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Finding the Vulnerable Plaque Editorial Finding the Vulnerable Plaque By C. Richard Conti, MD, MACC, Editor-in-Chief At a recent Transcatheter Therapeutics meeting in San Francisco the PROSPECT Trial was presented by Dr. Greg Stone. Prospect stands for Providing Regional Observations to Study Predictors of Events in the Coronary Tree. This was a natural history study of atherosclerosis using multi-modality intracoronary imaging to prospectively identify vulnerable plaque. More on this later. Plaque Disruption and Risk Factors to me that intracoronary ultrasound might be useful to In 1993, I wrote an editorial titled, ‘‘Vascular Events investigate the composition of less severe stenoses and Responsible for Thrombotic Occlusion of a Blood Vessel.’’1 might eventually lead to plaque rupture and coronary In that editorial, I commented on the relationship of thrombosis. So, in another editorial in 1996, I predicted plaque disruption to the usual risk factors (smoking, that intracoronary ultrasound will evolve to a highly hyperlipidemia, hypertension) and potential triggers (cat- sophisticated level and will be used in the future to identify echolamines, myocardial contractility, heart rate), but noth- intracoronary plaques prone to rupture.4 ing was known at that time about identifying the plaque that is prone to rupture (vulnerable plaque) prospec- Virtual Histology Intravascular Ultrasound (VH-IVUS) tively. I ended the editorial by saying that current and At the 2009 Trans Catheter Therapeutics meeting (TCT), future research should be directed at identifying vulnera- the PROSPECT investigators presented imaging data of ble plaques in the individual patient, so that measures can non-culprit arteries of 700 patients with acute coronary be taken to prevent plaque rupture. syndromes. Angiography was performed as usual, and virtual histology intravascular ultrasound (VH-IVUS) was Coronary Artery Occlusion Sites used in the proximal six to eight centimeters of each coro- In a later editorial in 1995, I noted that it was becoming nary artery. VH-IVUS is advanced spectral analysis of the common knowledge that occlusions resulting in acute ultrasound signal and was used to classify atherosclerosis myocardial infarction were occurring at sites with less than disease into different plaque components. The investiga- a 50% lumen diameter reduction.2 As early as 1988, Little tors were able to classify the plaques as fibrotic, fibro- and colleagues evaluated 42 patients before and one month calcific, pathological intimal thickening (PIT), thick cap after an acute myocardial infarction, and they found a high fibro-atheroma (ThCFA), and virtual histology thin cap percentage of occlusions occurred at sites with less than fibro-atheroma (VH-TCFA). This latter group was the pre- a 50% lumen diameter reduction on first angiogram and, sumed high risk group, i.e., the group with vulnerable with one exception, the remainder occurred at sites with plaques. less than 70% lumen diameter reduction.3 Intracoronary At the TCT conference, PROSPECT investigators ultrasoundwas coming of age, and many thought this might concluded from their observations that approximately 20% be a way to identify plaques that are prone to rupture. of all acute coronary syndrome patients treated with PCI/stents and modern medical therapy had a major Importance of the Vessel Wall adverse cardiac event (MACE) that occured over a three In 1995, I thought it was important to understand the year follow-up period. Approximately 13% of these patients pathology of the vascular wall, in order to identify developed MACE from culprit lesions and 11% from non- coronary artery plaques that will cause future events. I will culprit lesions during the three year follow-up. Most had readily admit that coronary angiography is lumenography progression of unstable angina and only a small percentage and does not answer questions about the status of the presented with cardiac death, cardiac arrest, or myocardial vascular wall. However, the procedure itself does provide infarction. The combination of large plaque burden and a an opportunity to use other methods to study plaque large necrotic core without a visible cap identified by VH- morphology and the vascular wall e.g. intracoronary TCFA is especially risky for future adverse cardiovascular ultrasound, optical coherence tomography etc. It seemed events. 320 Clin. Cardiol. 33, 6, 320–321 (2010) Published online in Wiley InterScience. (www.interscience.wiley.com) DOI:10.1002/clc.20809© 2010 Wiley Periodicals, Inc. Further Investigation of Coronary Arteries Using VH-IVUS coronary angiography. Obviously, all cardiologists agree More recently Kubo et al published a manuscript on the that aggressive lipid lowering, hypertension control, Dynamic Nature of Coronary Artery Lesion Morphology diabetes control, smoking cessation, weight control, and Assessed by serial VH-IVUS tissue characterization.5 use of all the drugs that we currently prescribe for According to the investigators, at 12 months follow up these patients are important. I wonder if it might be the major findings of their analysis were as follows. worthwhile to consider plain old balloon angioplasty for these lesions that are not ischemia-producing at the time 1) Most VH-TCFAs stabilized or healed during of angiography. If stable plaques can be differentiated from 12 months of follow-up. Only proximal VH-TCFAs unstable plaques, specific local therapy of the plaque that in larger vessels with more plaque appeared to heal does not limit blood flow could be undertaken: for example less often. angioplasty/stent/radiation or some other therapy not yet 6 2) New VH-TCFAs developed from Pathological Intimal identified. Maybe Bernie Meier is right. Thickening (PITs) or Thick Cap Fibro Atheromas (ThCFAs). References 3) Lesions classified as PIT, VH-TCFA, and ThCFA 1. Conti CR. Vascular Events Responsible for Thrombotic Occlusion showed significant progression (increase plaque and of a Blood Vessel. Clin Cardiol. 1993;16(11):761–762. 2. Conti CR. Identifying Coronary Stenoses Prone to Thrombosis. Clin decrease in lumen) compared with fibrotic and Cardiol. 1995;18(9):491 –2. fibrocalcific plaque. 3. Little WC, Constantinescu M, Applegate RJ, Cutcher MA, Burrows MT, Kahl FR, Santamore WP. Coronary angiography predicts the site of subsequent myocardial infarction in patients with mild to Clinical Relevance of These Observations moderate coronary disease? Circulation. 1988;78:1157–1166. The study by these investigators is a work in progress, 4. Conti CR. VascularDisease: ‘‘The Donut and the Hole.’’ Clin Cardiol. 1996;19(4):269. and I am quite confident that this technique will be refined 5. Kubo T, Maehara A, Mintz GS et al. The Dynamic Nature of and provide useful information that will identify patients Coronary Lesion Pathology Assessed by Serial Virtual Histology whose plaques are prone to rupture and possibly occlude a IntravascularUltrasound Tissue Characterization J Am Coll Cardiol. coronary artery. 2010;55:1590–7. 6. Meier, B. Use of IVUS and FFR do not improve outcomes for The issue here is what can be done when plaques patients with multivessel disease. ACCEL interview with Conti Cr that do not limit flow in any way, are found during Volume 41, No 7, July 2009. Clin. Cardiol. 33, 6, 320–321 (2010) 321 C. Richard Conti: Finding the vulnerable plaque Published online in Wiley InterScience. (www.interscience.wiley.com) DOI:10.1002/clc.20809© 2010 Wiley Periodicals, Inc..
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