What Should You Do If You Suspect Peripheral Artery Disease?

See your doctor for an ankle-brachial index (ABI) test — a painless, 15-minute screening that can diagnose PAD. If diagnosed, the immediate priorities are smoking cessation, starting antiplatelet and statin therapy, beginning a supervised exercise program, and managing blood pressure and blood sugar.

Strong Evidence2016 AHA/ACC Guideline on the Management of Patients With Lower Extremity PAD provides comprehensive evidence-based recommendations.

The ABI is the cornerstone diagnostic test for PAD. It compares systolic blood pressure at the ankle to that in the arm. An ABI of 0.91-1.30 is normal, 0.70-0.90 indicates mild PAD, 0.40-0.69 indicates moderate PAD, and below 0.40 indicates severe PAD. The test has a sensitivity of 95% and specificity of 100% for angiographically confirmed PAD. Screening is recommended for adults aged 65 and older, adults aged 50-64 with risk factors, and anyone with exertional leg symptoms.

Once diagnosed, aggressive cardiovascular risk reduction is paramount. PAD is a coronary artery disease equivalent — patients face the same cardiovascular event rates as those with established coronary disease. The AHA/ACC PAD guidelines recommend antiplatelet therapy (aspirin 75-325 mg or clopidogrel 75 mg), high-intensity statin therapy, blood pressure control below 130/80 mmHg, and glycemic management for diabetic patients. Smoking cessation is the single most impactful intervention, reducing all-cause mortality in PAD patients by up to 50%.

The ABI has sensitivity of 95% and specificity of 100% for angiographically confirmed PAD

What Causes Peripheral Artery Disease?

PAD is caused by atherosclerosis — the buildup of fatty plaques in the arteries supplying the legs. The same process that causes coronary artery disease narrows the peripheral arteries, reducing blood flow to the lower extremities. Smoking, diabetes, hypertension, and high cholesterol are the primary drivers of PAD development.

Atherosclerosis in PAD most commonly affects the superficial femoral and popliteal arteries (60-70% of cases), followed by the aortoiliac segment (25-30%) and tibial arteries (10-15%). The disease process is identical to coronary atherosclerosis — endothelial injury, lipid accumulation, inflammatory cell infiltration, and fibrous cap formation. Plaque progression gradually narrows the arterial lumen, reducing blood flow to the muscles during exercise and causing claudication.

Diabetes is a particularly important PAD risk factor, increasing risk 2-4 fold and being associated with more distal disease (tibial arteries), calcified lesions that are harder to treat, and higher amputation rates. The combination of PAD and diabetic neuropathy is especially dangerous because patients may not feel ischemic pain, presenting late with tissue loss. Chronic kidney disease is also a significant independent risk factor, with PAD prevalence exceeding 30% in dialysis patients.

How Is PAD Treated?

Treatment includes supervised exercise therapy as first-line for claudication, pharmacotherapy with cilostazol for symptom relief, aggressive cardiovascular risk reduction with statins and antiplatelets, and revascularization for severe or lifestyle-limiting disease unresponsive to conservative measures.

Strong EvidenceCLEVER trial and Cochrane meta-analysis provide strong evidence for supervised exercise therapy in PAD claudication.

Supervised exercise therapy (SET) is recommended as first-line treatment for claudication by all major guidelines. A structured program of walking exercise performed 3-5 times weekly for 30-60 minutes, progressively increasing intensity to the point of moderate-to-severe claudication pain, improves maximal walking distance by 50-200%. A Cochrane meta-analysis of 32 trials confirmed SET significantly improves walking ability compared to usual care. The CLEVER trial demonstrated that SET was superior to stent revascularization for improving peak walking time at 18 months.

Cilostazol (Pletal) 100 mg twice daily is the only FDA-approved medication for claudication symptoms. It acts as a phosphodiesterase-3 inhibitor with vasodilatory, antiplatelet, and anti-proliferative effects. Meta-analyses show it improves maximal walking distance by approximately 50% compared to placebo. It is contraindicated in patients with heart failure. For critical limb ischemia — characterized by rest pain, ulceration, or gangrene — revascularization (endovascular or surgical bypass) is essential to prevent amputation.

The CLEVER trial demonstrated SET was superior to stent revascularization for improving peak walking time