The ankle-brachial index (ABI) is a common noninvasive test used to determine if there is occlusive disease of the peripheral vasculature. It uses the brachial arterial systolic blood pressure as the control, assuming it to be nonocclusive, and compares it to either that of the posterior tibial (PT) or dorsalis pedis (DP) arteries. The ABI is calculated in each foot by dividing the higher systolic blood pressure reading of either of the PT or DP arteries by the higher systolic blood pressure reading of either the left or right brachial artery. This index suggests occlusive peripheral artery disease (PAD) when it is ≤0.9. Furthermore, the location of the occlusion may be inferred by using segmental blood pressure readings and supportive data such as pulse volume recordings (PVRs).
How to Use It
This test is ordered when there is a suspicion of obstructive vascular pathology, most commonly due to obstructive atherosclerosis of the lower extremities, but may also include obstruction due to vasculitis or thromboembolic disease. It is indicated in patients who are asymptomatic but have risk factors for atherosclerotic cardiovascular disease (ASCVD), who have symptoms of occlusive PAD (such as claudication or erectile dysfunction), or who have physical signs of limb ischemia such as poor wound healing.
How It Is Done
This test can be performed as either an inpatient or outpatient test, but is most commonly performed in the outpatient setting. A plethysmographic cuff is placed around the left and right arms, and the left and right lower calves just above the ankle. Segmental pressure readings require additional plethysmographic cuffs to be placed around the upper thighs, lower thighs, and upper calves. PVRs are used to help interpret the results of ABIs and may be obtained by the use of pneumoplethysmographic cuffs or alternatively obtained using continuous-wave Doppler. Testing is usually performed at rest but can also be performed post exercise using a standardized exercise protocol if there is clinical suspicion of obstructive PAD despite a normal resting ABI. In this case, the patient is exercised according to an institution’s protocol and, shortly after, ABIs are obtained at regular intervals. When there is suspicion of obstructive PAD in patients with calcified vessels (which often produces an ABI >1.4), a toe-brachial index may be performed by placing a small plethysmographic cuff usually around the great toe.
HOW IT IS INTERPRETED
Compared with the brachial artery, systolic arterial pressure should be similar or slightly higher in the more distal arteries. As such, the normal ABI is 1.0–1.4. An abnormal ABI is ≤0.9 and is suggestive of occlusive PAD. Borderline normal ABI is 0.91–0.99. An ABI >1.4 suggests noncompressible calcified vessels that may or may not be obstructed. An ABI >1.4 is an abnormal finding and is associated with an increased risk of stroke, heart failure, and a higher incidence of occlusive PAD compared with normal ABI.
Further testing in patients with ABI >1.4 using a toe-brachial index is indicated, as the small arterial vessels in the toes are rarely calcified. A normal toe-brachial index is >0.7. If the toe-brachial index is ≤0.7, it is abnormal and diagnostic of occlusive PAD. In addition, when there is further clinical suspicion of occlusive PAD in the setting of a normal or borderline normal ABI, an exercise ABI is indicated.
Segmental plethysmographic readings may help localize disease to various areas of the lower extremity such as the aortoiliac, femoropopliteal, or infrapopliteal regions. If blood pressure decreases from one contiguous segment to the next by more than 20 mmHg, it can be inferred that there is a focal arterial occlusion between those two segments.
Once occlusive PAD is diagnosed with an abnormal ABI, follow-up imaging may be indicated if the patient is symptomatic despite medical therapy and there is a goal for revascularization. Lower extremity arterial duplex ultrasound is a cost-effective and risk-free way of assessing the degree and level of occlusive PAD by using two-dimensional ultrasound and color Doppler ultrasound. Computed tomographic angiography (CTA) and magnetic resonance angiography (MRA) may also be used, but carry their specific risks. These tests have the benefit of evaluating the vasculature of the lower extremities in greater detail than lower extremity arterial duplex ultrasound. Finally, in symptomatic patients on goal-directed medical therapy who still have symptoms and whose quality of life may benefit from revascularization, invasive angiography is indicated.
Multiple double-blinded, randomized controlled trials have found that patients with occlusive, symptomatic PAD benefit from aspirin. In these patients, aspirin 75–325 mg orally once daily results in a reduction in the incidence of cerebral vascular accident (CVA), myocardial infarction (MI), and vascular-related deaths. This is because occlusive PAD is a regional manifestation of ASCVD and has significant overlap with coronary atherosclerosis and cerebral atherosclerosis. However, while aspirin has shown dramatic reduction in ASCVD-related events in patients with symptomatic PAD, no reductions have been demonstrated in asymptomatic patients with PAD. Even so, the American College of Cardiology and the American Heart Association, in collaboration with many other organizations, recommend the use of aspirin in asymptomatic patients with PAD, based on expert opinion.
In patients who had a recent CVA, recent MI, or have evidence of limb ischemia, the use of clopidogrel 75 mg orally once daily as monotherapy has been shown to reduce CVA, MI, or cardiovascular-related deaths compared with the use of aspirin 325 mg orally once daily. This benefit comes at no additional risk of bleeding. Current guidelines recommend the use of either aspirin or clopidogrel in patients with symptomatic PAD.
DUAL ANTIPLATELET THERAPY
Dual antiplatelet therapy with aspirin and clopidogrel, while beneficial to cardiovascular patients following an MI, has not been soundly proven to be as beneficial in patients with symptomatic PAD. In addition, there has not been strong evidence balancing the benefits of dual antiplatelet therapy with its risks of bleeding in patients with symptomatic PAD. Current guidelines state that it may be reasonable to consider its use in select high-risk populations with low bleeding risks. However, after revascularization, it is reasonable to use antiplatelet therapy with aspirin and clopidogrel to prevent limb ischemia.
Vorapaxar is a protease-activated receptor-1 antagonist that prevents platelet activation. Clinically, vorapaxar 2.08 mg orally once daily compared with placebo has been shown to reduce the incidence of acute limb ischemia and the need for peripheral revascularization in patients with stable coronary artery disease, CVA, or PAD. However, it did not reduce the incidence of MI, CVA, or cardiovascular-related deaths. In addition, vorapaxar is associated with increased moderate-severe bleeding compared with placebo, and its product labeling contains a boxed warning against use in patients with a history of CVA, transient ischemic attack, intracranial hemorrhage, or pathological bleeding. Currently, the use of vorapaxar has not been strongly recommended in guidelines by major professional organizations.
HMG-CoA REDUCTASE INHIBITORS (STATINS)
High-intensity statins are indicated in patients with clinical ASCVD including claudication or chronic limb ischemia. It is recommended that low-density lipoprotein cholesterol (LDL-C) goals are reduced to <50% of baseline LDL-C. In very high-risk patients, high-intensity statins should also be initiated and the goal LDL-C should be <50% of the baseline LDL-C. If LDL-C cannot be lowered to <70 mg/dL by using statins alone, ezetimibe or proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors may be added.
Cilostazol is a specific cyclic adenosine monophosphate phosphodiesterase inhibitor in platelets and vascular smooth muscle cells. It inhibits platelet aggregation, causes vasodilatation, and lowers lipids. It is used for the treatment of claudication in patients with stable PAD and may improve walking distances. Cilostazol 100 mg orally twice daily is the only medication that has been shown to decrease claudication. Its mechanism of action is multifactorial. Cilostazol is contraindicated in heart failure. Although it inhibits platelet aggregation, concurrent use with aspirin does not cause additional risk of bleeding.
Although approved to treat intermittent claudication in the United States, pentoxifylline is no longer recommended to treat claudication, as it has not been effective in prolonging maximal walking distances.