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A Natural History Study of Atherosclerosis Using Multimodality Intracoronary Imaging to Prospectively Identify Vulnerable Plaque Gregg W. Stone, MD PROSPECT.

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Presentation on theme: "A Natural History Study of Atherosclerosis Using Multimodality Intracoronary Imaging to Prospectively Identify Vulnerable Plaque Gregg W. Stone, MD PROSPECT."— Presentation transcript:

1 A Natural History Study of Atherosclerosis Using Multimodality Intracoronary Imaging to Prospectively Identify Vulnerable Plaque Gregg W. Stone, MD PROSPECT Investigators Providing Regional Observations to Study Predictors of Events in the Coronary Tree The PROSPECT Trial

2 Gregg W. Stone Gregg W. Stone Scientific Advisory Board, Abbott Vascular Devices Scientific Advisory Board, Abbott Vascular Devices Consultant to InfraReDx Consultant to InfraReDx

3 Most cases of sudden cardiac death and MI are believed to arise from plaque rupture with subsequent thrombotic coronary occlusion of angiographically mild lesions (vulnerable plaques), the prospective detection of which has not been achievedMost cases of sudden cardiac death and MI are believed to arise from plaque rupture with subsequent thrombotic coronary occlusion of angiographically mild lesions (vulnerable plaques), the prospective detection of which has not been achieved The event rate attributable to progression of vulnerable plaque has never been prospectively assessedThe event rate attributable to progression of vulnerable plaque has never been prospectively assessed Most cases of sudden cardiac death and MI are believed to arise from plaque rupture with subsequent thrombotic coronary occlusion of angiographically mild lesions (vulnerable plaques), the prospective detection of which has not been achievedMost cases of sudden cardiac death and MI are believed to arise from plaque rupture with subsequent thrombotic coronary occlusion of angiographically mild lesions (vulnerable plaques), the prospective detection of which has not been achieved The event rate attributable to progression of vulnerable plaque has never been prospectively assessedThe event rate attributable to progression of vulnerable plaque has never been prospectively assessed The PROSPECT Trial Background

4 PROVE-IT TIMI-22 4,162 Randomized Pts with ACS 16% RR 16% RR P = Pravastatin 40 mg/d Atorvastatin 80 mg/d 26.3% 22.4% Death, MI, UA requiring hosp, revasc >30d, or stroke (%) Cannon CP et al. NEJM 2004;350: How many events were attributable to: 1) Restenosis, stent thrombosis, etc. vs. 2) Significant disease left behind, vs. 3) VP with rapid lesion progression? ACS median 7d PCI 69%

5 We therefore performed a prospective, multicenter natural history study using 3 vessel multimodality intracoronary imaging to quantify the clinical event rate due to atherosclerotic progression and to identify those lesions which place pts at risk for unexpected adverse cardiovascular eventsWe therefore performed a prospective, multicenter natural history study using 3 vessel multimodality intracoronary imaging to quantify the clinical event rate due to atherosclerotic progression and to identify those lesions which place pts at risk for unexpected adverse cardiovascular events The PROSPECT Trial Background

6 700 pts with ACS UA (with ECGΔ) or NSTEMI or STEMI >24º undergoing PCI of 1 or 2 major coronary arteries at up to 40 sites in the U.S. and Europe at up to 40 sites in the U.S. and Europe PCI of culprit lesion(s) Successful and uncomplicated Formally enrolled Metabolic S. Waist circumWaist circum Fast lipidsFast lipids Fast gluFast glu HgbA1CHgbA1C Fast insulinFast insulin CreatinineCreatinineBiomarkers Hs CRPHs CRP IL-6IL-6 sCD40LsCD40L MPOMPO TNFαTNFα MMP9MMP9 Lp-PLA2Lp-PLA2 othersothers PI: Gregg W. Stone Sponsor: Abbott Vascular; Partner: Volcano The PROSPECT Trial

7 3-vessel imaging post PCI Culprit artery, followed by non-culprit arteries Angiography (QCA of entire coronary tree) IVUS Virtual histology Palpography (n=~350) Repeat imaging in pts with events Meds rec Aspirin Plavix 1yr Statin Repeat 30 days, 6 months Proximal 6-8 cm of each coronary artery MSCTSubstudyN= F/U: 1 mo, 6 mo, 1 yr, 2 yr, ±3-5 yrs F/U: 1 mo, 6 mo, 1 yr, 2 yr, ±3-5 yrs The PROSPECT Trial

8 PROSPECT: Primary Endpoint MACE attributable to rapid angiographic progression of a non-culprit lesion* Cardiac death Cardiac death Cardiac arrest Cardiac arrest Myocardial infarction Myocardial infarction Unstable angina Unstable angina - Requiring revascularization - Requiring rehospitalization Increasing angina Increasing angina - Requiring revascularization - Requiring rehospitalization MACE attributable to rapid angiographic progression of a non-culprit lesion* Cardiac death Cardiac death Cardiac arrest Cardiac arrest Myocardial infarction Myocardial infarction Unstable angina Unstable angina - Requiring revascularization - Requiring rehospitalization Increasing angina Increasing angina - Requiring revascularization - Requiring rehospitalization MACE during FU were adjudicated by the CEC as attributable to culprit lesions (those treated during or before the index hospitalization) or non culprit lesions (untreated areas of the coronary tree) based on angiography (+ECGs, etc.) at the time of the event; events occurring in pts without angiographic follow-up were considered indeterminate in origin. Rapid lesion progression = in QCA DS by >20% from baseline to FU. Hierarchical Most severe Least severe

9 PROSPECT: Methodology Angiographic Core Lab Analysis Performed on every coronary artery (main vessel and branch) visually 1.5 mm in diameter Performed on every coronary artery (main vessel and branch) visually 1.5 mm in diameter Detailed qualitative and quantitative parameters recorded for every 1.5 mm length segment Detailed qualitative and quantitative parameters recorded for every 1.5 mm length segment Distance from ostia and at major branch points were registered and corrected for foreshortening after IVUS co-registration Distance from ostia and at major branch points were registered and corrected for foreshortening after IVUS co-registration Lesions with DS 30% by visual assessment identified Lesions with DS 30% by visual assessment identified Output available as lesions, CASS segments, and vessels, by every mm, or any other parameter Output available as lesions, CASS segments, and vessels, by every mm, or any other parameter Performed on every coronary artery (main vessel and branch) visually 1.5 mm in diameter Performed on every coronary artery (main vessel and branch) visually 1.5 mm in diameter Detailed qualitative and quantitative parameters recorded for every 1.5 mm length segment Detailed qualitative and quantitative parameters recorded for every 1.5 mm length segment Distance from ostia and at major branch points were registered and corrected for foreshortening after IVUS co-registration Distance from ostia and at major branch points were registered and corrected for foreshortening after IVUS co-registration Lesions with DS 30% by visual assessment identified Lesions with DS 30% by visual assessment identified Output available as lesions, CASS segments, and vessels, by every mm, or any other parameter Output available as lesions, CASS segments, and vessels, by every mm, or any other parameter

10 Gray-scale IVUS volumetric and cross-sectional analysis performed Gray-scale IVUS volumetric and cross-sectional analysis performed Each IVUS/VH frame co-registered to corresponding QCA location using fiduciary branch points Each IVUS/VH frame co-registered to corresponding QCA location using fiduciary branch points IVUS lesions (3 consecutive frames with cross sectional plaque burden >40%) were characterized IVUS lesions (3 consecutive frames with cross sectional plaque burden >40%) were characterized IVUS-VH analysis performed using the latest classification tree (pcVH 2.1) IVUS-VH analysis performed using the latest classification tree (pcVH 2.1) Plaque characterized as fibrotic, fibrofatty, necrotic core or dense calcium, and reported as absolute and relative area/volumes Plaque characterized as fibrotic, fibrofatty, necrotic core or dense calcium, and reported as absolute and relative area/volumes Gray-scale IVUS volumetric and cross-sectional analysis performed Gray-scale IVUS volumetric and cross-sectional analysis performed Each IVUS/VH frame co-registered to corresponding QCA location using fiduciary branch points Each IVUS/VH frame co-registered to corresponding QCA location using fiduciary branch points IVUS lesions (3 consecutive frames with cross sectional plaque burden >40%) were characterized IVUS lesions (3 consecutive frames with cross sectional plaque burden >40%) were characterized IVUS-VH analysis performed using the latest classification tree (pcVH 2.1) IVUS-VH analysis performed using the latest classification tree (pcVH 2.1) Plaque characterized as fibrotic, fibrofatty, necrotic core or dense calcium, and reported as absolute and relative area/volumes Plaque characterized as fibrotic, fibrofatty, necrotic core or dense calcium, and reported as absolute and relative area/volumes PROSPECT: Methodology IVUS/VH Core Lab Analysis

11 Lesions are classified into 5 main types 1. Fibrotic 2. Fibrocalcific 3. Pathological intimal thickening (PIT) 4. Thick cap fibroatheroma (ThCFA) 5. VH-thin cap fibroatheroma (VH-TCFA) (presumed high risk) PROSPECT: Methodology Virtual histology lesion classification

12 Index 2/13/06 Event 2/6/07 QCA PLCX DS 28.6% QCA PLCX DS 71.3% PROSPECT : 52 yo 2/13/06: NSTEMI, PCI of MLAD 2/6/07 (51 weeks later): NSTEMI attributed to LCX

13 38 1. ThCFA * OM 5.3 mm 2 Lesion * 1 prox PROSPECT : Index 2/13/06 Baseline PLCX QCA: RVD 2.82 mm, DS 28.6%, length 6.8 mm IVUS: MLA 5.3 mm 2 VH: ThCFA

14 PROSPECT: Event Categories CEC adjudicated MACE during follow-up CEC adjudicated MACE during follow-up Culprit lesion (stent) related Culprit lesion (stent) related - Stent thrombosis - Restenosis - New side branch lesion Non culprit lesion related Non culprit lesion related - With rapid lesion progression (by QCA) (classic vulnerable plaque) - Without rapid lesion progression Indeterminate Indeterminate

15 PI: Gregg W. Stone; Co-PI: Patrick W. Serruys European Co-PI: Bernard de Bruyne PI: Gregg W. Stone; Co-PI: Patrick W. Serruys European Co-PI: Bernard de Bruyne Data management: Abbott Vascular; Zhen Zhang (lead statistician) Data management: Abbott Vascular; Zhen Zhang (lead statistician) Clinical events committee: CRF, Roxana Mehran (Chair), George Dangas Clinical events committee: CRF, Roxana Mehran (Chair), George Dangas Core laboratories Core laboratories QCA: CRF, Alexandra Lansky (Director), Ecaterina Cristea QCA: CRF, Alexandra Lansky (Director), Ecaterina Cristea IVUS, Virtual Histology: CRF, Akiko Maehara (Director), Gary S. Mintz IVUS, Virtual Histology: CRF, Akiko Maehara (Director), Gary S. Mintz Palpography: Cardialysis, Marie-Angèle Morel Palpography: Cardialysis, Marie-Angèle Morel MSCT: Thoraxcenter, Pim de Feyter (Director) MSCT: Thoraxcenter, Pim de Feyter (Director) Biomarkers: CRL Medinet Biomarkers: CRL Medinet DSMB: Steve Steinhubl (Chair) DSMB: Steve Steinhubl (Chair) Sponsor and Partner: Abbott Vascular and Volcano Corp. Sponsor and Partner: Abbott Vascular and Volcano Corp. Abbott Vascular Program Leads: Barry Templin and Wai-Fung Cheong Abbott Vascular Program Leads: Barry Templin and Wai-Fung Cheong PROSPECT: Organization

16 700 pts enrolled between Oct and June 2006 and followed for at least 3 years Europe: 403 pts enrolled at 18 sites Europe: 403 pts enrolled at 18 sites U.S.: 297 pts enrolled at 19 sites 66 pts Rotterdam (Serruys) 64 pts St. Thomas (McPherson) 54 pts Aalst (de Bruyne) 44 pts Elyria Memorial Hosp (Farhat) 40 pts St. Lukes Hosp (Marso) 38 pts Gothenburg (Wennerblom) 32 pts Vigo (Iniguez) 31 pts Toulouse (Fajadet) 30 pts South Carolina Heart (Foster) 28 pts Antwerp (Verheye) Top 10 enrollers PROSPECT: Enrollment

17 PROSPECT: Baseline Features N = 697* *3 patients who were never consented were de-registered

18 Age (yrs, median) 58 [50, 66] Gender (female) 24.0% Diabetes mellitus 16.9% - Insulin requiring - Insulin requiring3.0% Current cigarette use 47.1% Hypertension45.8% Hyperlipidemia40.0% Prior MI 10.5% Single / double / triple vessel disease 20% / 41% / 39% Total arteries with vs. without PCI 892, 1199 PCI performed in 1 or 2 arteries 72% / 28% PCI of LAD / LCX / RCA (per artery) 41% / 27% / 32% Median [IQR] follow-up (years) 3.4 [1.9, 3.9] PROSPECT: Baseline Features N = 697

19 PROSPECT: Imaging Summary Length of coronary arteries analyzed (core lab) Mean (mm) Angiography(N=697) IVUS and VH (N=615)LM 9.3 ± ± 6.3 LAD ± ± 33.2 LCX ± ± 35.9 RCA ± ± 38.0 Total per pt ± ± 81.6 Total all pts 311,016118,670

20 Virtual histology (N=2689 lesions in 615 pts) - Mean plaque composition- Plaque subtype N=2689Fibrotic2.5% Fibrocalcific1.1% PIT35.9% Fibroatheroma59.9% - Thick cap 37.8% - VH-TCFA 22.1% - Single, - Ca - Single, - Ca5.4% - Single, + Ca - Single, + Ca0.5% - Multiple, - Ca - Multiple, - Ca9.8% - Multiple, + Ca - Multiple, + Ca6.4% Unclassified0.7% PROSPECT: Imaging Summary

21 Per patient incidence of VH-TCFAs 51.2% of pts have 1 VH-TCFA 0.97 ±1.30 VH-TCFAs per pt (range 0 – 7 per pt) Total of 594 VH-TCFA lesions in 615 pts N lesions/patient: PROSPECT: Imaging Summary

22 PROSPECT: MACE MACE (%) Time in Years 0123 All Culprit lesion (CL) related Non culprit lesion (NCL) related Indeterminate Number at risk ALL CL related NCL related Indeterminate % 20.4% 11.6% 2.7%

23 PROSPECT: MACE MACE (%) Time in Years 0123 All Culprit lesion (CL) related Non culprit lesion (NCL) related Indeterminate Number at risk 20.4% 12.9% 11.6% 2.7%13.2% 7.9% 6.4% 0.9% 18.1% 11.4% 9.4% 1.9%ALL CL related NCL related Indeterminate

24 PROSPECT: MACE 3-year follow-up, non hierarchical All Culprit lesion related Non culprit lesion related Indeter- minate Cardiac death 1.9% (12) 0.2% (1) 0% (0) 1.8% (11) Cardiac arrest 0.5% (3) 0.3% (2) 0% (0) 0.2% (1) MI (STEMI or NSTEMI) 3.3% (21) 2.0% (13) 1.0% (6) 0.3% (2) Unstable angina 8.0% (51) 4.5% (29) 3.3% (21) 0.5% (3) Increasing angina 14.5% (93) 9.2% (59) 8.5% (54) 0.3% (2) Composite MACE 20.4% (132) 12.9% (83) 11.6% (74) 2.7% (17) Cardiac death, arrest or MI 4.9% (31) 2.2% (14) 1.0% (6) 1.9% (12) Rates are 3-yr Kaplan-Meier estimates (n of events)

25 PROSPECT: MACE Sensitivity analysis*: 3-year FU, non hierarchical All Culprit lesion related Non culprit lesion related* Cardiac death 1.9% (12) 0.2% (1) 1.8% (11) Cardiac arrest 0.5% (3) 0.3% (2) 0.2% (1) MI (STEMI or NSTEMI) 3.3% (21) 2.0% (13) 1.3% (8) Unstable angina 8.0% (51) 4.5% (29) 3.8% (24) Increasing angina 14.5% (93) 9.2% (59) 8.8% (56) Composite MACE 20.4% (132) 12.9% (83) 13.3% (85) Cardiac death, arrest or MI 4.9% (31) 2.2% (14) 2.9% (18) Rates are 3-yr Kaplan-Meier estimates (n of events) *Assuming all indeterminate events are non culprit related

26 MACE (%) Time in Years 0123 NCL related, all without RLP - without RLP with RLP - with RLP Number at risk Non-culprit lesion (NCL) related, all - Without rapid lesion progression (RLP) - Without rapid lesion progression (RLP) - With rapid lesion progression (RLP) - With rapid lesion progression (RLP) PROSPECT: NCL MACE %6.7% 6.4%

27 MACE (%) Time in Years 0123 Number at risk Non-culprit lesion (NCL) related, all - Without rapid lesion progression (RLP) - Without rapid lesion progression (RLP) - With rapid lesion progression (RLP) - With rapid lesion progression (RLP) %6.7% 6.4% 2.9% 4.1% 6.4% 5.5% 4.9% 9.4% NCL related, all without RLP - without RLP with RLP - with RLP PROSPECT: NCL MACE Median time to event No RLP: 223 [85, 663] days RLP: 401 [229, 666] RLP: 401 [229, 666] days

28 PROSPECT: Correlates of Non Culprit Related Events Baseline variables examined (n=152) Demographic, history and PE (n=19) Labs (n=7; including CrCl, lipids, hgbA1C, CRP) Angio non core lab (n=1; visible lesions >30% DS) QCA measures (n=12) IVUS area and volumetric measures (n=22) Virtual histology measures (n=74) Treatment related (n=1; # vessels stented) Medications in-hosp. and at discharge (n=16)

29 PROSPECT: Correlates of Non Culprit Lesion Related Events Patient level events at median 3.4 yrs (76 events in 689 pts*) Baseline Demographic and Angiographic Variables VariableKM Rate (n)HR [95% CI]HR [95% CI]P Insulin DM (n=21)41.4% (6)4.07 [1.75, 9.46]0.001 Non insulin DM (n=96)16.3% (14) Non insulin DM (n=96)16.3% (14)1.55 [0.86, 2.79]0.14 Non diabetic (n=569)10.7% (56) Hypertension (n=314)14.7% (42)1.64 [1.03, 2.60]0.04 No hypertension (n=369)9.1% (31) Prior PCI (n=75)23.1% (15)2.20 [1.25, 3.86]0.006 No prior PCI (n=613)10.8% (61) 1 visible angio lsn* (n=582)13.7% (73)4.72 [1.49, 14.98]0.008 No visible angio lsn (n=107)3.2% (3) *Visually assessed DS >30% Univariate, unadjusted. * 8 patients with indeterminate events were excluded.

30 VariableRate (n)HR [95% CI]HR [95% CI]P MLA < median 5.9 mm 2 (n=1336)3.4% (45)]< MLA < median 5.9 mm 2 (n=1336)3.4% (45)7.53 [3.21, 17.65]< MLA median 5.9 mm 2 (n=1337)0.4% (6) MLA 4.0 mm 2 (n=496) 5.4% (27)] < MLA 4.0 mm 2 (n=496) 5.4% (27)5.01 [2.89, 8.68] < MLA > 4.0 mm 2 (n=2177) 1.1% (24) PB MLA median 0.55 (n=1337)3.3% (44)6]< PB MLA median 0.55 (n=1337)3.3% (44)6.37 [2.87, 14.15]< PB MLA < median 0.55 (n=1336)0.5% (7) PB MLA 0.70 (n=242)9.1% (22)< PB MLA 0.70 (n=242)9.1% (22)7.94 [4.56, 13.81] < PB MLA < 0.70 (n=2431)1.2% (29) EEM MLA med 14.3 mm 2 (n=1337) 1.4% (19)0.60 [0.34, 1.06]0.08 EEM MLA < med 14.3 mm 2 (n=1336) 2.4% (32) Lsn length < med 11.6 mm (n=1336) 0.7% (10)] < Lsn length < med 11.6 mm (n=1336) 0.7% (10)4.01 [2.01, 8.02] < Lsn length med 11.6 mm (n=1337) 3.1% (41) PROSPECT: Correlates of Non Culprit Lesion Related Events Lesion level events (51 events from 2673 lesions in 609 pts at median 3.4 yrs) IVUS Characteristics (area data) MLA = minimal luminal area; PB MLA = plaque burden at the MLA; EEM MLA = external elastic membrane at the MLA. Data represent univariate associations, unadjusted

31 VariableRate (n)HR [95% CI]HR [95% CI]P VH-TCFA (n=590)4.4% (26)3]< VH-TCFA (n=590)4.4% (26)3.84 [2.22, 6.65]< Not VH-TCFA (n=2065)1.2% (25) ThCFA (n=1005)1.8% (18)]0.69 ThCFA (n=1005)1.8% (18)0.89 [0.50, 1.58]0.69 Not ThCFA (n=1650)2.0% (33) PIT (n=964)0.6% (6)]0.001 PIT (n=964)0.6% (6)0.23 [0.10, 0.53]0.001 Not PIT (n=1691)2.7% (45) Fibrotic (n=67)0% (0)0.99 Fibrotic (n=67)0% (0)-0.99 Not Fibrotic (n=2588)2.0% (51) Fibrocalcific (n=29)3.4% (1)]0.58 Fibrocalcific (n=29)3.4% (1)1.75 [0.24, 12.63]0.58 Not fibrocalcific (n=2626)1.9% (50) PROSPECT: Correlates of Non Culprit Lesion Related Events TCFA = thin cap fibroatheroma; ThCFA = thick cap fibroatheroma; PIT = pathologic intimal thickening. Univariate, unadjusted. Lesion level events (51 events from 2655 lesions in 609 pts at median 3.4 yrs) Virtual Histology Plaque Type

32 PROSPECT: Multivariable Correlates of Non Culprit Lesion Related Events Independent predictors of lesion level events by logistic regression analysis Variables entered into the model: Minimal luminal area (MLA); plaque burden at the MLA (PB MLA ); external elastic membrane at the MLA (EEM MLA )

33 PROSPECT: Correlates of Non Culprit Lesion Related Events Lesion HR Lesion HR 3.8 (2.2, 6.6) 5.0 (2.9, 8.7) 7.9 (4.6, 13.8) 6.4 (3.4, 12.2) 6.7 (3.4, 13.0) 10.8 (5.5, 21.0) 10.8 (4.3, 27.2) P value < < < < < < < P value < < < < < < < Prevalence*51.2%49.1%30.7% 17.4% 15.4%11.0% 4.6% Prevalence*51.2%49.1%30.7% 17.4% 15.4%11.0% 4.6% *Likelihood of one or more such lesions being identified per patient. PB = plaque burden at the MLA

34 PROSPECT: VH-TCFA and Non Culprit Lesion Related Events Lesion HR Lesion HR 3.84 (2.22, 6.65) 6.41 (3.35, 12.24) (5.53, 21.00) (4.30, 27.22) P value < < <0.0001< P value < < <0.0001< Prevalence*51.2%17.4%11.0% 4.6% Prevalence*51.2%17.4%11.0% 4.6% *Likelihood of one or more such lesions being present per patient. PB = plaque burden at the MLA

35 PROSPECT: PIT and Non Culprit Lesion Related Events Lesion HR Lesion HR 0.24 (0.10, 0.56) 1.15 ( ) 1.36 (0.19, 9.86) 2.85 (0.39, 20.67) P value P value Prevalence*68.6%17.2%5.7% 2.6% Prevalence*68.6%17.2%5.7% 2.6% *Likelihood of one or more such lesions being present per patient. PB = plaque burden at the MLA

36 PROSPECT: Conclusions From this trial, the first prospective, natural history study of atherosclerosis using multimodality imaging to characterize the coronary tree, we can conclude that:From this trial, the first prospective, natural history study of atherosclerosis using multimodality imaging to characterize the coronary tree, we can conclude that: Approximately 20% of pts with ACS successfully treated with stents and contemporary medical Rx develop MACE within 3 years, with adverse events equally attributable to recurrence at originally treated culprit lesions (treatment failure) and to previously untreated non culprit coronary segmentsApproximately 20% of pts with ACS successfully treated with stents and contemporary medical Rx develop MACE within 3 years, with adverse events equally attributable to recurrence at originally treated culprit lesions (treatment failure) and to previously untreated non culprit coronary segments Approximately 12% of pts develop MACE from non culprit lesions during 3 years of follow-upApproximately 12% of pts develop MACE from non culprit lesions during 3 years of follow-up Patients treated with contemporary medical therapy who develop non culprit lesion events present most commonly with progressive or unstable angina, and rarely with cardiac death, cardiac arrest or MIPatients treated with contemporary medical therapy who develop non culprit lesion events present most commonly with progressive or unstable angina, and rarely with cardiac death, cardiac arrest or MI From this trial, the first prospective, natural history study of atherosclerosis using multimodality imaging to characterize the coronary tree, we can conclude that:From this trial, the first prospective, natural history study of atherosclerosis using multimodality imaging to characterize the coronary tree, we can conclude that: Approximately 20% of pts with ACS successfully treated with stents and contemporary medical Rx develop MACE within 3 years, with adverse events equally attributable to recurrence at originally treated culprit lesions (treatment failure) and to previously untreated non culprit coronary segmentsApproximately 20% of pts with ACS successfully treated with stents and contemporary medical Rx develop MACE within 3 years, with adverse events equally attributable to recurrence at originally treated culprit lesions (treatment failure) and to previously untreated non culprit coronary segments Approximately 12% of pts develop MACE from non culprit lesions during 3 years of follow-upApproximately 12% of pts develop MACE from non culprit lesions during 3 years of follow-up Patients treated with contemporary medical therapy who develop non culprit lesion events present most commonly with progressive or unstable angina, and rarely with cardiac death, cardiac arrest or MIPatients treated with contemporary medical therapy who develop non culprit lesion events present most commonly with progressive or unstable angina, and rarely with cardiac death, cardiac arrest or MI

37 PROSPECT: Conclusions While plaques which are responsible for unanticipated future MACE are frequently angiographically mild, most untreated plaques which become symptomatic have a large plaque burden and a small lumen area (which are detectable by IVUS but not by angiography)While plaques which are responsible for unanticipated future MACE are frequently angiographically mild, most untreated plaques which become symptomatic have a large plaque burden and a small lumen area (which are detectable by IVUS but not by angiography) Only about half of new events due to non culprit lesions exemplify the classic notion of vulnerable plaque (rapid lesion progression of mild angiographically lesions), while half are attributable to unrecognized and untreated severe disease with minimal change over timeOnly about half of new events due to non culprit lesions exemplify the classic notion of vulnerable plaque (rapid lesion progression of mild angiographically lesions), while half are attributable to unrecognized and untreated severe disease with minimal change over time The prospective identification of non culprit lesions prone to develop MACE within 3 years can be enhanced by characterization of underlying plaque morphology with virtual histology, with VH-TCFAs representing the highest risk lesion typeThe prospective identification of non culprit lesions prone to develop MACE within 3 years can be enhanced by characterization of underlying plaque morphology with virtual histology, with VH-TCFAs representing the highest risk lesion type The combination of large plaque burden (IVUS) and a large necrotic core without a visible cap (VH-TCFA) identifies lesions which are at especially high risk for future adverse cardiovascular eventsThe combination of large plaque burden (IVUS) and a large necrotic core without a visible cap (VH-TCFA) identifies lesions which are at especially high risk for future adverse cardiovascular events While plaques which are responsible for unanticipated future MACE are frequently angiographically mild, most untreated plaques which become symptomatic have a large plaque burden and a small lumen area (which are detectable by IVUS but not by angiography)While plaques which are responsible for unanticipated future MACE are frequently angiographically mild, most untreated plaques which become symptomatic have a large plaque burden and a small lumen area (which are detectable by IVUS but not by angiography) Only about half of new events due to non culprit lesions exemplify the classic notion of vulnerable plaque (rapid lesion progression of mild angiographically lesions), while half are attributable to unrecognized and untreated severe disease with minimal change over timeOnly about half of new events due to non culprit lesions exemplify the classic notion of vulnerable plaque (rapid lesion progression of mild angiographically lesions), while half are attributable to unrecognized and untreated severe disease with minimal change over time The prospective identification of non culprit lesions prone to develop MACE within 3 years can be enhanced by characterization of underlying plaque morphology with virtual histology, with VH-TCFAs representing the highest risk lesion typeThe prospective identification of non culprit lesions prone to develop MACE within 3 years can be enhanced by characterization of underlying plaque morphology with virtual histology, with VH-TCFAs representing the highest risk lesion type The combination of large plaque burden (IVUS) and a large necrotic core without a visible cap (VH-TCFA) identifies lesions which are at especially high risk for future adverse cardiovascular eventsThe combination of large plaque burden (IVUS) and a large necrotic core without a visible cap (VH-TCFA) identifies lesions which are at especially high risk for future adverse cardiovascular events


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