Atherosclerosis is considered to be a systemic disease. Therefore, patients with a clinical manifestation of a particular atherosclerotic disease are likely to have atherosclerotic lesions in other vascular beds. Epidemiological and clinical studies have shown that peripheral arterial occlusive disease (PAOD) is a common disorder associated with the presence of coronary (CHD) or cerebrovascular disease (CVD) and a profoundly increased risk of cardiovascular and cerebrovascular events and mortality (1,2). It was also shown that not only clinical but also the preclinical stages of PAOD, represented by a borderline decrease of the ankle-brachial index (ABI), have a strong predictive value and that the risk of cardiovascular mortality increases with the severity of PAOD (3,4).
Easy accessibility enables to use peripheral arteries as surrogate markers of cerebrovacular and systemic atherosclerosis. Moreover, for detection of PAOB a simple and reliable diagnostic techiques are available. Especially, ABI is a very useful, diagnostic (and risk assessment) tool that also predicts carotid atherosclerosis.
Interrelationship between peripheral arterial occlusive disease and carotid atherosclerosis was confirmed in different studies. House and co-workers reported that 35 % of the patients with peripheral arterial occlusive disease have in internal carotid stenosis (ICAS) greater that 50 %. Males presented associated carotid stenosis at a younger age than females and in females the greatest prevalence of internal carotid artery stenosis was associated with abdominal aortic aneurism (5). The SMART Study (Second Manifestation of ARTerial disease) showed that in PAOD patients ICAS is present in 14 % and that the prevalence of ICAS increased to as much as 50% in patients who had additional risk indicators (age 67 years, pulse pressure 74 mmHg, ABI 0.78) (6). Not only symptomatic, but also asymptomatic PAOD (ABI ≤ 0.9) is related to the higher prevalence of cerebrovascular disease. In the Limburg – PAOD study the prevalence of CVD in asymptomatic PAOD patients was even two times higher than in symptomatic (7). Increased morbidity, caused by simultaneous presence of PAOD and carotid atherosclerosis results in increased mortality. Cricqui with co-workers showed that the mortality because of CVD in PAOD patients was 2.5 times as great as in those without PAOD (2).
Mostly used indicator of the presence and severity of PAOD is ABI. Irrespective if the PAOD disease is symptomatic or asymptomatic, decreased ABI represents an increased risk for cardiovascular, including cerebrovascular incidents. ARIC Study showed inverse linear trend between ABI and ischemic stroke incidence. The lowest ABI group (≤ 0.80) had a risk ratio of 5.68 for CVD and it was shown that there also exists an interrelationship between ABI and preclinical carotid atherosclerosis – intima media thickness (IMT). Individuals with decreased ABI (≤ 0.9) had significantly greater carotid IMT and were twice as likely to have preclinical plaques than those with normal ABI (3). Similarly, the Rotterdam Study showed significant inverse association between common carotid artery IMT and ABI. The calculations showed that an increase of IMT for 0.1 mm is associated with reduction of ABI of 0.026. This study also showed that the prevalence of symptomatic and asymptomatic PAOD is strongly increased among subjects with IMT > 0.89 mm (8). Therefore, low ABI reflects not only clinical, but also preclinical atherosclerotic lesions in carotid arteries.
In one of our studies we investigated morphological characteristics of carotid arteries in PAOD patients in comparison to healthy subjects. It was shown that only 7 % of patients had normal morphological characteristics of carotid arteries (including IMT), 23 % of them had increased intima-media thickness and in 70 % atherosclerotic plaques were detected. In healthy subjects IMT was increased in only 15 % and atherosclerotic plaques were found in 8 %. Further, a close interrelationship between ABI and PAOD and between ABI and number of atherosclerotic plaques on carotid arteries was found (9). However, these results arose the question if low ABI would add substantial prognostic ability beyond determination of traditional risk factors of atherosclerosis. In the ARIC Study it was shown that after adjustment for other risk factors of stroke (age, gender, blood pressure and fibrinogen) the relation between ankle-brachial pressure index and incidence of cerebrovascular disease was substantially reduced and was not more significant. However, in our study the association of ABI with IMT and carotid plaques retained statistical significance even after adjustment for risk factors of atherosclerosis. Therefore we concluded that lower values of ABI (0.34 - 0.82) charasteristic for0 symptomatic PAOD patients (claudicants) are (independently of risk factors for atherosclerosis related) to intima-media thickness of carotid arteries.
Determination of ABI improves identification of subjects at high risk of cardiovascular (including cerebrovascular) events, especially in asymptomatic patients. Since asymptomatic PAOD patients are at very high risk for an ischemic event (like the patients with multifocal symptomatic disease), they deserve special interventive effort and are likely to experience the greatest profit of risk reduction procedures. Therefore, in some populations determination of ABI has additional prognostic value beyond traditional risk factor identification.
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