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Vuln plaque poster burke

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Vuln plaque poster burke

  1. 1. The “Vulnerable” Plaque: Frequencies in Sudden Coronary Death Allen P. Burke, M.D. Frank Kolodgie, Ph.D. Andrew Farb, M.D. Renu Virmani, M.D. Armed Forces Institute of Pathology Washington, D.C.
  2. 2. We serially sectioned the epicardial coronary arteries of 92 hearts from 59 men and 23 women dying with severe coronary disease ( 1≥ epicardial artery with 75% cross sectional luminal area narrowing).≥ The causes of death were assigned as incidental coronary disease, dying of other causes; coronary thrombosis overlying plaque erosion; acute thrombus overlying plaque rupture; stable plaque with healed infarct, no other cause of death found at autopsy; stable plaque with no other cause of death found at autopsy and no healed infarct. The purpose of the study was to determine the frequency and distribution of “unstable” or “vulnerable” plaques by mechanism of death. The number of thin cap atheromas was greatest in hearts with acute ruptures (2.2 ± 0.4), fewest in incidental coronary disease (0.4 ± 0.2), and intermediate in stable plaque (1.2 ± 0.4). The distribution of thin cap atheroma, fibroatheromas with hemorrhage, acute ruptures, and healed plaque ruptures was similar to one another, and concentrated in proximal segments. We conclude that the number of “vulnerable” plaques varies by acute coronary syndrome, and that they are concentrated in proximal segments, mirroring the distribution of plaque ruptures. ABSTRACT
  3. 3. Introduction The identification of “vulnerable plaques,” a term coined by Little in 1990 and further defined by Muller in 1992, is of paramount importance in potential imaging screening techniques. It has been shown that acute narrowing in the coronary arteries often occurs in areas of only moderate pre-existing atherosclerosis, and that plaque progression occurs largely as a result of episodic thrombosis and organization. There is a paradigm for the progression of plaques that lead to rupture; namely, formation of a large necrotic core, intraplaque hemorrhage, thinning of the fibrous cap, and ultimate breaking of the cap leading to thrombus in the lumen. Other forms of acute thrombus, such as plaque erosion, are less common than ruptures and do not have candidate precursor lesions at this time that potential imaging strategies can target. The purpose of this study is to identify the numbers and distribution of coronary thrombi and precursor lesions in a series of autopsy hearts, focusing on thin cap atheromas and their relationship to plaque rupture.
  4. 4. Materials A series of 92 consecutively hearts were examined, with epicardial coronary arteries sectioned serially at 3-5 mm intervals. Cases were selected on the basis of sudden unexpected death and 1≥ epicardial artery showing 75% cross sectional luminal narrowing.≥ Mechanisms of death were classified as noncoronary (incidental severe coronary disease after another cause of death was found after complete autopsy, n = 19), sudden death due to plaque erosion with or without acute myocardial infarction (n=5), sudden death due to acute plaque rupture, with or without acute myocardial infarction (n=32), sudden death due to atherosclerosis in the absence of healed infarct or coronary thrombus (n=17), and sudden death due to atherosclerosis in the absence of coronary thrombus, but in the presence of healed infarct (n=19).
  5. 5. Methods Every lesion with >50% cross sectional luminal narrowing was studied histologically and classified by the Virmani classification. The mean numbers of each type of plaque were compared by mechanism of death, and the association between thin cap atheromas and acute rupture was determined, based on relationship between the site of thin cap atheroma (same vessel or remote site) compared to the site of the ruptured plaque. The proximal regions consisted of the first 3 centimeters for the right coronary, before the first diagonal branch for the left anterior descending, and the obtuse marginal for the left circumflex. Middle segments were between 1st and 2nd diagonals for left anterior descending, between left obtuse marginal 1 and left obtuse marginal 2 for circumflex and beyond 3 cm of the right to the right marginal branch.
  6. 6. Case characteristics Mechanism of death Age, yrs (mean ± SD) Number of segments studied Mean heart weight (gm) Male: female Non- coronary (19) 54 ± 11 20 ± 12 534 ± 162 15:4 Plaque erosion (5) 45 ± 3 17 ± 7 486 ± 133 2:3 Stable plaque (17) 57 ± 15 28 ± 22 471 ± 92 9:8 Healed infarct (19) 59 ± 13 31 ± 15 558 ± 142 13:6 Acute plaque rupture (32) 52 ± 11 29 ± 28 506 ± 107 30:2
  7. 7. Classification of plaques Plaque type n Fibroatheroma 229 Fibroatheroma with hemorrhage 133 Plaque rupture 32 Plaque erosion 5 Healed rupture 75 Organized thrombus 68 Total 542
  8. 8. Frequency of fibroatheroma, by mechanism of death 00 22 44 66 88 1010 1212 NumbersoffibroatheromasNumbersoffibroatheromas noncoronarynoncoronary erosionerosion stableplaquestableplaque healedmihealedmi acuteruptureacuterupture
  9. 9. Frequency of intraplaque hemorrhage, by mechanism of deathNumbersofintraplaquehemorrhageNumbersofintraplaquehemorrhage noncoronarynoncoronary erosionerosion stableplaquestableplaque healedmihealedmi acuteruptureacuterupture 00 11 22 33 44 55 66
  10. 10. Frequency of healed rupture, by mechanism of death 00 11 22 33 44 55 66 77 NumbersofhealedrupturesNumbersofhealedruptures noncoronarynoncoronary erosionerosion stableplaquestableplaque healedmihealedmi acuteruptureacuterupture
  11. 11. Frequency of thin cap atheroma, by mechanism of death 00 .5.5 11 1.51.5 22 2.52.5 33 NumbersofthincapatheromasNumbersofthincapatheromas noncoronarynoncoronary erosionerosion stableplaquestableplaque healedmihealedmi acuteruptureacuterupture
  12. 12. Hearts with plaque rupture: distribution of thin cap atheromas # TCFA, same artery #TCFA, same side (r vs. left)* #TCFA, different side Mean number .48 ± .7 .43 ± .9 .70 ± .9 % with 1 TCFA 37% 32% 41% * different artery
  13. 13. Proportion of types of “unstable” plaques, by approximate distance from ostium 0 10 20 30 40 50 60 Fibro- atheroma hemorrhage into plaque thin cap acute rupture healed rupture left main proximal mid distal %distribution
  14. 14. Conclusions • The number of “vulnerable” plaques varies in patients dying with severe coronary disease by mechanism of death • Plaques with large cores, plaque hemorrhage and thin caps are most frequent in patients dying with acute plaque rupture, and infrequent in incidental severe disease and plaque erosion • Healed ruptures are most frequent in patients dying with acute ruptures and healed myocardial infarcts • Thin cap atheromas are are most predominant in the proximal segments, and are distributed similarly to other “unstable” plaques

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