The Ankle-brachial index (ABI) is the ratio between systolic pressure on ankle and arm. It is the basic and simplest technique for the detection of arterial occlusive disease of the lower limbs.
In healthy subjects in the lying position, ankle-pressure is equal to or a little bit higher than arm pressure and therefore ABI is equal or higher than 1.0.
An ABI of 0.9 or less has been accepted as a cut-off level that indicates vascular disease both, in clinical practice and in epidemiological studies.
ABI inversely correlates with PAD-progression and its values are related to clinical stages of PAD. Therefore, ABI is a non-invasive method to assess the patency of the lower extremity arterial system and to detect the presence of arterial occlusive disease.
It is a very specific test for the detection of PAD. Its sensitivity and specificity are very high – they are about 90% accountable.
The technique fails only in some diabetic patients in whom, due to medial classification, peripheral arteries are not compressible and ankle pressures are falsely high and therefore the ankle-brachial index does not show real haemodynamic conditions as well (1).
At least as important as the usefulness of ABI in assessing clinical PAD is the ability to detect preclinical atherosclerosis, using this technique. Namely there is a large group of people in the elderly population who are without any symptoms of PAD, but who have low ABIs (usually 0.75 - 0.9) . Their low ABIs indicate the presence of atherosclerotic disease, which, significantly worsenes their prognosis.
In contrast to other techniques used for the detection of very early – preclinical stages of atherosclerosis, like intima-media thickness and endothelial dysfunction measurement, the pathological ABI shows advanced disease. Atherosclerotic lesions namely cause haemodynamic disturbances with blood pressure decreases in distal regions, from the moment that vessel lumen is reduced by more than 50% or 70%.
On top of the diagnostic value of ABI for screening of PAD (preclinical or clinical), ABI is also accepted as a risk-assessment tool. An ABI of < 0.9 has shown to be a strong predictor of total and cardiovascular morbidity and mortality in those without prior history of clinical cardiovascular disease at the base-line examination (2).
PAD, as measured by progressive decrements in ABI, was associated with the stepwise increase in cardiovascular risk factor levels as well as with the prevalence of myocardial infarction, stroke and congestive heart failure (3).
In the Cardiovascular Health-Study (CHS) the association of ABI with cardiovascular events was strong, regardless of the presence or absence of other risk factors. The risk for incident congestive heart-failure and for total mortality with low ABI remains significantly elevated after the adjustment to cardiovascular risk factors.
In patients with a previous myocardial infarction or stroke, and in patients preferred for coronary angiography, the occurrence of peripheral arterial disease has been shown to increase their risk further (4).
Additionally, data has shown that clinical, but also the preclinical stages of PAD characterised by a border-line decrease in ABI are related to a higher risk of cardiovascular incidents when compared to subjects with normal ABI.
Criqui with co-workers first illustrated that the risk is markedly increased, even in subjects with preclinical PAD (5).
In the Heart Outcomes Prevention Evaluation (HOPE) study, ABI was measured by digital palpation of the foot pulse at the base-line in 8986 patients that were followed for 4.5 years.
They found that low ABI is a strong predictor of morbidity and mortality during the follow-up. This was in both, for the primary end–point (cardiovascular mortality, myocardial infarction or stroke) and for each individual component.
A low ABI also predicted the development of heart-failure and diabetic complications.
A very important finding of this study was that low ABI is also, in the absence of the clinical PAD, a strong predictor of cardiovascular events.
However, also in this group of subjects the risk increased with the decrease of ABI (all the cause of death: ABI 0.9 to 0.6 - 12.8%, ABI < 0.6 - 14.7%) and was in both groups significantly higher than in subjects with ABI > 0.9 (8.8%).
The benefit of Ramipril, whose preventive effect was investigated in this study was about twice as large in the group of patients with ABI < 0.9 than in those with ABI > 0.9 and its preventive effect was in patients with preclinical PAD comparable to symptomatic subjects (6).
This should also suggest that in patients with other atherosclerotic diseases and no clinical evidence of PAD, utilising ABI can identify patients the patients with a higher risk who can benefit from intensive preventive strategies.
The editorial of the European Heart Journal concluded, on the basis of these data, that ABI should be used to help define cardiovascular risk patients with and without symptomatic cardiovascular disease and it added that the HOPE-study brings hope for the use of ankle-brachial index as a cardiovascular risk marker (7). In contrast to other methods used for the determination of cardiovascular risk (scores), the determination of ABI enables the identification of subjects who already have asymptomatic or symptomatic atherosclerotic disease and may benefit from preventive treatments. They then represent the first priority group for aggressive prevention of atherosclerosis.
The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.