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Arterial disease can be broadly classified into two categories: occlusive and aneurysmal. The major sequelae of arterial obstruction are tissue ischemia and necrosis, whereas those of aneurysmal disease are typically rupture and hemorrhage in the aortic position and thrombosis and embolization in the peripheral arteries.


Although atherosclerosis is the dominant cause of arterial occlusive disease in Western countries, other etiologies such as congenital and anatomical anomalies, autoimmune diseases, and remote thromboembolism can also result in arterial obstruction. Symptoms of occlusive vascular disease primarily are end-organ dysfunction and, in the muscle beds, pain with exercise and tissue necrosis.


Atherosclerosis can occur in any artery, with plaques most commonly developing in areas of low shear stress, such as at arterial branch points. Lesions are usually symmetrically distributed, although the rate of progression may vary. Early lesions are confined to the intima. In advanced lesions, both intima and media are involved, but the adventitia is spared. Preservation of the adventitia is essential for the vessel’s structural integrity and is the basis for all cardiovascular interventions.

When hemodynamically significant disease affects a major artery, a parallel system of collateral vessels may preserve flow to the peripheral runoff bed. Collateral vessels are smaller, more circuitous, and always have a higher resistance than the original unobstructed artery. The stimuli for collateral development include abnormal pressure gradients across the collateral system and increased flow velocity through intramuscular channels that connect to reentry vessels. Adequate collateral vessels take time to develop but often maintain tissue viability in patients with chronic major arterial occlusions.

Generally, arterial insufficiency occurs in medium-sized and large arteries with at least a 50% reduction in arterial diameter. This correlates with a 75% narrowing of cross-sectional area and enough resistance to decrease downstream flow and pressure. Early in the process, compensatory dilation of the vessel wall may preserve lumen diameter as the atherosclerotic lesion develops, but with continued growth, lesions overcome this adaptation and result in flow-limiting stenoses. If there is adequate collateral flow, single stenoses or even occlusions are reasonably well-tolerated. Severe ischemia occurs when there are inadequate collaterals or there are multiple levels of disease.

Davì  G, Patrono  C: Platelet activation and atherothrombosis. N Engl J Med. 2008;358:1638.  [PubMed: 18403776]
Libby  P, Ridker  PM, Hansson  GK: Inflammation in atherosclerosis: from pathophysiology to practice. J Am Coll Cardiol. 2009;54:2129.  [PubMed: 19942084]


General Considerations

Peripheral arterial insufficiency is predominantly a disease of the lower extremities. Upper extremity arterial lesions are uncommon and confined mostly to the subclavian arteries. Even when present, upper extremity atherosclerosis rarely produces symptoms due to abundant collateral pathways. In the lower extremities, however, obstructive lesions are distributed widely, with lesions of ...

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