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14th Vietnam National Congress of Cardiology Da Nang City Vietnam 2014 New Insights In AMI: From Vulnerable to Ruptured Plaque Dr Tan Huay Cheem MBBS, M Med(Int Med) MRCP(UK), FRCP(Edinburgh), FAMS, FACC, FSCAI Director, National University Heart Centre, Singapore Associate Professor of Medicine, Yong Loo Lin School of Medicine National University of Singapore President, Asia Pacific Society of Interventional Cardiologhy 100 Years Ago! “……that thrombosis in the coronary artery leads to the symptoms and abnormalities of heart attacks…… and that this was not inevitably fatal ” JB Herrick JAMA 59:2015-2020, 1912 Non Progressive and Progressive Coronary Plaques Virmani R et al Arterioscler Thromb Vasc Biol 2000; 20: 1262 Early Stages of Atherosclerosis Development Pathologic Intimal Thickening (PIT) vs Atheroma • PIT poorly defined entity sometimes referred to as an "intermediate lesion" • PIT fibrous cap overlying the areas of lipid is rich in smooth muscle cells and proteoglycans Sparsely scattered macrophages and lymphocytes may be present • In contrast, fibrous cap atheroma, classically shows a "true" necrotic core (NC) containing cholesterol esters, free cholesterol, phospholipids, and triglycerides The fibrous cap consists of smooth muscle cells in a proteoglycan-collagen matrix, with a variable number of macrophages and lymphocytes Virmani R et al Arterioscler Thromb Vasc Biol 2000; 20: 1262 Mechanisms of Early Necrotic Core Formation in Human Atherosclerosis Pathologic intimal thickening and lipid pool is converted to necrotic core from macrophages infiltration and apoptosis leading to early necrotic core formation Mechanisms of Late Necrotic Core Formation in Human Atherosclerosis Late necrotic core is likely the result of defective efferocytosis as well as plaque hemorrhage which contribute to free cholesterol within necrotic core Coronary Thrombosis Types of Lesions That Cause Coronary Thrombosis • Plaque Rupture • Plaque Erosion • Calcified Nodule Virmani R et al Arterioscler Thromb Vasc Biol 2000; 20: 1262 Gross and Light Microscopic Features of Plaque Rupture 60 to 65% of thrombi in sudden coronary death occurs from plaque rupture Virmani R et al Arterioscler Thromb Vasc Biol 2000; 20: 1262 Are Mildly Obstructive Lesions More Likely To Cause Acute Coronary Events? Stenosis Severity of Culprit Atherosclerotic Plaque Causing AMI 5-Year Frequency (%) Frequency Luminal Stenosis 14% >70 18% 50-70% 68% [...]... carried out after coronary flow was restored in: (1) 73% patients by aspiration thrombectomy (2) 24% by balloon dilatation (3) 3% following guidewire passage alone across the lesion • Post-procedural TIMI 2/3 flow was established in 98% • Mean minimal luminal diameter (MLD) was 1.1±0.5mm, Mean ref vessel diameter 2.8±0.6mm, mean diameter stenosis 61±16%, and mean lesion length 16±6mm The majority of... 55.2% 51.1% 41.0% 38.6% 24.5% 10.2% 5.9% 3.8% 75% FA 75% 75% PR % Stenosis Categories with Plaque Types • Plaques that rupture are substantially narrowed at the time of the acute event • Rare to find disrupted but nonstenotic plaque TCFA may need to grow bigger before they rupture Narula J et al J Am Coll Cardiol 2013; 61: 1041-51 PROSPECT Study: Event Rates Stratified... • Fibroatheromas with cores in late stage of necrosis or thin caps had marked increase in glycophorin A surrounded by iron deposits • Erythrocyte membranes in plaque may represent potent atherogenic stimulus which contribute to deposition of free cholesterol, macrophage infiltration and enlargement of the necrotic core FD Kolodgie et al N Engl J Med 2003; 349: 2316-25 Plaque Rupture & Healing = Progression