Atherosclerosis in the Legs

Peripheral Artery Disease

By Ruth Werner
[Pathology Perspectives]

Picture this: your client is a 76-year-old man who is moderately overweight. Since his mild heart attack three years ago, he is fairly active and careful about his diet. He does his best to manage his diabetes, but he has been unsuccessful in his attempts to quit smoking. He likes to try to walk a mile every day, but he recently began experiencing some pain in his left calf after about half that distance.

He describes the pain as sharp and knife-like, and it is only relieved when he stops walking. He tried a stationary bicycle, and the same thing happened. He is hoping he just pulled a muscle in his leg, and he wants your help so he can start exercising again.

Sounds pretty straightforward, right? Wrong.

My advice: proceed with caution.

What is Peripheral Artery Disease?

Most readers are probably familiar with the term coronary artery disease (CAD). This describes the condition of having fatty plaques in the arteries that supply the heart. The same process commonly occurs in the carotid arteries leading up to the brain, which of course raises the risk for cerebrovascular accident (CVA), otherwise known as stroke. But the coronary and carotid arteries are not the only structures vulnerable to plaque development. This process can also occur at the renal arteries and in the legs. When it occurs away from the heart and brain, this condition is called peripheral artery disease (PAD); when it is specifically in the legs, specialists call it lower extremity atherosclerotic disease.


The pathophysiology of PAD is similar to that of coronary artery disease. Because heart attack and stroke are the first and third leading causes of death in the United States, and because they are closely linked to the development of atherosclerosis, it is in every massage therapist’s best interest to be familiar with the course of these conditions.

The process of developing fatty plaques in the arteries is complex and probably has subtle differences in each individual, but in broad strokes the sequence has three main steps: fat is deposited in the tunica intima, plaques develop, and eventually they may complicate into more serious lesions.

Fatty Streaks

These are lesions that indicate damage inside medium and large arteries. When the tunica intima is damaged, monocytes (small,

mobile white blood cells) arrive to help clean up the debris. Then, they may

move in and become permanently installed macrophages that specialize in

taking up LDL: low density lipoproteins that carry cholesterol. Eventually this becomes visible to the naked eye in deposits of cholesterol called fatty streaks. At this point no obstruction is present, no symptoms occur, and the whole process may be reversible. Chronic high blood pressure,

chemicals derived from cigarette smoke, and blood that is high in glucose

(i.e., uncontrolled diabetes) are particularly damaging to artery linings.

Fatty streaks are most likely to develop in places where arteries divide: the turbulence of blood appears to be an important factor in the erosion


Investment of Plaque

Chemicals released by fat-filled macrophages trigger the production of connective tissue in the area: collagen and elastin fibers are spun, and smooth muscle cells may proliferate around the new material. At this point, the lesion is big enough to intrude into the lumen of the artery, and it infiltrates both the tunica intima and the muscular layer of the vessel wall.

Plaques Complicate

The development of a fatty plaque in an arterial wall triggers a sequence of reactions that can make the situation much worse. The plaque may accumulate calcium deposits, which causes the artery to lose its ability to appropriately dilate and constrict. Any roughness in a blood vessel attracts platelets (thrombocytes), which then secrete pro-inflammatory chemicals and clotting factors. When clots accumulate around the site of the lesion, this obviously increases the size of the obstruction.

An obstruction composed primarily of clotted blood that is stationary and grows on-site is called a thrombus. If a portion of a thrombus or other debris breaks loose and travels, this is an embolism. Plaques can grow large enough to limit blood flow, but they can also rupture, and fragments of blood clot, fat, and other substances can travel or embolize further along the artery. Any tissue that was meant to receive oxygen and nutrients from that blood vessel will die. When this happens with the coronary artery, it is called a heart attack or myocardial infarction. Anywhere else, it is just called an infarction. Regardless of location, the result is dead tissue and loss of function.

There is good news, however. The wonderful thing about human physiology is that we have a remarkable ability to grow new blood vessels wherever existing vessels are not keeping up with our needs. This process, called angiogenesis, allows us to create collateral vasculature that does the work of the obstructed arteries. Angiogenesis takes time, however, so a new situation may be more threatening than an older one.

Who Has PAD?

So far this discussion has focused on PAD as a variant of cardiovascular disease. It is important to point out that this condition can develop under other circumstances as well. Any circumstance that involves damage or injury to peripheral blood vessels can lead to PAD. This includes chronic inflammatory diseases like lupus, or trauma. Clotting disorders can also contribute to PAD, as can exposure to radiation or anatomical anomalies that make the arteries vulnerable to ongoing damage. These cases are in the minority, however. Most people with PAD have it in combination with other cardiovascular compromise and are consequently at a very increased risk for both heart attack and stroke.

Because PAD is virtually silent until damage is extensive, it is difficult to project how many people may live with this condition. A simple test has been developed that compares blood pressure readings from the arm and the ankle: this is called ankle-brachial index (ABI). When the ratio is under .95, PAD may be present. Estimates suggest that about 3 percent of the adult population under age 60 have a positive ABI. Not surprisingly, this number goes up with age: about 20 percent of people over age 70 have a positive ABI.[1]

Risk factors for PAD are the same as those for other forms of cardiovascular disease. Age, activity levels, a body mass index of 30 or above, and personal or family history with other forms of heart disease are predictive of a risk for damage to both core and peripheral arteries. But the two most common risks are poorly managed diabetes and smoking. Fortunately, these are risk factors that are controllable.

Signs and Symptoms

In its early stages, PAD is essentially silent: it causes virtually no symptoms until the artery is significantly occluded. The first symptom most people report is a condition called intermittent claudication (literally “occasional limping”). This is a result of leg muscles needing more oxygen than they can get: during exercise (usually walking), the person experiences sudden sharp pain and cramping in one calf. The pain ranges from mild to debilitating, and it is relieved only when exercise stops.

This is a progressive condition, and as the arterial blockage becomes greater other signs develop. These include a difference in temperature between legs (the blocked side is cooler); erectile dysfunction is common in men with PAD; and eventually pain along with numbness in the leg may be present even at rest—although many people report that weight-bearing relieves the pain.

Signs that medical professionals may observe in a person with PAD include a pulse that is decreased or even absent in the affected ankle; a characteristic sound called a bruit that is heard through a stethoscope over the clogged artery; very slow wound healing; hair loss on the affected leg; and thickened toe nails along with shiny, thinned skin.

These skin and nail changes are related to severely challenged circulation. In very extreme and advanced cases, the skin may completely degenerate and form ulcers that don’t heal or that heal so slowly they are vulnerable to infection and gangrene. This progression is more rare than it used to be, because treatment options for PAD are much more effective than they were even a decade ago.


Untreated peripheral artery disease can have serious consequences. Pain that had been triggered only during exercise can progress to be a constant problem. Skin that is starved of nutrition can develop non-healing ulcers that are an invitation to infection and gangrene: the only safe option in this case is amputation of the affected leg. And while this discussion has focused on PAD in the lower extremity, the same problem can also develop in the renal arteries, leading to two very complicated conditions called renal artery stenosis and renovascular hypertension. Both of these conditions create a vicious circle with hypertension: obstruction of the renal artery changes kidney function, and they secrete hormones that consequently raise blood pressure, which puts more force on the damaged arteries.

Treatment Options

Treatment options for PAD have two main goals: to limit symptoms and to prevent progression to the more serious consequences of the condition. This typically begins with specific attention to managing diabetes and quitting smoking. Medications may include anti-platelet drugs to reduce clotting, aggressive hypertension management drugs, and some drugs that can delay the onset of intermittent claudication symptoms so that exercise is more comfortable. Careful and often supervised exercise—this is exercise done in a medical facility with sensors to track cardiovascular stress—is also part of many treatment plans; this may help speed the process of angiogenesis to restore circulation to the starved tissues.

Until recently, the standard treatment for a recognized case of PAD was to surgically replace the damaged section of artery in what amounts to a type of bypass surgery. However the risk for infection and other complications was significant, and it often didn’t lead to a successful outcome. The more current intervention involves balloon angioplasty along with the insertion of a stent to prevent the artery from becoming occluded again. This can be done as a closed surgery and has a high success rate. Consequently, the prospect of dangerous ulcers, infections, and amputation is quite rare for PAD patients today.


Obstructed blood flow in the legs (or anywhere) is a significant red flag for massage therapists and other bodywork practitioners. If the obstruction is in the veins (deep vein thrombosis, or DVT), the risks are quite different than if it is in the arteries. With DVT, if a piece of debris breaks off, then it can flow unobstructed up the leg, into the vena cava, through the right side of the heart, and into the lungs: this is a pulmonary embolism, and it kills about 200,000 people every year.[2] By contrast, a clot or plaque on the arterial side that becomes disrupted by massage or other interventions can rupture, and the movement of debris “downstream” can create a complete blockage in a more distal part of the artery: as discussed, this is an infarction, and it can lead to extensive tissue damage from ischemia. Further, a client who has PAD has a significantly increased vulnerability to both heart attack and stroke.

However, because the body is so adept at growing new pathways for blood to flow, a long-standing and stable obstruction may not be such a dangerous situation. Decisions about bodywork need to be made in the context of what the client can tolerate in terms of exercise and increased load on the circulatory system. After all, careful exercise may actually promote the creation of helpful new arteries. In short, this is an excellent example of a client who needs to compile a health-care team so that all of his or her providers, including a massage therapist, can work together for the best results.

 Ruth Werner is the president of the Massage Therapy Foundation. She is a writer and NCBTMB-approved provider of continuing education. She wrote A Massage Therapist’s Guide to Pathology (Lippincott Williams & Wilkins, 2009), now in its fourth edition, which is used in massage schools worldwide. Her latest book, Disease Handbook for Massage Therapists (Lippincott Williams & Wilkins, 2009), is also available at Werner can be reached at or


1. C. Chahin, B. Rose, and S. Stuhlmiller, “Lower-Extremity Atherosclerotic Arterial Disease,” Medscape. Available at (accessed July 2010).

2. D. Schreiber, “Deep Venous Thrombosis and Thrombophlebitis,” Medscape. Available at (accessed spring 2010).