Cardiopatía isquémica por la Dra. Luxely Toledo

1. CARDIOPATÍA ISQUÉMICA DRA. TOLEDO PA-200

10. INFARTO TRANSMURAL

14. TROMBOS CORONARIOS

15. EVENTOS Cambio súbito en la morfología de una placa Agregación y adhesión plaquetaria Activación y liberación de favorecedores de la agregación Vasoespasmo estimulado por la agregación plaquetaria Activación de la Vía extrínseca de la coagulación lo que Aumenta el volumen del trombo Oclusión por completo de la luz del vaso coronario

20. Figure 12-14 Schematic representation of the progression of myocardial necrosis after coronary artery occlusion. Necrosis begins in a small zone of the myocardium beneath the endocardial surface in the center of the ischemic zone. This entire region of myocardium (shaded) depends on the occluded vessel for perfusion and is the area at risk. Note that a very narrow zone of myocardium immediately beneath the endocardium is spared from necrosis because it can be oxygenated by diffusion from the ventricle. The end result of the obstruction to blood flow is necrosis of the muscle that was dependent on perfusion from the coronary artery obstructed. Nearly the entire area at risk loses viability. The process is called myocardial infarction, and the region of necrotic muscle is a myocardial infarct. Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 9 September 2009 06:10 AM) © 2007 Elsevier

21. EVOLUCIÓN DE LOS CAMBIOS MORFOLÓGICOS EN EL INFARTO DEL MIOCARDIO Table 12-5. Evolution of Morphologic Changes in Myocardial Infarction Table 12-5. Evolution of Morphologic Changes in Myocardial Infarction Time Gross Features Light Microscope Electron Microscope Reversible Injury 0-½ hr None None Relaxation of myofibrils; glycogen loss; mitochondrial swelling Table 12-5. Evolution of Morphologic Changes in Myocardial Infarction Tiempo Caract. macro Microscopia óptica Microscopia electrónica Lesión reversible 0-½ hr Ninguna Ninguna Relajación de miofibrillas; pérdida de glucógeno; tumefacción mitocondrial.

22. EVOLUCIÓN DE LOS CAMBIOS MORFOLÓGICOS EN EL INFARTO DEL MIOCARDIO Lesión irreversible Tiempo Caract. macro Microscopia óptica Microscopia electrónica ½-4 hr Ninguna Usualmente ninguna; ondulación variable de las fibras en el borde Alteración del sarcolema; densidades mitocondriales amorfas

23. 4-12 hr. En ocasiones moteado oscuro Comienza necrosis por coagulación; edema; hemorragia. 12-24 hr. Moteado oscuro Continúa la necrosis por coagulación; picnosis de núcleos; hipereosinofilia de los miocitos; necrosis de banda de contracción marginal; comienza infiltrado neutrófilo. 1-3 días Moteado con centro de infarto pardo amarillento Necrosis por coagulación con pérdida de núcleos y estriaciones; infiltrado intersticial de neutrófilos. 3-7 días Borde hiperémico; ablandamiento central amarillo pardo Comienza desintegración de miofibras muertas, con neutrófilos moribundos; fagocitosis precoz de células muertas por macrófagos en el borde del infarto.

24. 7-10 días Máximo grado de ablandamiento y coloración pardo amarillenta, con márgenes deprimidos rojo-morenos. Fagocitosis bien desarrollada de células muertas; formación precoz de tejido de granulación fibrovascular en los márgenes. 10-14 días Bordes deprimidos rojo-grisáceos del infarto Tejido de granulación bien establecido, con nuevos vasos sanguíneos y depósito de colágeno. 2-8 sem. Cicatriz gris-blanca, progresiva desde el borde hacia el centro del infarto Depósito aumentado de colágeno, con celularidad disminuida. >2 mes Cicatrización completa Cicatriz de colágeno denso

26. Figure 12-15 Acute myocardial infarct, predominantly of the posterolateral left ventricle, demonstrated histochemically by a lack of staining by the triphenyltetrazolium chloride (TTC) stain in areas of necrosis (arrow). The staining defect is due to the enzyme leakage that follows cell death. Note the myocardial hemorrhage at one edge of the infarct that was associated with cardiac rupture, and the anterior scar (arrowhead), indicative of old infarct. (Specimen the oriented with the posterior wall at the top.) Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 9 September 2009 07:21 AM) © 2007 Elsevier

27. Figure 12-16 Microscopic features of myocardial infarction and its repair. A, One-day-old infarct showing coagulative necrosis along with wavy fibers (elongated and narrow), compared with adjacent normal fibers (at right). Widened spaces between the dead fibers contain edema fluid and scattered neutrophils. B, Dense polymorphonuclear leukocytic infiltrate in area of acute myocardial infarction of 3 to 4 days' duration. C, Nearly complete removal of necrotic myocytes by phagocytosis (approximately 7 to 10 days). D, Granulation tissue characterized by loose collagen and abundant capillaries. E, Well-healed myocardial infarct with replacement of the necrotic fibers by dense collagenous scar. A few residual cardiac muscle cells are present. Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 9 September 2009 07:57 AM) © 2007 Elsevier

28. Figure 12-16 Microscopic features of myocardial infarction and its repair. A, One-day-old infarct showing coagulative necrosis along with wavy fibers (elongated and narrow), compared with adjacent normal fibers (at right). Widened spaces between the dead fibers contain edema fluid and scattered neutrophils. B, Dense polymorphonuclear leukocytic infiltrate in area of acute myocardial infarction of 3 to 4 days' duration. C, Nearly complete removal of necrotic myocytes by phagocytosis (approximately 7 to 10 days). D, Granulation tissue characterized by loose collagen and abundant capillaries. E, Well-healed myocardial infarct with replacement of the necrotic fibers by dense collagenous scar. A few residual cardiac muscle cells are present. Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 9 September 2009 07:42 AM) © 2007 Elsevier

29. Figure 12-16 Microscopic features of myocardial infarction and its repair. A, One-day-old infarct showing coagulative necrosis along with wavy fibers (elongated and narrow), compared with adjacent normal fibers (at right). Widened spaces between the dead fibers contain edema fluid and scattered neutrophils. B, Dense polymorphonuclear leukocytic infiltrate in area of acute myocardial infarction of 3 to 4 days' duration. C, Nearly complete removal of necrotic myocytes by phagocytosis (approximately 7 to 10 days). D, Granulation tissue characterized by loose collagen and abundant capillaries. E, Well-healed myocardial infarct with replacement of the necrotic fibers by dense collagenous scar. A few residual cardiac muscle cells are present. Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 9 September 2009 07:46 AM) © 2007 Elsevier

30. Figure 12-16 Microscopic features of myocardial infarction and its repair. A, One-day-old infarct showing coagulative necrosis along with wavy fibers (elongated and narrow), compared with adjacent normal fibers (at right). Widened spaces between the dead fibers contain edema fluid and scattered neutrophils. B, Dense polymorphonuclear leukocytic infiltrate in area of acute myocardial infarction of 3 to 4 days' duration. C, Nearly complete removal of necrotic myocytes by phagocytosis (approximately 7 to 10 days). D, Granulation tissue characterized by loose collagen and abundant capillaries. E, Well-healed myocardial infarct with replacement of the necrotic fibers by dense collagenous scar. A few residual cardiac muscle cells are present. Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 9 September 2009 07:50 AM) © 2007 Elsevier

31. Figure 12-16 Microscopic features of myocardial infarction and its repair. A, One-day-old infarct showing coagulative necrosis along with wavy fibers (elongated and narrow), compared with adjacent normal fibers (at right). Widened spaces between the dead fibers contain edema fluid and scattered neutrophils. B, Dense polymorphonuclear leukocytic infiltrate in area of acute myocardial infarction of 3 to 4 days' duration. C, Nearly complete removal of necrotic myocytes by phagocytosis (approximately 7 to 10 days). D, Granulation tissue characterized by loose collagen and abundant capillaries. E, Well-healed myocardial infarct with replacement of the necrotic fibers by dense collagenous scar. A few residual cardiac muscle cells are present. Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 9 September 2009 07:53 AM) © 2007 Elsevier

43. Aneurisma ventricular que muestra una pared delgada con formación de trombo mural

44. Figure 12-19 Complications of myocardial infarction. Cardiac rupture syndromes (A, B, and C). A, Anterior myocardial rupture in an acute infarct (arrow). B, Rupture of the ventricular septum (arrow). C, Complete rupture of a necrotic papillary muscle. D, Fibrinous pericarditis, showing a dark, roughened epicardial surface overlying an acute infarct. E, Early expansion of anteroapical infarct with wall thinning (arrow) and mural thrombus. F, Large apical left ventricular aneurysm. The left ventricle is on the right in this apical four-chamber view of the heart. (A-E, Reproduced by permission from Schoen FJ: Interventional and Surgical Cardiovascular Pathology: Clinical Correlations and Basic Principles, Philadelphia, WB Saunders, 1989.) (F, Courtesy of William D. Edwards, M.D., Mayo Clinic, Rochester, MN.) Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 9 September 2009 09:23 AM) © 2007 Elsevier

45. Figure 12-19 Complications of myocardial infarction. Cardiac rupture syndromes (A, B, and C). A, Anterior myocardial rupture in an acute infarct (arrow). B, Rupture of the ventricular septum (arrow). C, Complete rupture of a necrotic papillary muscle. D, Fibrinous pericarditis, showing a dark, roughened epicardial surface overlying an acute infarct. E, Early expansion of anteroapical infarct with wall thinning (arrow) and mural thrombus. F, Large apical left ventricular aneurysm. The left ventricle is on the right in this apical four-chamber view of the heart. (A-E, Reproduced by permission from Schoen FJ: Interventional and Surgical Cardiovascular Pathology: Clinical Correlations and Basic Principles, Philadelphia, WB Saunders, 1989.) (F, Courtesy of William D. Edwards, M.D., Mayo Clinic, Rochester, MN.) Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 9 September 2009 09:27 AM) © 2007 Elsevier