Peripheral arterial disease pathophysiology

Peripheral arterial disease Microchapters
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AHA/ACC Guidelines on Management of Lower Extremity PAD
Guidelines for Clinical Assessment of Lower Extremity PAD
Guidelines for Diagnostic Testing for suspected PAD
Guidelines for Screening for Atherosclerotic Disease in Other Vascular Beds in patients with Lower Extremity PAD
Guidelines for Medical Therapy for Lower Extremity PAD
Guidelines for Structured Exercise Therapy for Lower Extremity PAD
Guidelines for Minimizing Tissue Loss in Lower Extremity PAD
Guidelines for Revascularization of Claudication in Lower Extremity PAD
Guidelines for Management of CLI in Lower Extremity PAD
Guidelines for Management of Acute Limb Ischemial in Lower Extremity PAD
Guidelines for Longitudinal Follow-up for Lower Extremity PAD
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Pathophysiology

• PAD is a manifestation of systemic atherosclerosis that has developed over many years.
• Atherosclerosis is a complex process that involves endothelial dysfunction, lipid disturbances, platelet activation, thrombosis, oxidative stress, vascular smooth muscle activation, altered matrix metabolism, remodeling and genetic factors
• Atherosclerosis frequently develops at arterial bifurcations and branches where endogenous atheroprotective mechanisms are impaired as a result of the effects of disturbed flow on endothelial cells
• The stages of atherosclerosis are divided into the following:

  • Lesion initiation

    • Results from endothelial dysfunction

  • Formation of the fatty streak

    • Results from an inflammatory lesion that develops first
    • Affects the intima of the artery and leads to formation of the foam cell
    • Fatty streak consists primarily of smooth muscle cells, monocytes, macrophages, and T and B cells

  • Fibroproliferative atheroma development

    • Originates from the fatty streak
    • Contains larger numbers of smooth muscle cells frlled with lipids

  • Advanced lesion development

    • Results from continued accumulation of cells that make up the fatty streak and fibroproliferative atheroma
    • Highly cellular
    • Contains intrinsic vascular cell walls (both endothelial and smooth muscle), and inflammatory cells (monocytes, macrophages, and T lymphocytes)
    • Also contains a lipid core covered by a fibrous cap

• Arteries initially compensate for atherosclerosis by remodeling, which causes the blood vessels to increase in size
• Advanced lesions eventually intrude into the lumen, resultsing in flow-limiting stenoses and chronic ischemic syndromes
• Acute arterial events occur if the fibrous cap is disrupted, the resulting exposure of the "prothrombotic" necrotic lipid core and subendothelial tissue leads to thrombus formation and flow occlusion
• In addition to coronary artery disease and cerebrovascular disease, PAD is one of the three major syndromes of atherothrombosis
• Atherothrombosis is the term currently used to describe the process of thrombus formation on top of a ruptured plaque located at a disease arterial segment
• Such atherosclerotic plaques tend to occur at vessel bifurcations, presumed to be due to both impaired atheroprotective mechanisms and disturbed blood flow leading to local intimal injury
• Panvascular disease refers to clinically significant atherosclerosis is present in multiple vascular beds

Diagram of arterial lumen (Image courtesy of Amjad Almahameed)

Associated Disorders

Many PVD patients also have angina pectoris or have had myocardial infarction. There is also an increased risk for stroke.

References

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