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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, while those of aneurysmal disease are 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, other etiologies such as congenital and anatomical anomalies, arterial dissection, 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 be seen 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.

The hemodynamic circuit consists of the diseased major artery, a parallel system of collateral vessels, and 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 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. 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.

Atherosclerosis develops over decades. Significant luminal narrowing with reduced flow may produce ischemia with increased demand (exercise), or the presenting event may be sudden thrombosis. If there is adequate collateral flow, single stenoses or even occlusions are reasonably well tolerated. Severe ischemia is usually associated with multiple levels of disease.

Libby P: Atherosclerosis: the new view. Sci American 2002;286:46.  [PubMed: 11951331]
Davì G, Patrono C: Platelet activation and atherothrombosis. N Engl J Med 2008;358:1638.  [PubMed: 19476184]

Essentials of Diagnosis


  • Decreased pulses.
  • Low ankle-brachial index.
  • Intermittent claudication.
  • Cramping calf pain with walking.

Critical Limb Ischemia:

  • Rest pain of the foot relieved by dependency.
  • Ulceration of the foot or ankle.
  • Pallor of foot on elevation, rubor on dependency.
  • Gangrene and atrophy.

General Considerations

Peripheral arterial insufficiency is predominantly a disease of ...

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