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- 1. ENFERMEDAD CORONARIA Dr. Pablo Potthoff N. Residente 3er año MedInt UFRO/Temuco
- 30. Atherosclerosis: An Inflammatory Disease III.2 © 2002 PPS ® C MMP-9 Oxidized
- 38. Estudio Angina Estable (+) Test de Esfuerzo Cuadro clínico ECG Test de Provocación Cintigrama Mioc Eco Stress Coronariografía .
- 43. 30-45 min. moderate intensity 5 x/week Physical Activity Initial BMI Weight Loss Goal 25-27.5 BMI <25 >27.5 10% relative weight loss Body Weight by Body Mass index <130/85 mmHg Blood Pressure HbA1c <7.0% Diabetes <200 mg/day Dietary Cholesterol 60-85 mg/dL LDLc (primary goal) >40 mg/dL HDLc (secondary goal) <150 mg/dL Triglyceride (secondary goal) <30% calories / <7% calories Total Dietary Fat / Saturated Fat Cessation Smoking Goal Variable
- 45. Statins Reducing thrombogenicity Opposing vasospasm Decreasing inflammation Stabilizing fibrous cap
- 46. PCI + Optimal Medical Therapy will be Superior to Optimal Medical Therapy Alone Hypothesis
- 48. COURAGE Trial 35,539 2,287 (6.4%)
- 49. Survival Free of Death from Any Cause and Myocardial Infarction Number at Risk Medical Therapy 1138 1017 959 834 638 408 192 PCI 1149 1013 952 833 637 417 200 Years 0 1 2 3 4 5 6 0.0 0.5 0.6 0.7 0.8 0.9 1.0 PCI + OMT Optimal Medical Therapy (OMT) Hazard ratio: 1.05 95% CI (0.87-1.27) P = 0.62 7
- 50. Overall Survival Number at Risk Medical Therapy 1138 1073 1029 917 717 468 302 38 PCI 1149 1094 1051 929 733 488 312 44 Years 0 1 2 3 4 5 6 0.0 0.5 0.6 0.7 0.8 0.9 1.0 PCI + OMT OMT 7 Hazard ratio: 0.87 95% CI (0.65-1.16) P = 0.38
- 51. Survival Free of Hospitalization for ACS Number at Risk Medical Therapy 1138 1025 956 833 662 418 236 PCI 1149 1027 957 835 667 431 246 Years 0 1 2 3 4 5 6 0.0 0.5 0.6 0.7 0.8 0.9 1.0 PCI + OMT OMT 7 Hazard ratio: 1.07 95% CI (0.84-1.37) P = 0.56
- 52. Survival Free of Myocardial Infarction Number at Risk Medical Therapy 1138 1019 962 834 638 409 192 PCI 1149 1015 954 833 637 418 200 Years 0 1 2 3 4 5 6 0.0 0.5 0.6 0.7 0.8 0.9 1.0 PCI + OMT OMT 7 Hazard ratio: 1.13 95% CI (0.89-1.43) P = 0.33
- 56. Evolution of Atherosclerotic Risk
Hinweis der Redaktion
- Atherosclerosis: An Inflammatory Disease* Atherosclerosis, once regarded largely as a disorder of lipid accumulation, is now generally viewed as an inflammatory disease. The process begins with endothelial dysfunction caused, for example, by modified LDL, an infectious microorganism, or free radicals associated with cigarette smoking. Modified LDL is a major cause of endothelial injury in patients with type 2 diabetes and results from such factors as oxidation and glycation. Post-insult endothelial changes include increased leukocyte adhesion and migration into the arterial wall, increased permeability to lipoproteins and other plasma constituents, a switch from anticoagulant to procoagulant activity, and formation of cytokines, growth factors, and vasoactive molecules. As the inflammation continues, circulating monocytes and T lymphocytes migrate into the subendothelial space, and macrophages ingest oxidized LDL and are transformed into foam cells. The resulting fatty streak is augmented by migrating/proliferating smooth muscle cells and adherent/aggregating platelets to form an intermediate atherosclerotic lesion. Activation of T lymphocytes and macrophages also leads to the release of hydrolytic enzymes, cytokines, chemokines, and growth factors, which induce further damage. Eventually, a fibrous cap, which represents a healing response, will form over the mixture of leukocytes, lipid, and debris to wall off the lesion from the lumen. The core of such an advanced lesion may become necrotic. Subsequent thinning and rupture of the fibrous cap appears to be caused by the continued influx and activation of macrophages. Their release of metalloproteinases and other proteolytic enzymes causes degradation of the matrix, followed by possible hemorrhage, thrombus formation, and arterial occlusion. Ross R. N Engl J Med . 1999;340:115-126. *An animated version of this slide is located in the folder “Animated Slides.” Slide III.2
- 4 Slide 3L The pathologic process of atherothrombosis begins with the development of atherosclerotic plaque within the arterial lumen. A number of factors may lead to fissuring, cracking, or rupture of the plaque, exposing thrombogenic components such as collagen and von Willebrand factor, which cause platelets to adhere to the damaged area, forming a thrombus. Thrombi may then become incorporated into atheroma, thereby increasing the size of the plaque and further constricting the arterial lumen. These events may be clinically silent. If the plaque is then stabilized, the process may remain asymptomatic. However, if the thrombus is unstable and becomes dislodged, the resulting embolus may be carried throughout the circulation or become lodged, most often in a vascular bifurcation, thereby obstructing circulation. Alternatively, a burgeoning thrombus may itself occlude the artery. In either of these cases, an acute vascular event—myocardial infarction, unstable angina, ischemic stroke, transient ischemic event, or even cardiovascular death—may ensue.