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Infark Miokard Akut (IMA). Mohammad Saifur Rohman , dr.SpJP , PhD.FICA. Outlines. Anatomy of coronary artery Coronary artery disease : atherosclerosis Progression of CAD IMA Diagnosing IMA IMA Treatment. Major components. Muscle; contractile apparatus
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Infark Miokard Akut (IMA) Mohammad SaifurRohman, dr.SpJP, PhD.FICA
Outlines • Anatomy of coronary artery • Coronary artery disease : atherosclerosis • Progression of CAD IMA • Diagnosing IMA • IMA Treatment
Major components • Muscle; contractile apparatus • Nerve; conducting system and innervation • Vessel; Supporting oxygen from the blood • Extra cellular matrix • Endocardium; valves • Pericardium • Etc.
Coronary Arteries • Coronary arteries branch off at base of aorta & supply blood to the electrical conduction system & myocardium. • 3 main arteries: • RCA • LCA • Circumflex
Coronary Arteries • Originates from the aorta just beyond the aortic valve • Coronary blood flow to the myocardium occurs primarily during diastole * To maintain adequate blood flow through the coronaries, mean arterial pressure (MAP) must be at least 60 mmHg
Coronary Arteries • Left main coronary artery (LCA) - Left anterior descending artery (LAD) >descends toward the anterior wall & apex of LV > supplies LV, ventricular septum, chordae, papillary muscle & RV - Left circumflex artery (LXA) > descends toward the lateral wall of LV & apex > supplies LA, lateral & posterior LV surfaces *45% supplies SA node
Coronary Arteries • LCA • Branches into LAD & L Circumflex • Left Anterior Descending • Anterior wall of LV & anterior 2/3 septum • RBB & part of LBB • LA • Circumflex Supplies • AV node in 10% hearts • SA node in 45% hearts • Posterior surface of LV
Coronary Arteries • Right main coronary artery (RCA) - descends toward the apex of RV - supplies the RA, RV, & inferior portions of LV
Coronary Arteries • RCA Supplies • SA node in 55% of hearts • AV node in 90% hearts • RA & RV heart muscle • Inferior wall of LV • Posterior 1/3 of intraventricular septum • In 85% of hearts, RCA provides the posterior descending branch.
Atherosclerosis • Disease of cardiovascular system affecting vessel wall. • It leads to the narrowing of arteries or complete blockage. • Its main components are endothelial disfunction, lipid deposition, inflammatory reaction in the vascular wall. • Remodeling of vessel wall.
The process of atherogenesis – an overview Risk Factors
Family history: Man < 55 yo Women < 65 yo
The development of atherosclerosis • The key event – damage to the endothelium caused by excess of lipoproteins, hypertension, diabetes, components of cigarette smoke. • Endothelium becomes more permeable to lipoproteins. • Lipoproteins move below the endothelial layer (to intima). • Endothelium loses its cell-repelent quality. • Inflammatory cells move into the vascular wall.
Triggers for inflammation in atherosclerosis • LDL retained in the intima (in part by binding to proteoglycan) undergoes oxidative modification. • Lipid hydroperoxides, lysophospholipides, carbonyl compounds localize in the lipid fraction. • Oxygen free-radicals inactivate NO rapidly. • NO + superoxide (O2.-) peroxynitrite (ONOO-). • NO has no longer vasoprotective function.
The process of atherogenesis • Lipid entry into the arterial wall is a key process in atherogenesis. • Hypercholesterolemia – factor for VCAM-1 and MCP-1 induction. • LDL and VLDL are most atherogenic, enter vascular wall more easily. • LDL – in plasma are protected against oxidation by vit. E, ubiquinon, plasma antioxidants (b-carotene, vit. C). • Out of plasma, LDL phospholipides and fatty acids oxidize.
The process of atherogenesis • Activated macrophages produce enzymes – lipoxygenases, myeloperoxidase, NADPH oxidase ROS • Oxidized LDL are cytotoxic to endothelial cells, mitogenic for macrophages. • Oxidized LDL apolipoprotein apoB100 bind to the scavenger receptor. • Scavenger receptors are not subjected to regulationby intracellular cholesterol level. • Macrophages take up oxidized LDL, overload with lipids.
The process of atherogenesis • Foam cells ruptured (apoptosis). • Lipid release to intima and their acumulation becomes centre of atherosclerotic plaques. • The lipid center and fibrous cap are the main parts of a mature atherosclerotic plaque. • Plaque emerges from the structurally changed vascular wall. • So-called vulnerable plaque ruptures easily. • The thrombus formed at the rupture site.
Morphologic stages: • Type I – Fatty dots - Foam cells • Type II – Fatty streak • Type III – Extracellular lipid pool • Type IV – Atheroma – Core of lipid • Type V – Fibroatheroma – Fibrotic layer • Type VI – Complicated – Ulcer, Ca+ • Hemorrhage, thrombus, embolism, aneurysm.
Stages of Atheroma - Aorta Stage VI III II
Morphologic types: Fatty dots F.Atheroma Plaques Complicated
Spektrum ACS • Unstable Angina Pectoris : (EKG normal, Trop T/I (-)) • Acute Non ST-Elevation Myocardial Infarction (NSTEMI) : (EKG normal/ST depresi/T inversi dan Trop T/I (+)) • Acute ST-Elevation Myocardial Infarction (STEMI) : EKG ST elevasi dan Trop T/I(+)
Prevalensi IMA • Di Amerika : kejadian IMA lebih 1 Juta/tahun • 200,000 – 300,000 pasien IMA meninggalsebelumsampai RS • Total : WarganegaraAmerikamengalami IMA setiap 29 detikdanmeninggalsetiapmenit. • Indonesia ? • Tahun 2008: PJN Harapan Kita 7 pasien ACS , 50-60% IMA • 10% IMA < 40 thn • Penyebabkematian no 2 di UGD RSSA Topol EJ. CV med 2009 Saifur et al. unpublished data, 2008, 2011
Nyeri dada ACS? • 1. Cardiac or non cardiac • 2. Cardiac : Ischemic non Ischemic • 3. Ischemic : Coronary non Coronary • 4. Angina pektorisstabilatau ACS
Nyeri (tidak enak) dada ….. ? • Sifat :Berat/ tertindih (pressure, tightness, or heaviness, strangling, constricting, or compression),Panas (burning) ; Masukangin, Sesak,”maag” • Lokasi: Di dada kiri/tengahtidakbisaditunjuk • Penjalaran : kebahu/lengan, leher, dagu, • belakang,epigastrium • Lama : 5-30’ • Pencetus :aktifitas/stres/dingin • Berkurang: Nitrat/Istirahat • Tidakkhas: Pingsan/kejang/tidaksadar/berdebar ESC guidelines for SAP 2006 ESC AMI ST elevation guidelines 2008
Angina Pectoris • A syndrome resulting from myocardial ischemia • Demand and supply imbalance • Careful history taking; mode of onset, location, quality of pain, duration, precipitating factors, pattern of disappearance, risk factor, etc
Stable vs. Unstable • Stable : There is no substantial deterioration in symptoms over several weeks. Stability or quiescence of an atherosclerotic plaque; depending on increased oxygen demand • Unstable : symptom pattern worsen abruptly without an obvious caused of increased oxygen consumption, decreased supply . Unstable plaque: ACS
Stable Angina Pectoris Canadian Class : • I Ordinary physical activity does not cause angina • II Slight limitation of ordinary activity • III Marked limitation of ordinary activity • IV Inability to carry on any activity without discomfort
Nyeri dada khas ACS • Angina awitan baru derajat 3 menurut klasifikasi kanada kardiovaskuler group ( nyeri dada timbul pada aktifitas ringan sehari-hari) • Angina saat istirahat > 20 menit • Perburukan derajat angina menjadi derajat 3 dalam beberapa hari – 1 bln terakhir (Crescendo angina) • Atypical
Hati-hati : Angina Equivalent • Indigestion, belching, dyspnea • DM, wanita, manula (post operative) • Didapatkan 5% dari ACS • 2% dipulangkan ternyata ACS Braunwalds Heart Disease 8th Ed 2008
DD Chest pain Ischemic • Stenosis Aorta • Regurgitasi Aorta • Hypertrophic Cardiomyopathy • Angina pada Hypertensi • Hipertensi pulmonal berat 11th ed Hurst’s the heart 2005
DD Chest Pain Non Ischemic • Diseksi Aorta • Pericarditis • Mitral valve prolaps 11th ed Hurst’s the heart 2005
DD Chest Pain Gastro intestinal • Esophageal spasm/reflux/rupture • Peptic Ulcer Neuromusculoskeletal • Costochondritis • Herpes zoster • Chest wall pain dan tenderness etc 11th ed Hurst’s the heart 2005
DD chest pain Pulmonary • Pulmonary emboli • Pneumothorax • Penumonia with pleural involvement Pleurisy Psychogenic • Axiety/depression/cardiac psychosis etc 11th ed Hurst’s the heart 2005