Cholesterol Embolism 

  • Author: Lisa Kirkland, MD, FACP, CNSP, MSHA; Chief Editor: Vincent Lopez Rowe, MD   more...
 
Updated: Aug 31, 2011
 

Background

Cholesterol embolism syndrome, shown below, should be suspected in a patient who develops worsening renal function, hypertension, distal ischemia, or acute multisystem dysfunction after an invasive arterial procedure. Atheroemboli may also occur spontaneously. The protean manifestations of this syndrome make the diagnosis challenging. As the population ages, the incidence of cholesterol embolism syndrome will increase.

See the image below.

Cholesterol crystal embolization from upstream corCholesterol crystal embolization from upstream coronary artery plaque after percutaneous transluminal coronary angioplasty.
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Pathophysiology

Key components of cholesterol embolism syndrome include the following:

  • Proximal, large caliber arterial plaque
  • Plaque rupture with embolization of debris
  • Mechanical occlusion of small arteries
  • Intense foreign body inflammation
  • End organ damage from mechanical obstruction
  • Inflammatory vascular changes

Any organ system, with the exception of the lungs, may be directly affected. Cholesterol embolism syndrome has 2 mechanisms of action.

In the first, cholesterol crystals spontaneously break off from severely atherosclerotic plaques and shower into downstream organs, occluding arterioles 100-200 micrometers in diameter. The crystals induce an inflammatory body reaction and adventitial fibrosis, which eventually obliterate the vessel lumen. Local vasospastic mediators compound tissue ischemia and produce progressive, irreversible organ damage.

With the second mechanism, larger cholesterol plaques break off and occlude larger arteries, causing tissue infarction with acute organ dysfunction. This can occur after local trauma to the atherosclerotic plaque, such as that caused by angiography or aortic trauma, or it can occur after destabilization of the protective clot overlying the plaque, which can occur as a result of anticoagulation.

Cholesterol crystal embolization occurs from the arterial system, and crystals are trapped in the arterioles where they either immediately occlude the vessels or induce an intense inflammatory response that leads to tissue ischemia. Crystals do not travel to the lungs; however, inflammatory mediators released by ischemic tissue may result in acute lung injury.

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Epidemiology

Frequency

United States

See Internationally below.

International

Estimates of the incidence of cholesterol embolic disease are usually based on autopsy data. Tissue sections from patients with the following diseases or indicate the incidence of atheroembolic events: aortic aneurysms (31%), abdominal aortic aneurysm repair (up to 77%), severe aortic disease (13-16%), and mild aortic disease (1-2%). Of patients undergoing angiography, 25-30% may have atheroembolic events, while 2.5-3% of patients who receive percutaneous coronary transluminal angioplasty vein grafts and 1.4-3% of patients undergoing renal artery angioplasty or cardiac catheterization have been reported to have clinical signs of atheroemboli.

Mortality/Morbidity

  • The mortality rate of acute multisystem organ failure resulting from cholesterol embolism syndrome is 58-90%. Jucgla found an overall incidence of 58% at 15 months, increasing to 65% if visceral organs were involved.[1] Pre-existing chronic renal insufficiency had a relative risk of death of 4.54.
  • The mortality rate of severe cholesterol embolism is 90% at 3 months.
  • Mild cases with renal dysfunction with or without skin findings had a mortality of 16%.

Sex

Men have a higher risk than women.

Age

Cholesterol embolism is a disease of persons ranging from middle-aged to elderly, with a minimum age of 50 years.

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Contributor Information and Disclosures
Author

Lisa Kirkland, MD, FACP, CNSP, MSHA  Assistant Professor, Department of Internal Medicine, Division of Hospital Medicine, Mayo Clinic; ANW Intensivists, Abbott Northwestern Hospital

Lisa Kirkland, MD, FACP, CNSP, MSHA is a member of the following medical societies: American College of Physicians, Society of Critical Care Medicine, and Society of Hospital Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Richard M Stillman†, MD, FACS  Honorary Medical Staff, Northwest Medical Center; Former Chief of Staff and Medical Director, Wound Healing Center, Department of Surgery, Northwest Medical Center

Richard M Stillman†, MD, FACS is a member of the following medical societies: American College of Angiology, American College of Surgeons, Association for Academic Surgery, and Society of University Surgeons

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Travis J Phifer, MD  Chief, Division of Vascular Surgery, Professor, Department of Surgery and Radiology, Louisiana State University Health Sciences Center in Shreveport

Travis J Phifer, MD is a member of the following medical societies: American College of Emergency Physicians, American College of Surgeons, American Medical Association, Association for Academic Surgery, Society for Academic Emergency Medicine, Society for Vascular Surgery, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Paolo Zamboni, MD  Professor of Surgery, Chief of Day Surgery Unit, Chair of Vascular Diseases Center, University of Ferrara, Italy

Paolo Zamboni, MD is a member of the following medical societies: American Venous Forum and New York Academy of Sciences

Disclosure: Nothing to disclose.

Chief Editor

Vincent Lopez Rowe, MD  Associate Professor of Surgery, Department of Surgery, Division of Vascular Surgery, University of Southern California Medical Center

Vincent Lopez Rowe, MD is a member of the following medical societies: American College of Surgeons, American Heart Association, Pacific Coast Surgical Association, Peripheral Vascular Surgery Society, Society for Clinical Vascular Surgery, Society for Vascular Surgery, and Western Vascular Surgical Society

Disclosure: Nothing to disclose.

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Cholesterol crystal embolization from upstream coronary artery plaque after percutaneous transluminal coronary angioplasty.
Necrosis of the abdominal wall in a patient with cholesterol embolism syndrome who received anticoagulation.
 
 
 
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