Atherosclerotic vascular diseases (peripheral arterial disease (PAD), coronary artery disease (CAD) and cerebrovascular disease (CVD)) are leading causes of global morbidity and mortality. While manifesting in different vascular territories, these diseases all share the common pathophysiological process of atherothrombosis. Given the overlap that exists between these different territories, once atherosclerosis is established in one territory, risk factor modification is vital for the secondary prevention of cardiovascular events. Hypertension is the most common cardiovascular risk factor, as well as a risk factor for atherosclerosis. The mechanisms by which it contributes to this have not been fully elucidated but include abnormalities in platelet activation and fibrinolysis, endothelial cell dysfunction and abnormal levels of haemostatic factors. Hypertension perhaps exerts similar effects on the arterial wall to hyperlipidaemia. For example, the increase in oxidative stress, common in both conditions, may activate genes involved in generating an inflammatory response that in the presence of hyperlipidaemia leads to the formation of atherosclerotic plaques. In hypertension, there is an increase in mean arterial pressure and total peripheral resistance reflecting a reduction in arteriolar calibre. With it there is also an increase in arterial stiffness, resulting in changes in amplitude of pulse pressure waves and timing of central wave reflections. Several components of blood pressure (BP), including systolic BP (SBP), diastolic BP (DBP) and pulse pressure, have been reported to be independent cardiovascular risk factors. The risk of cardiovascular disease increases progressively and continuously with increases in SBP and DBP independent of other risk factors; in particular, increased SBP levels are more important than increased DBP. Peripheral arterial disease and hypertension are associated diseases with 35–55% of patients with PAD also having hypertension at presentation. In PAD, hypertension is a risk factor for the development of both asymptomatic and symptomatic disease. A recent study on Chinese hypertensives found that SBP, but not DBP, was an independent risk factor for low ankle–brachial pressure index and that low ankle–brachial pressure index in these patients was associated with higher all cause and cardiovascular mortality. Increased systolic hypertension is more frequently observed in patients with cerebrovascular complications, including both ischaemic and haemorrhagic stroke. Treating hypertension is therefore extremely important in the secondary prevention of cardiovascular complications. The antihypertensive of choice may also differ according to the dominant site of vascular disease as different drug classes are more efficient at preventing either cardiovascular or cerebrovascular complications. In this issue of the Journal of Human Hypertension, Safar et al. report the associations between different forms of hypertension (isolated systolic hypertension (ISH), systolic–diastolic hypertension) with cardiovascular disease in different vascular territories as part of the ATTEST study. This relationship has been poorly evaluated in the past, and the ATTEST study comprised 37.6% isolated PAD, 37.6% PAD with associated CAD and/or CVD and 24.8% CAD/CVD without PAD, reflecting the participant selection methods of the study (notably, two patients with PAD selected for every patient with CAD/CVD identified from general practice registers). The ATTEST study reported ISH to be the most prevalent form of hypertension, overall suggesting that this may be an important factor for consideration in the secondary prevention of cardiovascular complications. In the cohort of isolated PAD, ISH was more prevalent than systolic–diastolic hypertension, as opposed to the CAD/CVD cohort in whom the latter form was more prevalent. Safar et al. also report that all cardiovascular risk factors Correspondence: PC Bennett, University Department of Medicine, City Hospital, Birmingham B18 7QH, UK. E-mail: philip.bennett@doctors.org.uk Published online 16 October 2008 Journal of Human Hypertension (2009) 23, 213–215 & 2009 Macmillan Publishers Limited All rights reserved 0950-9240/09 $32.00