Extent of Cholesterol Crystals in Coronary Artery Aspirates During Acute Myocardial Infarction

Abela, George S.; Shamoun, Fadi; Vedre, Ameeth; Pathak, Dorothy R.; Shah, Ibrahim; Dhar, Guarav; Leffler, Dale

doi:10.1016/s0735-1097(10)61020-0

Cited by 3 publications

(6 citation statements)

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“…Thus, released cholesterol crystals do flow downstream from the site of plaque rupture. Moreover, Gadeela et al Cholesterol Crystals, Vasospasm, and No-Reflow cholesterol crystals have been isolated from both atherectomy specimens and aspirates obstructing coronary arteries during acute coronary syndromes, confirming their presence during the acute event (8,15). Furthermore, we had previously demonstrated that cholesterol crystallizes under certain physical conditions (i.e., increase cholesterol saturation and drop in temperature) that may trigger plaque rupture (24).…”

Section: Discussionsupporting

confidence: 56%

“…There has been much controversy regarding the exact mechanism of no-reflow in the coronary arteries after interventional procedures. However, given our observations, it would be reasonable to infer that 2 mechanisms contribute to the no-reflow, one is vasospasm from endothelial injury and the other is obstruction by the particulate materials including cholesterol crystals (15,16). Moreover, recent studies have demonstrated that cholesterol crystals also trigger an inflammatory response not dissimilar to that described with uric acid crystals (25)(26)(27).…”

Section: Discussionmentioning

confidence: 57%

“…The crystals ranged in length from 200 to 300 m. After being injected into the artery and allowed to circulate for a period of 30 min, they were washed out of the system with PBS and the artery was allowed to stabilize for 20 min before the post-exposure pharmacological challenge. These synthetic crystals are almost identical in size and shape to those seen in human plaques (14,15,23). Microspheres.…”

Section: Methodsmentioning

confidence: 76%

“…However, the subsequent release of plaque material laden with cholesterol crystals traveling downstream may produce intimal injury that impairs vascular function that worsens ischemia and contributes to no-reflow after intervention (4 -13). Recently, we have demonstrated that plaque rupture is associated with cholesterol crystals extensively perforating the intima and their release into the arterial lumen (14,15). Once the plaque cap is torn, the contents, composed mostly of cholesterol crystals, are released into the arterial circulation and embolize distally, constituting a major component of the occlusive thromboatheroma.…”

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confidence: 99%

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The Impact of Circulating Cholesterol Crystals on Vasomotor Function

Gadeela

Rubinstein

Tamhane

et al. 2011

JACC: Cardiovascular Interventions

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Section: Discussionsupporting

confidence: 56%

Section: Discussionmentioning

confidence: 57%

Section: Methodsmentioning

confidence: 76%

mentioning

confidence: 99%

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The Impact of Circulating Cholesterol Crystals on Vasomotor Function

Gadeela

Rubinstein

Tamhane

et al. 2011

JACC: Cardiovascular Interventions

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“…). These crystals were similar in size and shape to CC found in human plaques (Abela et al, ; Abela et al, ; Gadeela et al, ).…”

Section: Methodssupporting

confidence: 72%

Role of cholesterol crystals in atherosclerosis is unmasked by altering tissue preparation methods

Nasiri

Janoudi

Vanderberg

et al. 2015

Microscopy Res & Technique

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Standard tissue preparation for light and scanning electron microscopy (SEM) uses ethanol as a dehydrating agent but that can also dissolve cholesterol crystals (CC) leaving behind empty tissue imprints or "clefts". Cholesterol crystals may contribute to plaque rupture by their sharp tips that can tear membranes and trigger inflammation. Therefore, use of ethanol in tissue processing can mask the pathological role of CC. Here we evaluated the amount of cholesterol dissolved from CC with single and complete series of standard graded ethanol concentrations (25-100%) used in tissue preparation. Also, solubility of CC in ethanol at physiological levels was measured. Furthermore, we compared the effect of ethanol on CC in fresh human atherosclerotic plaques to matched segments dehydrated using vacuum (-1 atm, 12h). Tissue crystal density ranging from 0 to +3 was measured semi-quantitatively by SEM. For CC exposed to 25% and 100% ethanol for 10 min each, 0.38% and 95% of CC were dissolved respectively. Also, increase in CC solubility was significant at physiological levels of ethanol (0.16%) compared to water (43.4 ± 18.0 ng/mL vs. 30.9 ± 13.9 ng/mL; p < 0.05). We speculate that this could represent a potential mechanism of cardio-protective effects of alcohol consumption. In atherosclerotic plaques, CC density was lower in ethanol vs. saline treatment (+1.2 vs. +2.8; P < 0.01) with visible dissolving noted by SEM. Ethanol has been used for centuries in tissue preparation for microscopy. Here we demonstrate how current tissue preparation methods greatly alter histological findings with SEM by masking the potential mechanism of plaque rupture.

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Cholesterol crystal embolization following plaque rupture: a systemic disease with unusual features

et al. 2017

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Cholesterol crystal embolic (CCE) syndrome is often a clinically challenging condition that has a poor prognostic implication. It is a result of plaque rupture with release of cholesterol crystals into the circulation that embolize into various tissue organs. Plaque rupture seems to be triggered by an expanding necrotic core during cholesterol crystallization forming sharp tipped crystals that perforate and tear the fibrous cap. Embolizing cholesterol crystals then initiate both local and systemic inflammation that eventually lead to vascular fibrosis and obstruction causing symptoms that can mimic other vasculitic conditions. In fact, animal studies have demonstrated that cholesterol crystals can trigger an inflammatory response via NLRP3 inflammasome similar to that seen with gout. The diagnosis of CCE syndrome often requires a high suspicion of the condition. Serum inflammation biomarkers including elevated sedimentation rate, abnormal renal function tests and eosinophilia are useful but non-specific. Common target organ involvement includes the skin, kidney, and brain. Various testing including fundoscopic eye examination and other non-invasive procedures such as trans-esophageal echocardiography and magnetic resonance imaging may be helpful in identifying the embolic source. Treatment includes aspirin and clopidogrel, high dose statin and possibly steroids. In rare cases, mechanical intervention using covered stents may help isolate the ruptured plaque. Anticoagulation with warfarin is not recommended and might even be harmful. Overall, CCE syndrome is usually a harbinger of extensive and unstable atherosclerotic disease that is often associated with acute cardiovascular events.

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Extent of Cholesterol Crystals in Coronary Artery Aspirates During Acute Myocardial Infarction

Cited by 3 publications

References 0 publications

The Impact of Circulating Cholesterol Crystals on Vasomotor Function

The Impact of Circulating Cholesterol Crystals on Vasomotor Function

Role of cholesterol crystals in atherosclerosis is unmasked by altering tissue preparation methods

Cholesterol crystal embolization following plaque rupture: a systemic disease with unusual features

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