Cholesterol embolism syndrome 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.
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 two mechanisms of action.
With the first mechanism, cholesterol crystals spontaneously break off from severely atherosclerotic plaques and shower into downstream organs, occluding arterioles 100-200 μm in diameter. The crystals induce an inflammatory foreign-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 (see the image below) 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.
Any risk factor for atherosclerotic disease is a risk factor for cholesterol embolism.
Preoperative risk factors for cholesterol embolism syndrome after coronary artery bypass surgery (CABG) include the following:
Age greater than 60 years
Mitral annular calcification
Although the other factors have been well known for some time, it was only comparatively recently that the association between mitral annular calcification and aortic atherosclerosis was identified.
Identifying patients at risk and making efforts to minimize aortic wall trauma help reduce the chance of cholesterol embolism. The risk that cholesterol embolism will develop may be reduced by using a brachial or axillary approach in patients known to have severely ulcerated aortic plaque, using soft flexible catheters, and avoiding high-pressure jets of contrast material.
Estimates of the incidence of cholesterol embolic disease are usually based on autopsy data. Tissue sections from patients with the following diseases or procedures indicate the incidence of atheroembolic events:
Aortic aneurysms (31%)
Abdominal aortic aneurysm repair (up to 77%)
Severe aortic disease (13-16%)
Mild aortic disease (1-2%)
Of patients undergoing angiography, 25-30% may have atheroembolic events, whereas 2.5-3% of patients who receive percutaneous transluminal coronary angioplasty (PTCA) vein grafts and 1.4-3% of patients undergoing renal artery angioplasty or cardiac catheterization have been reported to have clinical signs of atheroemboli. Cholesterol embolism syndrome has been reported as occurring months after thrombolytic therapy for stroke, but the true incidence is unknown. [1, 2]
Age and sex-related demographics
Cholesterol embolism is a disease of persons ranging from middle-aged to elderly, with a minimum age of 50 years. The risk is greater for men than it is for women.
Patients with multisystem cholesterol embolism syndrome have a poor prognosis. The mortality 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.  Preexisting chronic renal insufficiency had a relative risk of death of 4.54.
The mortality of severe cholesterol embolism is 90% at 3 months. Mild cases with renal dysfunction, with or without skin findings, have a mortality of 16%.
Cholesterol crystal showers can become stabilized, leaving patients with varying degrees of organ dysfunction. Renal function can recover if no further insults occur, even to the degree that dialysis can be discontinued. However, patients remain at risk for recurrence of emboli.
Patients should be educated to watch for ulcerations and infections in chronically ischemic areas, particularly feet and toes. Ischemic neuropathy may exacerbate injury and tissue loss, predisposing the patient to gangrene.
For patient education resources, see the Cholesterol Center, as well as High Cholesterol, Cholesterol Charts (What the Numbers Mean), Lifestyle Cholesterol Management, and Cholesterol Lowering Medications.
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