Demystifying atherosclerosis and peripheral arterial disease
Aaron Schoenkerman, M.D., FACC
Cardiologist, Providence St. Vincent Medical Center
Published February 2011
In an earlier issue of eCardioVascular Beat, Providence Heart and Vascular Institute's physician newsletter, Dr. Brad Evans wrote about the important relationship between peripheral arterial disease (PAD), coronary artery disease and cerebrovascular disease.
He identified the ABI (ankle-brachial index), a noninvasive measurement of the blood pressures in the arms and ankles, as a method of making this important diagnosis.
I'd like to specifically discuss the pathophysiology of the relationship between these diseases, and outline the evaluation and treatment ramifications of diagnosing PAD.
The basic mechanism behind the development of most diseases affecting the arterial circulation is atherosclerosis. Atherosclerosis is a syndrome in which fatty materials – caused by LDL cholesterol, circulating inflammatory mediators and arterial shear stress – build up within an artery’s walls.
Risk factors for PAD include hypertension, hyperlipidemia (elevated bad cholesterol levels), tobacco use, diabetes, aging (men over 55 and women over 65) and family history. The disease can be clinically silent, or it can lead to obstructive, aneurysmal or embolic sequelae.
Further, a patient may have a combination of these abnormal occurrences and may be diagnosed by different modalities. It follows that identifying any manifestation of peripheral arterial disease mandates evaluation for other covert sequelae. Once this evaluation is complete, a treatment and follow-up plan can be developed.
While there are many ways to diagnose atherosclerosis, the initial evaluation is relatively uniform, involving a complete vascular review of systems and a physical examination. This is typically followed by laboratory and imaging evaluations.
Patients at risk for PAD will be asked about leg fatigue or leg pain with ambulation (claudication). They also will be asked about poor healing in the lower extremities, stroke or stroke-like symptoms, abdominal pain with eating, or weight loss. They will be asked about family history of aortic aneurysms.
Next: a focused physical exam
Second, a focused physical examination is performed. This includes bilateral arm blood pressures, cardiac examination, palpation of the abdomen, examination of the legs and feet, and a comprehensive pulse examination from the carotid arteries in the neck to the small arteries of the foot and ankle. Depending on the patient’s medical history, review of systems and physical examination, laboratory testing may be required to determine cholesterol, kidney function and fasting glucose.
Noninvasive modalities may be used, such as segmental blood pressure analysis, ultrasound with Doppler, CT scan or MRI. In some cases cardiac stress testing may be appropriate.
The rationale for this extensive evaluation is to identify modifiable risk factors for atherosclerosis, and to initiate a treatment plan to prevent major events such as a heart attack or stroke. The risk of these two acute illnesses is a high concern no matter what manifestation of atherosclerosis is diagnosed.
Treatment includes aspirin or another platelet inhibitor, certain antihypertensive medications if indicated to treat high blood pressure, cholesterol-lowering medications and a smoking-cessation plan. These strategies have been proven to slow progression of the disease and to decrease the risk of stroke, heart attack and death.
Noninvasive imaging is necessary to define the type and location of disease present – especially if it is being targeted for invasive treatment – and to confirm atherosclerosis as the mechanism. Treatment decisions beyond optimal pharmacologic therapy, such as invasive revascularization, are highly individual. Generally, however, treatment depends on symptoms, severity of risk and anatomic location of disease.
There are many different clinical presentations of atherosclerosis and many methods to diagnose this common disease. Early diagnosis is essential to maximize the effect of medical therapy, and ultimately to eliminate symptoms and decrease the burden of disease and its associated risk.