This is a power point presentation titled "Chronic Stable Angina" . For more medical power points, PDFs, ECGs, X-rays, please visit www.medicaldump.com
2. A 47-year-old man reports a six-month history of intermittent chest discomfort while playing squash. He describes lower substernal tightness with numbness of the left upper arm only during exertion. He does not smoke. His father died suddenly at the age of 49 years. His blood pressure is 138/84 mm Hg. The level of total cholesterol is 261 mg per deciliter (6.7 mmol per liter), of low-density lipoprotein cholesterol 172 mg per deciliter (4.4 mmol per liter), and of high-density lipoprotein cholesterol 50 mg per deciliter (1.3 mmol per liter), and the triglyceride level is 113 mg per deciliter (2.9 mmol per liter). The result of an exercise test is positive, with pain and 1.5 mm of horizontal ST-segment depression at stage 4 of the Bruce protocol. How should the patient's case be managed? Abrams,NEJM,2005;352:2524-2533 Case history
11. Boden WE, ORourke, RA, Teo KK, Hartigan P, Maron D, et al. Optimal Medical Therapy with or without PCI for Stable Coronary Disease. N Engl J Med 2007;356:1503-16.
18. Chronic Stable Angina References 1. Abrams J. Chronic Stable Angina. N Engl J Med 2005;352:2524-33. 2 . Fraker TD Jr, Fihn SD. 2007 Chronic Angina Focused Update of the ACC/AHA 2002 Guidelines for the Management of Patients With Chronic Stable Angina: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Writing Group to Develop the Focused Update of the 2002 Guideline for the Management of Patients with Chronic Stable Angina . J. Am. Coll. Cardiol . 2007;50:2264-2274. 3. Boden WE, ORourke, RA, Teo KK, Hartigan P, Maron D, et al. Optimal Medical Therapy with or without PCI for Stable Coronary Disease . N Engl J Med 2007;356:1503-16. 4. Hochman JS, Steg PG. Does Preventive PCI Work? N Engl J Med 2007;356:1572-1574. 5. Peterson ED, Rumsfeld JS. Finding the Courage to Reconsider Medical Therapy for Stable Angina . N Engl J Med 2008;359:7:751-753. 6. Hochman JS, Lamas GA, Buller CE, Dzavik V, Reynolds HR, et al. Coronary Intervention for Persistent Occlusion after Myocardial Infarction. N Engl J Med 2006;355:2395-407. 7. Mark DB, Pan W, Clapp-Channing NE, Anstrom KJ, et al. Quality of Life after Late Invasive Therapy for Occluded Arteries. N Engl J Med 2009;360:774-83.
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Editor's Notes
Figure 1. Typical Progression of Coronary Atherosclerosis. As the plaque burden increases, the atherosclerotic mass tends to stay external to the lumen, which allows the diameter of the lumen to be maintained; this is known as the Glagov effect, or positive remodeling.1 As plaque encroaches into the lumen, the coronary artery diameter decreases. Myocardial ischemia results from a discordant ratio of coronary blood supply to myocardial oxygen consumption. Luminal narrowing of more than 65 to 75 percent may result in transient ischemia and angina. In acute coronary syndromes, vulnerable plaque is a more important factor than is the degree of stenosis; acute coronary events result from ulceration or erosion of the fibrous cap, with subsequent intraluminal thrombosis. 2, 3 Vulnerable plaque within the vessel wall may not be obstructive and thus may remain clinically silent until it causes rupture and associated consequences. (The figure has been modified from Greenland et al., 4 with permission.)
Figure 2. Kaplan-Meier Survival Curves. In Panel A, the estimated 4.6-year rate of the composite primary outcome of death from any cause and nonfatal myocardial infarction was 19.0% in the PCI group and 18.5% in the medical-therapy group. In Panel B, the estimated 4.6-year rate of death from any cause was 7.6% in the PCI group and 8.3% in the medical-therapy group. In Panel C, the estimated 4.6-year rate of hospitalization for acute coronary syndrome (ACS) was 12.4% in the PCI group and 11.8% in the medical-therapy group. In Panel D, the estimated 4.6-year rate of acute myocardial infarction was 13.2% in the PCI group and 12.3% in the medical-therapy group.