Richard J Frink1. 1. Heart Research Foundation of Sacramento, 1007 39th Street, Sacramento, CA 95816-5502, USA. rjfrink@hrfsac.org
Abstract
BACKGROUND: Currently, there are no available methods that can reliably predict when or if an atheroma will rupture. Recent reports suggest cholesterol crystals (CCs), present within the necrotic core, are sharp and can penetrate and disrupt the fibrous cap, contributing to plaque rupture. Our aim is to show CC, normally distributed at random within the necrotic core, often develop a parallel configuration at the site of plaque disruption (PD) which may be a sign of impending plaque rupture. METHODS AND RESULTS: The coronary arteries of 83 patients who died of acute coronary disease (ACD) were injected with a colored barium gelatin mass. The arteries were dissected, decalcified, cut at 2-3 mm intervals, and all segments mounted for microscopic study. All segments were reviewed to identify PDs and to determine the frequency of parallel cholesterol crystals (P-CCs) at the site of these PDs. There were 215 separate PDs in 83 patients, with 64 (77%) patients showing more than one PD. P-CCs were present in 126 (59%) of all PDs regardless of plaque size or the severity of luminal stenosis and were present with or without luminal thrombosis. Luminal thrombosis was present in 105 PDs (49%), primarily in those segments showing significant luminal stenosis. There was no significant difference in the frequency of luminal thrombosis in those PDs with or without P-CCs. CONCLUSIONS: P-CCs are commonly present at the site of PD and may contribute to PD by penetrating and disrupting the fibrous cap. The ability to recognize this parallel configuration may help to identify plaques with impending plaque rupture.
BACKGROUND: Currently, there are no available methods that can reliably predict when or if an atheroma will rupture. Recent reports suggest cholesterol crystals (CCs), present within the necrotic core, are sharp and can penetrate and disrupt the fibrous cap, contributing to plaque rupture. Our aim is to show CC, normally distributed at random within the necrotic core, often develop a parallel configuration at the site of plaque disruption (PD) which may be a sign of impending plaque rupture. METHODS AND RESULTS: The coronary arteries of 83 patients who died of acute coronary disease (ACD) were injected with a colored barium gelatin mass. The arteries were dissected, decalcified, cut at 2-3 mm intervals, and all segments mounted for microscopic study. All segments were reviewed to identify PDs and to determine the frequency of parallel cholesterol crystals (P-CCs) at the site of these PDs. There were 215 separate PDs in 83 patients, with 64 (77%) patients showing more than one PD. P-CCs were present in 126 (59%) of all PDs regardless of plaque size or the severity of luminal stenosis and were present with or without luminal thrombosis. Luminal thrombosis was present in 105 PDs (49%), primarily in those segments showing significant luminal stenosis. There was no significant difference in the frequency of luminal thrombosis in those PDs with or without P-CCs. CONCLUSIONS: P-CCs are commonly present at the site of PD and may contribute to PD by penetrating and disrupting the fibrous cap. The ability to recognize this parallel configuration may help to identify plaques with impending plaque rupture.