Cholesterol Embolization Syndrome

Kronzon, Itzhak; Sarić, Muhamed

doi:10.1161/circulationaha.109.886465

Cited by 157 publications

(162 citation statements)

References 80 publications

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“…Advanced atherosclerosis is the most important independent risk factor for the development of CES. [1,2] The present patients had all risk factors except diabetes mellitus. CES may, rarely, occur spontaneously, but often follows invasive cardiovascular procedures such as cardiac catheterization, coronary or peripheral angiography, cardiovascular surgery, cardiopulmonary resuscitation, and anticoagulant and thrombolytic treatments.…”

Section: Case Reportmentioning

confidence: 62%

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Cholesterol embolization syndrome: report of two cases

Dizman

Bahat

Özkanlı

et al. 2016

Arch Turk Soc Cardiol

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Section: Case Reportmentioning

confidence: 62%

“…One of the most important characteristic features of CES is AKI with poor prognosis causing high incidence of irreversible organ damage. [1,2] Two cases of CES that developed after peripheral angiography are described in the present report.…”

mentioning

confidence: 77%

Cholesterol embolization syndrome: report of two cases

Dizman

Bahat

Özkanlı

et al. 2016

Arch Turk Soc Cardiol

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“…The five most commonly affected organs are skin, kidneys, lower extremity skeletal muscles, gastrointestinal tract, and brain [10]. It clinically manifests as livedo reticularis, blue toe/purple toe syndrome, renal failure, abdominal pain and neurological deficits.…”

Section: Discussionmentioning

confidence: 99%

“…It clinically manifests as livedo reticularis, blue toe/purple toe syndrome, renal failure, abdominal pain and neurological deficits. In the kidney, it primarily affects the arcuate and interlobar arteries, and can present as acute, subacute or chronic renal impairment [10,11]. Renal involvement is seen in more than 50% of the cases, with progression to dialysis in 28-61%, and 1 year mortality rate up to 83% [12].…”

Section: Discussionmentioning

confidence: 99%

Atheroembolic Renal Disease and Anticoagulants use: A Case Report and Literature Review

Pasupala

2012

World J Nephrol Urol

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Warfarin therapy is associated with improved clinical outcomes in several conditions including atrial fibrillation and thromboembolic disease. However, it can cause peripheral embolization by destabilizing the atherosclerotic plaque. This usually manifests as purple or blue toe syndrome, but isolated cases of renal manifestations are also reported. We report the case of a 77-year-old man who has been hemodialysis dependent due to warfarin induced atheroembolic renal disease. This is the most common cause of death in patients with cholesterol crystal embolization. Better understanding of the clinicopathological manifestations and high index of suspicion for the condition in predisposed patients can facilitate early diagnosis and potentially decrease the mortality risk.

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“…3 The prevalence of cholesterol crystal embolism in autopsy studies in unselected patients ranges from 0.7% to 4%. 4 This has also been shown to occur spontaneously in 1% of patients with transesophageal echocardiography-confirmed extensive thoracic aortic athersosclerotic disease when followed over 3 years.…”

mentioning

confidence: 99%

18F-FDG for imaging microvascular injury

Harikrishnan

Gerard

Jain

2018

Journal of Nuclear Cardiology

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Atherosclerosis is an inflammatory process where oxidation of low-density lipoproteins (LDL) in the arterial wall causes initiation and progression of the atherosclerotic plaque by attracting macrophages. 1 The necrotic core of the vulnerable atherosclerotic plaque is rich in free cholesterol crystals derived from apoptotic lipid-laden macrophages and from the membranes of red blood cells which enter the core during intraplaque hemorrhage. 2 Vulnerable plaque is more prone to rupture. The plaque rupture triggers macrophage activation, tissue factor release, platelet aggregation, thrombus formation, thromboembolization, cholesterol embolization, arterial obstruction, end organ ischemia and necrosis. Atherosclerosis is a dynamic process and many of its clinical manifestations such as myocardial infarction, ischemic stroke, transient ischemic attack, acute mesenteric ischemia, acute limb ischemia, and renal injury occur as a consequence of rupture of the vulnerable atherosclerotic plaque. So it is very important to understand the various mechanisms behind the distal organ injury caused by acute plaque rupture.Cholesterol crystal embolization (CCE) is one known mechanism of organ injury from atherosclerotic plaque rupture and it may happen spontaneously or by the endothelial trauma during instrumentation of an artery. 3 The prevalence of cholesterol crystal embolism in autopsy studies in unselected patients ranges from 0.7% to 4%. 4 This has also been shown to occur spontaneously in 1% of patients with transesophageal echocardiography-confirmed extensive thoracic aortic athersosclerotic disease when followed over 3 years. 5 CCE occurs in 3% of patients who underwent infrarenal aortic and infrainguinal vascular surgery or angiographic manipulation, 6 in 0.8% of patients undergoing cardiac catheterization, 7 and in 0.2% of patients undergoing cardiac surgery. 8 CCE causes organ injury by multiple mechanisms. In this issue of the Journal of Nuclear Cardiology, Pervaiz MH et al 9 examine the nonobstructive, non-ischemic, direct toxicity of cholesterol crystals as a cause of left thigh muscle inflammation and injury in a controlled animal study after injecting cholesterol crystals, polystyrene microsphere control, or saline control into the left femoral artery of rabbits. Thigh muscle inflammation and injury was assessed by 18 F-FDG PET/CT and angiography, which were then correlated with inflammatory markers such as tissue macrophage infiltration density and muscle injury markers such as creatine phosphokinase (CPK) levels. There was more muscle inflammation and injury in the cholesterol crystal group compared to the control groups as demonstrated by high maximum standardized uptake values of the left thigh muscles by PET/CT (0.40 ± 0.16 vs 0.21 ± 0.11 and 0.23 ± 0.06; P = .038 and P = .036, respectively), high CPK levels at 24 hours (7.46 ± 4.32 vs 1.57 ± 0.84 and 1.43 ± 0.57; P = .007 and P = .023, respectively), and high macrophage density in the muscle biopsy.CCE may cause organ injury by multiple mechanisms such as ...

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Cholesterol Embolization Syndrome

Cited by 157 publications

References 80 publications

Cholesterol embolization syndrome: report of two cases

Cholesterol embolization syndrome: report of two cases

Atheroembolic Renal Disease and Anticoagulants use: A Case Report and Literature Review

18F-FDG for imaging microvascular injury

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