According to the Rose questionnaire, the prevalence of PAD in males is approximately 1.5 % in men under the age of 50 and reaches 4–5 % in the age group of 50 and older. In females under the age of 50, the prevalence is lower than in men, but contrary to common belief, it is as high and even higher as in males over the age of 60 [5]. Moreover, in women, the clinical picture of PAD is more peculiar and in particular, the symptoms are more severe, more often leading to more profound ischemia and ulceration.

Hypertension is a risk factor for vascular disorders such as PAD; follow-up data from the Framingham study [6] demonstrated an almost doubling of intermittent claudication in hypertensive men and women; in elderly patients, similar data have been shown. Of hypertensives at presentation, about 2–5 % have intermittent claudication, with increasing prevalence with age [7–9]. Conversely, 35–55 % of patients with PAD at presentation also show hypertension, and this is particularly thru in elderly patients. Thus, in patients with PAD there is a higher prevalence of hypertension [10]; among several possible mechanisms, the presence of associated renal artery disease in many patients plays an important role.

When making up these figures, it is important to remember that the prevalence of asymptomatic PAD is clearly higher than that of symptomatic PAD [7–9]. Remarkably, as said above, at least half to two-thirds of individuals with PAD are asymptomatic or have atypical limb exertional symptoms, especially in female patients; this will in any way further increase the figures on prevalence published so far.

Ankle-brachial pressure expressed as an index will not significantly change with the treatment of arterial hypertension [7].

However, ankle pressure by itself is depending on the central blood pressure and its changes besides the local hemodynamic conditions; as said above, it can change in function of time with age, diabetes, etc. [9]. In all of these, the increase in stiffness of the arteries will increase the measured value of ankle pressure, while in reality, local perfusion is not significantly altered; the higher value of ankle pressure in such case is due to the lower compressibility of the arteries resulting in a false higher number; this phenomenon, also seen at the brachial arteries but to a lesser degree, can lead to very high figures of ankle pressure and consequently of ABI what is most often encountered in diabetic patients. Real values can be obtained in such cases by measurements at the toe by oscillography or pulse/volume recordings. Because ABI in these conditions can become surprisingly high, the problem, in most cases, is easily detected.

Much more misleading is when there is hardening of the arteries in patients with a minor degree of obstruction in the arteries; this can increase the calculated index, for example, from 0.8 to 1.1, and lead to a false “normal” value and in fact causing under diagnosis or underestimation of an existing arterial stenosis. It is not well known how frequently such a phenomenon misleads the physician in regular practice. Most likely, it only plays a role in borderline cases. Other information, for example, coming from palpation of the arteries, should help to correct such a “false normal” reading.

Another problem to be mentioned here is the situation of a severe stenosis in the arterial tree of the lower limbs, in a patient with systemic hypertension; treatment of the high blood pressure can in such condition bring the ankle perfusion pressure to lower than 50 mmHg, what can lead to critical ischemia. This phenomenon needs to be known by the physician and is by itself a good reason to measure ankle blood pressure in every hypertensive patient, especially in elderly people and diabetic patients.