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(Circulation. 2003;107:2979.)
© 2003 American Heart Association, Inc.
Clinical Cardiology: New Frontiers |
From the Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minn (R.J.G.); the University of North Carolina/Chapel Hill (S.S.), Chapel Hill; and the Cardiovascular Division, Brigham and Womens Hospital, Boston, Mass (E.A.).
Correspondence to Raymond J. Gibbons, MD, Division of Cardiovascular Disease, Mayo Clinic, Rochester, MN. E-mail gibbons.raymond{at}mayo.edu
| Introduction |
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On physical examination, his blood pressure is 145/95 mm Hg. His heart rate is 72 beats per minute and regular. His cardiac examination is normal. His resting ECG is normal.
The patient undergoes a treadmill exercise test. He completes 6 minutes of exercise according to a Bruce protocol. He stops because of fatigue but does note some mild chest pressure at peak exercise. Peak exercise heart rate is 135 beats per minute, and the peak exercise blood pressure is 190/100 mm Hg. Exercise electrocardiography shows 0.5 mm of up-sloping ST depression measured 80 seconds after the J point at peak exercise.
To better define the patients diagnosis and prognosis, he then undergoes exercise myocardial perfusion imaging with sestamibi. He again exercises for 6 minutes according to a Bruce protocol and achieves a peak heart rate of 132 beats per minute and a peak blood pressure of 185/98 mm Hg. He again stops because of fatigue, but still describes some chest pressure at peak exercise. Electrocardiographic findings are similar to his previous exercise test. The perfusion images show a small area of inferior ischemia. The ejection fraction shown by gated single photon emission computed tomography is 61% with normal regional wall motion.
After discussion of these findings with the patient, his physician decides to manage the patient medically. What is appropriate therapy for this patient, as outlined in the American College of Cardiology/American Heart Association/American College of Physicians-American Society of Internal Medicine (ACC/AHA/ACP-ASIM) Guidelines for Management of Stable Angina?1
The flow diagram for appropriate therapy is shown in Figure 1. The left portion of this flow diagram focuses on antianginal drug treatment. The specific recommendations in the guideline for pharmacotherapy to prevent myocardial infarction and death and reduce symptoms are reproduced in Table 1. This patient clearly requires therapy with aspirin, ß-blockers, and sublingual nitroglycerin. The right portion of the flow diagram focuses on risk factor modification. The specific guideline recommendations for treatment of risk factors are detailed in Table 2. This patient clearly merits a smoking cessation program, a recheck of his lipids with initiation of drug therapy to bring his LDL cholesterol to less than 100 (if his LDL cholesterol remains >130 on recheck), recheck of his hypertension on ß-blockers to make certain that it is better controlled, initiation of an exercise program, review of his diet, and education.
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This illustrative case example is intended to demonstrate the application of ACC/AHA practice guidelines. The purpose of this review is to provide an overview of the guidelines process and its fundamental principles.
| Rationale for Guidelines |
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The perceived need for clinical practice guidelines has increased in recent years with the publication of data regarding the overall quality of cardiovascular care. The Worcester Heart Study (Figure 2) demonstrated that the prevalence of aspirin use in patients presenting to the hospital with acute myocardial infarction who had a history of previous infarction gradually increased over the late 1980s and early 1990s, but that this percentage remained less than 50% (in patients without contraindications to aspirin) as recently as 1995 (Figure 2). Surveys of the use of angiotensin-converting enzyme (ACE) inhibitors in patients with heart failure have shown that less than 50% of eligible patients are taking ACE inhibitors and that the dosages are optimal in less than 50% of them.
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Regional practice variations have provided another source of concern.5 The rate of utilization of percutaneous intervention, ß-blockers after myocardial infarction, and ACE inhibitors after myocardial infarction vary enormously in different regions of the country, even after adjustment for basic demographic variables (Figure 3). In response to data like these, both the ACC and AHA have committed considerable resources to their joint effort for the development of clinical practice guidelines, consistent with their stated mission to improve the quality of care in the country.
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| Selection of Topics and Writing Committees |
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| Principles of Guideline Development |
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| Conflict of Interest |
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| Classes of Recommendations |
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| Levels of Evidence |
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| Review Process |
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Some of the reviewers may identify pertinent new evidence that has been published since the writing committee submitted its draft for review. For example, the text of the stable angina guideline regarding vitamin E was modified to reflect the publication of the Heart Protection Study (Figure 8), which provided further support for the Class III recommendation from the committee.8 This process is overseen by a designated "lead reviewer" from the Task Force, who consults with the task-force chair regarding controversial or unresolved issues. When appropriate, the chair may choose to ballot the Task Force regarding these issues, or commission additional reviewers (which was done for stable angina). When this extensive review process is complete, the fully revised document is submitted to the ACC Board of Trustees and the AHA Science Advisory and Coordinating Committee (as well as to other organizations who are partners or who wish to consider the guideline for endorsement) for a formal endorsement vote. This process usually leads to additional suggestions for minor edits.
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| Publication Issues |
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| Commitment to Quality Improvement |
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In the next article in this series, we will describe the recent evolution of the guideline process, including its efforts to provide more rapid updates, its international extension, its increasing focus on patient conditions rather than procedures, and its interface with data standards, performance measures, and efforts at implementation.
Let us now return to our patient. His care, as well as the care of the 10 million patients with stable angina in the United States, will be improved if physicians, nurses, and other health professionals involved remember the treatment mnemonic recommended in the guideline.913
| Footnotes |
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| References |
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2. Frye RL, Collins JJ, DeSanctis RW, et al. Guidelines for permanent cardiac pacemaker implantation, May 1984: a report on the Joint American College of Cardiology/American Heart Association Task Force on Assessment of Cardiovascular Procedures (Subcommittee on Pacemaker Implantation). Circulation. 1984; 70; 331339.[Medline] [Order article via Infotrieve]
3. Greenspan AM, Kay HR, Bergor BC, et al. Incidence of unwarranted implantation of permanent cardiac pacemakers in a large medical population. N Engl J Med. 1988; 318: 158163.[Abstract]
4. McCormick D, Gurwitz JH, Lessard D, et al. Use of aspirin, beta-blockers, and lipid-lowering medications before recurrent acute myocardial infarction: missed opportunities for prevention? Arch Intern Med. 1999; 159: 561567.
5. Wennberg JE, Birkmeyer JD, Birkmeyer NJO, et al. The Dartmouth Atlas of Cardiovascular Health Care. Chicago, Ill: AHA Press; 1999.
6. American College of Cardiology. Manual for ACC/AHA Guideline Writing Committees. Available at: http://www.acc.org/clinical/manual/manual_introltr.htm and http:/circ.ahajournals.org/manual./ Accessed January 27, 2003.
7. Choudry NK, Stelfox HT, Detsky AS. Relationships between authors of clinical practice guidelines and the pharmaceutical industry. JAMA. 2002; 287: 612617.
8. Heart Protection Study Collaborative Group. MRC/BHF Heart Protection Study of antioxidant vitamin supplementation in 20 536 high-risk individuals: a randomised placebo-controlled trial. Lancet. 2002; 360: 2333.[CrossRef][Medline] [Order article via Infotrieve]
9. Berthold HK, Sudhop T, von Bergmann K. Effect of a garlic oil preparation on serum lipoproteins and cholesterol metabolism: a randomized controlled trial. JAMA. 1998; 279: 19001902.
10. Isaacsohn JL, Moser M, Stein EA, et al. Garlic powder and plasma lipids and lipoproteins: a multicenter, randomized, placebo-controlled trial. Arch Intern Med. 1998; 158: 11891194.
11. Jain AK, Vargas R, Gotzkowsky S, et al. Can garlic reduce levels of serum lipids? A controlled clinical study. Am J Med. 1993; 94: 632635.[CrossRef][Medline] [Order article via Infotrieve]
12. Warshafsky S, Kamer RS, Sivak SL. Effect of garlic on total serum cholesterol: a meta-analysis. Ann Intern Med. 1993; 119: 599605.
13. Silagy CA, Neil HA. A meta-analysis of on the effect of garlic on blood pressure. J Hypertens. 1994; 12: 463468.[Medline] [Order article via Infotrieve]
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