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Aterogenesis Dr Fleming
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2. Lípidos Hipertensión Edad Enfermedad Vascular Tabaquismo Obesidad Diabetes Dieta Historia familiar Sedentarismo AMBIENTAL GENETIC A Sexo Factores Trombogénicos
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5. Chronology of the interface between the patient and the clinician through the progression of plaque formation and the onset of complications of STEMI. Management Before STEMI 4 1 2 3 4 5 6 Onset of STEMI - Prehospital issues - Initial recognition and management in the Emergency Department (ED) - Reperfusion Hospital Management - Medications - Arrhythmias - Complications - Preparation for discharge Secondary Prevention/ Long-Term Management Presentation Working Dx ECG Cardiac Biomarker Final Dx UA NQMI QwMI No ST Elevation NSTEMI Ischemic Discomfort Acute Coronary Syndrome Unstable Angina Myocardial Infarction ST Elevation Modified from Libby. Circulation 2001;104:365, Hamm et al. The Lancet 2001;358:1533 and Davies. Heart 2000;83:361.
6. Aterotrombosis: un Proceso Generalizado y Progresivo Normal Estría lipídica Placa fibrosa Placa ateros- clerótica Ruptura/fisura/ de la placa & trombosis IM Isquemia crítica m.inferior Clínicamente silente Muerte cardiovascular Aumento de la edad Angina estable Claudicación intermitente Angina inestable SCA SCA, síndrome coronario agudo; TIA, “transient ischemic attack” isquemia cerebral transitoria ACV isquémico/ TIA
11. Angiographically unrecognised coronary artery disease Nissen et al. In: Topol (ed.) Interventional Cardiology Update 14;1995. Ultrasound reveals a large crescent-shaped atheroma (arrow) that narrows the lumen by about 50% Arrow indicates a site in the left main coronary artery where the intravascular ultrasound catheter was positioned
13. Different Types of Vulnerable Plaque CP1130695-18 Circ 108:1666, 2003 A B C D E F G Rupture- prone vulnerable plaque Ruptured/ healing vulnerable plaque Erosion- prone vulnerable plaque Eroded vulnerable plaque Vulnerable plaque with intra-plaque hemorrhage Vulnerable plaque with calcified nodule Critically stenotic vulnerable plaque Normal Macrophage Thin cap Large lipid core Collagen Ruptured cap Non-occlusive clot Smooth muscle cells Dysfunctional endothelium Platelets Proteoglycans Non-occlusive mural thrombus/ fibrin Intact cap Leaking vasa vasorum/ angiogenesis Calcium node Extensive calcification Old thrombus
15. Characteristics of Unstable and Stable Plaques Thin Fibrous Cap Inflammatory Cells Few SMCs Unstable Eroded Endothelium Activated Macrophages Thick Fibrous Cap Lack of Inflammatory Cells Foam Cells Intact Endothelium More SMCs Stable Libby et al. Circulation 1995; 91:2844-50
19. FISIOPATOLOGIA DE PLACA VULNERABLE Lumen EROSION O FISURA DE CAPSULA FIBROSA GRAN NUCLEO LIPIDICO PRESENCIA CELS.INFLAMATORIAS REMODELACION ARTERIAL EXCENTRICA MAS CALCIFICACION ALTO STRESS DE PARED INCREMENTO DE NEOVASCULARIZACION
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21. Fern á ndez-Real and Ricart: Endocrine Reviews 24:278, 2003 Possible Pathways Leading to Chronic Inflammation, Resulting in Atherosclerosis Aterosclerosis Inflamacion intrarterial Vejez Estimulo extravascular Inflamacion cronica subclinica Tabaco Obesidad Citoquinas proinflamatorias infecciones mucosa oral CP1158202-69 Sd. Resistencia Insulina HTA Hiperinsulinemia Dislipidemia Intolerancia Glucosa Obesidad abdominal
22. adventitia lipid core lipid core Site of previous plaque rupture Resolving thrombus Recruitment of new smooth muscle cells PLAQUE GROWTH Weissberg PL Eur Heart J. 1999 Courtesy of P Weissberg
30. Strategies to Treat Plaque Inhibit Platelet Aggregation Stabilize the Plaque Passivate the Plaque LDL-C HDL-C TG Reduce Sheer Stress Endothelial function Suppress Inflammation Stent the Vessel