768-6 Lipid Rich Plaques with Thrombus are Common in Unstable Rest Angina: Observations from Atherectomy Tissue Analysis

Abstract

Several autopsy studies indicate that disrupted atherosclerotic plaques particularly those rich in lipid with associated thrombus. are the cause of acute MI. Other plaques without disruption are fibrocellular without lipid. Although unstable rest angina (UA) shares a common pathogenesis to acute MI, there are little pathological data on plaque composition in UA. Directional Coronary Atherectomy (DCA) provides the opportunity to study plaque composition in UA. We prospectively analyzed the DCA tissue specimens of 60 pts with de novo culprit lesions for fibrocellular and lipid constituents by hematoxylin & eosin and oil red O stains. A fibrous plaque (FP) was defined as one which had predominantly fibrous and sclerotic tissue with no or minimallipid (0 or 1 + on scale of 3). A lipid plaque (LP) was defined as one with moderate or high lipid (2 or 3+) content. The presence of inflammatory cells and thrombus were also noted. Histopathology was analyzed independent of clinical presentation. Clinical syndrome FP(%) LP(%) P Stable/asymptomatic (10) 9(90) 1(10) New or Crescendo (16) 9 (56) 7 (44) Rest Angina (21) 4 (19) 17 (81) Post-MI (13) 2 (15) 11 (85) Coronary thrombus on histologic analysis was present in 23/36 (64%) of LP vs. in 5/24 (21%) of FP (p < 0.01). Coronary thrombus was present in 88% and 82% of LP in rest angina and post MI respectively. Inflammatory cells were noted in 12 LP and 2 FP (p = 0.02) — in 38% of both rest angina and post MI specimens. Lipid rich plaque are very common in rest angina and post MI, moderately common in crescendo or new onset and rare in stable angina. LP are usually associated with thrombus and inflammation particularly in rest angina and post MI pts. These DCA tissue analyses confirm and expanded on prior autopsy studies in acute syndromes and support the pathogenetic link between unstable rest angina and acute MI.