Factors determining the clinical manifestations of peripheral arterial disease
THE CONTEXT
The effects of peripheral arterial disease depend on the affected circulation, available collateral supply, speed of arterial occlusion and mechanism of injury.
Anatomical site
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Cerebral arterial disease may cause transient ischaemic attack, amaurosis fugax or vertebrobasilar insufficiency.
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Renal arterial disease may cause hypertension and renal failure.
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Mesenteric arterial disease may cause mesenteric angina or acute intestinal ischaemia.
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Limb involvement is much more common in the legs than the arms and may present as intermittent claudication, critical limb ischaemia or acute limb ischaemia.
Collateral supply and speed of onset
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A complete circle of Willis may allow occlusion of one carotid artery to remain asymptomatic; without cross-circulation, stroke is likely.
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Slowly developing disease permits collateral supply to develop.
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Sudden occlusion of a previously normal artery is likely to cause severe distal ischaemia.
Haemodynamic and thrombotic injury
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A plaque must reduce arterial diameter by 70% to reduce flow and pressure at rest; this is termed critical stenosis. During exertion, a moderate stenosis may become critical.
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Haemodynamic disease tends to follow a relatively benign course because collateralisation develops.
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Thrombotic occlusion of a long-standing critical stenosis may be asymptomatic because of collateralisation.
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Acute rupture and thrombosis of a plaque that was not haemodynamically significant usually has severe consequences.
Embolic injury
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In atheroembolic injury, symptoms depend on embolic load and size. Carotid plaque may cause transient ischaemic attack, amaurosis fugax or stroke; peripheral arterial plaque may cause blue toe or finger syndrome.
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Thromboembolic injury is usually secondary to atrial fibrillation.
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Thromboembolic consequences are usually dramatic because a large thrombus can suddenly and completely occlude a major, previously healthy artery without collateral supply.