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.
Davì G, Patrono C: Platelet activation and atherothrombosis.
N Engl J Med 2008;358:1638.
- Decreased pulses.
- Low ankle-brachial index.
- Intermittent claudication.
- Cramping calf pain with walking.
- 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.
Peripheral arterial insufficiency is predominantly a disease of ...