Peripheral arterial disease clinical presentation

MN is a 48-year-old man with a history of hypertension and smoking who presents to the clinic for evaluation of his cholesterol. He denies having chest pain or history of myocardial infarction, stroke, or peripheral artery disease. He has no siblings and both parents are alive with no history of CHD. MN says that he smokes about 1 pack of cigarettes per day. He does not exercise on a regular basis. He has been fasting for approximately 11 hours. 

The peripheral vasculature is considered a target organ. Physical examination of the systemic vasculature can detect evidence of atherosclerosis, which may present as bruits (in the aortic, abdominal, and peripheral arteries), distended veins, diminished or absent peripheral arterial pulses, or lower extremity edema. Peripheral arterial disease is a clinical condition that can result from atherosclerosis, which is accelerated in hypertension. Other cardiovascular risk factors (e.g., smoking) can increase the hkelihood of peripheral arterial disease as well as all other forms of target-organ damage. 

The clinical presentation of peripheral arterial disease is variable and includes a range of symptoms. The two most common characteristicsof peripheral arterial disease are intermittent claudication and pain at rest in the lowerextremities. 

Peripheral arterial occlusion can be the initial manifestation of cardiac or systemic disease. At times, patients with chronic stable claudication may experience abrupt shortening of the distance at which claudication occurs, and this may be the only symptomatic evidence of an acute arterial occlusion either by embolization of by thrombus formation on a pre-existing arterial stenosis. The situation is not chronic and stable any more, but acute and unstable. As ischemia becomes more severe, the patient with chronic peripheral arterial disease develops ischemic pain at rest. The pathophysiologic mechanisms and the clinical presentation parallel the evolution of chronic stable angina pectoris to unstable angina and acute coronary syndromes. 

Epidemiologic studies have indicated a very strong inverse association between HDL-cholesterol levels and the incidence of arteriosclerotic cardiovascular disease [32]. HDL is thought to promote efflux of cholesterol from peripheral cells in the vascular wall and return of that cholesterol to the liver for excretion in bile, a process known as reverse cholesterol transport [21]. HDL has also been shown to have anti-inflammatory and anti-thrombotic activities [21]. Therefore, HDL levels may influence both the hyperlipidemia and inflammatory processes proposed as factors in the development of atherosclerosis. Although clinical data in support of HDL-raising are limited, in the VA-HIT trial gemfibrozil therapy in men with coronary artery disease and low HDL-cholesterol modestly increased HDL levels and reduced coronary events by 22% [33]. Presently, other methods of effectively and safely increasing HDL-cholesterol levels have not been discovered. 

Intermittent claudication is a clinical diagnosis. Usually lower extremity ischemia is caused by flow-limiting atherosclerotic plaques. Intermittent claudication is the presenting symptomatology in half of the patients with chronic lower extremity ischemia. The other one-third to half of patients with documented peripheral arterial occlusive disease are asymptomatic or silent (8). Other symptoms and physical findings indicating more severe ischemia are pain at rest, pale and cold extremity(s), ischemic ulcers, peripheral cyanosis, and gangrene (12). 

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