Peripheral Arterial Disease - Diagnosing and Managing

Dr Paul Chiam, Consultant, Department of Cardiology, National Heart Centre Singapore
Dr Victor Chao, Consultant, Department of Cardiothoracic Surgery, National Heart Centre Singapore

How does lower extremity Peripheral Arterial Disease develop?

Peripheral Arterial Disease develops when the arteries in the lower extremities become narrowed with plaque - such as fatty deposits and cholesterol - which limit or completely block blood flow in the legs. This prevents oxygen rich blood from reaching the muscles when the muscles need it most, resulting in pain in the buttocks, thighs and calves when engaging in activity.

Peripheral Arterial Disease is also a marker of increased risk of heart attack and stroke. The good news is that Peripheral Arterial Diseasecan be easily diagnosed and treated.

With pain limiting their movements, the patients move gradually from an active lifestyle to a sedentary one. This results in immobility and a shorter life expectancy due to the increased risk of high blood pressure, heart attack, and stroke.

The risk factors for Peripheral Arterial Disease include hypertension, high cholesterol, and diabetes – all of which are common illnesses in our population. One third of diabetics over the age of 50 develop the disease.

Perhaps the strongest risk factor is smoking. This brings on the disease much sooner, and can lead to Peripheral Arterial Disease in patients as early as their 50s or 60s.

Symptoms and treatment

The symptoms include intermittent claudication, which is an aching pain reproduced by walking a certain distance. For example, a patient with lower extremity Peripheral Arterial Disease may start developing pain in the calf muscle of the affected leg when he walks 100 metres. He stops and rests for a few minutes; the pain goes away and he can go another 100 metres before it comes on again.

In the most extreme cases, if left unchecked, it may result in rest pain, ulcers, gangrene, and amputation.

One way of detecting lower extremity Peripheral Arterial Disease is to check ankle and arm pressures during routine clinic consultations, which should be the same. The ankle-brachial index (ABI) is calculated by dividing ankle pressures by arm pressures. A value of 0.9 to 1 is normal. If it comes back as 0.5, then that implies that the patient has significant disease.

Specific management of Peripheral Arterial Disease involves:

1. Lifestyle changes
These include smoking cessation; a diet that is high in fibre and low in cholesterol, fat and sodium; and exercise.

2. Management of other related health problems, such as high blood pressure, diabetes or high cholesterol.

3. Practise good foot and skin care to prevent infection and reduce the risk of complications.

4. Aggressive exercise (walking) therapy.
This helps to improve collateral flow to the lower extremities and improves walking distance. It is a very effective treatment, is safe and costs practically nothing!

5. Medications
Medications may be recommended to treat conditions such as high blood pressure (anti-hypertensive medications) or high cholesterol (statin medications). An antiplatelet medication such as aspirin or clopidogrel (Plavix) may be prescribed to reduce the risk of heart attack and stroke. Cilostazol (a platelet aggregation inhibitor) has been shown to improve the walking distance.

6. Intervention
More advanced Peripheral Arterial Disease can be treated with interventional procedures such as angioplasty (to widen or clear the blocked vessel), angioplasty with stent placement (to support the cleared vessel and keep it open), or atherectomy (to remove the blockage). In some cases, surgical procedures such as peripheral artery bypass surgery may be performed to re-route blood flow around the blood vessel blockage.

Despite the availability of healthcare in Singapore, Peripheral Arterial Disease is still “under-diagnosed” for several reasons. Patients tend to ignore the symptoms as being part of the “aging process” or simply learn to bear with it and do not report it to their physicians. The other is that checking of arm and ankle pressures (ABI) is not as widely practised as it should be.

In the US, the determination to increase awareness has recently led to increased training for vascular medicine specialists for routine ankle-brachial check-ups and early detection for treatment.

The goal of therapy is to improve blood supply to their leg muscles so that patients maintain their functional level of activity. Once patients become couch potatoes, it will be hard to get them off the couch. They need to be kept active to maintain their health.

Carotid artery stenosis

Carotid artery disease usually involves the internal carotid artery and the common carotid artery at the carotid artery bifurcation. Progressive plaque deposition leads to carotid artery stenosis. Unlike the lower extremities, the reduced cerebral blood flow does not usually cause symptoms since the contralateral carotid artery or vertebrobasilar system (posterior circulation) can provide collateral cerebral supply via the Circle of Willis. Carotid stenosis is the etiologic factor in up to 10% – 20% of large artery ischemic strokes. Thus the main purpose of treating carotid stenosis is to reduce the risk of future stroke.

Symptoms and treatment

Carotid stenosis can be detected during the workup of a patient presenting with stroke, transient ischemic attack or amaurosis fugax (symptomatic disease), or during screening (for example with duplex ultrasound) for other indications (asymptomatic disease).

In symptomatic patients, there is a greatly elevated risk of recurrent ipsilateral stroke of approximately 26% over the next two years, whereas in asymptomatic patients the five-year risk of ipsilateral stroke is 11% – 12%. Several large randomised studies (NASCET, ECST, ACAS and ACST) have demonstrated that carotid endarterectomy (CEA) can significantly reduce the risk of recurrent stroke from 26% to 9% over two years in symptomatic patients and from 11% – 12% to 5% – 6% over five years in asymptomatic patients, when compared to medical therapy alone. The caveat is that the peri-procedural stroke or death rate from CEA must not exceed 6% and 3% for symptomatic and asymptomatic patients respectively. Therefore, in patients with carotid stenosis and suitable for surgery, CEA is the standard of care.

In the last decade, carotid stenting (CS) which is less invasive than CEA has emerged as an alternative modality. Increasing experience with this technique, improved distal filter devices and dedicated stent technology have made this therapeutic option safer.

The SAPPHIRE trial demonstrated that CS and CEA were equivalent in patients at high surgical-risk, for both symptomatic and asymptomatic disease. The SPACE trial however, could not demonstrate non-inferiority of CS compared to CEA for standard surgical-risk patients with symptomatic disease, and the EVA-3S trial showed that CS was associated with a higher complication rate for the same group of patients. Because of these data, reimbursement for CS in the US healthcare system is only approved for symptomatic patients at high surgical-risk.

Many single-centre and multi-centre registries however, demonstrate that CS can be performed with low complication rates in a wide range of patients, most likely due to appropriate case selection. Surgery, though, remains the gold standard therapy to which CS is compared. The results of CREST (one of the largest ongoing randomised trials of CS vs CEA in both symptomatic and asymptomatic patients at standard surgical-risk) will shed further data for this subset of patients.

It must be emphasised that optimal medical therapy MUST always be part of the treatment for carotid stenosis. Antiplatelet therapy, management of dyslipidemia, control of hypertension and / or diabetes, and smoking cessation are imperative, whether or not CEA or CS is performed.