatment of leg pain on walking (intermittent claudication (IC)). This is the fourth update of a review first published in 1998. Objectives Our goal was to determine whether an exercise programme was effective in alleviating symptoms and increasing walking treadmill distances and walking times in people with intermittent claudication. Secondary objectives were to determine whether exercise was effective in preventing deterioration of underlying disease, reducing cardiovascular events, and improving quality of life. Search methods For this update, the Cochrane Vascular Information Specialist searched the Specialised Register (last searched 15 November 2016) and the Cochrane Central Register of Controlled Trials (CENTRAL; 2016, Issue 10) via the Cochrane Register of Studies Online, along with trials registries. Selection criteria Randomised controlled trials of an exercise regimen versus control or versus medical therapy for people with IC due to peripheral arterial disease (PAD). We included any exercise programme or regimen used for treatment of IC, such as walking, skipping, and running. Inclusion of trials was not affected by duration, frequency, or intensity of the exercise programme. Outcome measures collected included treadmill walking distance (time to onset of pain or pain-free walking distance and maximum walking time or maximum walking distance), ankle brachial index (ABI), quality of life, morbidity, or amputation; if none of these was reported, we did not include the trial in this review. Data collection and analysis For this update (2017), RAL and AH selected trials and extracted data independently. We assessed study quality by using the Cochrane 'Risk of bias' tool. We analysed continuous data by determining mean differences (MDs) and 95% confidence intervals (CIs), and dichotomous data by determining risk ratios (RRs) and 95% CIs. We pooled data using a fixed-effect model unless we identified significant heterogeneity, in which case we used a random-effects model. We used the GRADE approach to assess the overall quality of evidence supporting the outcomes assessed in this review.

Thrombotic risk factors may be important in determining cardiovascular outcome in patients with symptomatic peripheral arterial disease. A cohort study with a 6-year follow-up period was established to determine the relationships between haemostatic and rheological factors and incident ischaemic heart disease (IHD) and stroke events in patients with peripheral arterial disease. A consecutive series of 607 patients with intermittent claudication was examined between 1989 and 1990 at the Peripheral Vascular Clinic, Royal Infirmary of Edinburgh. Main outcome measures were combined fatal and non-fatal stroke, non-fatal myocardial infarction (MI), coronary death and total coronary events. A total of 210 patients died during follow-up. 203 patients did not experience a vascular event or deterioration of limb ischaemia. Median levels of fibrinogen, von Willebrand factor (VWF), tissue plasminogen activator (t-PA) antigen, fibrin D-dimer and whole blood viscosity were significantly higher in those who experienced an event compared with those who did not. After adjusting for age and sex, fibrin D-dimer was significantly associated with risk of non-fatal myocardial infarction (RR 1.50, 95% CI 1.09-2.06, P < or = 0.01). Both fibrinogen and fibrin D-dimer were associated with risk of total coronary events (P < or = 0.05). The risk of stroke was related to baseline levels of t-PA antigen (RR 1.87, 95% CI 1.04-3.34, P < or = 0.05) and whole blood viscosity (RR 1.33, 95% CI 1.07-1.65, P < or = 0.01). All the relationships became weaker and statistically non-significant after further adjustment for cigarette smoking, systolic blood pressure, glucose and baseline IHD. The associations of these factors to IHD and stroke may therefore be partly related to cardiovascular risk factors, but are likely to be important in the pathogenesis of future atherothrombotic events in subjects with peripheral arterial disease.

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