This Article Free upon publication Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Grundy, S. M. Articles by Washington, R. Search for Related Content PubMed PubMed Citation Articles by Grundy, S. M. Articles by Washington, R.

(Circulation. 1997;95:1683-1685.)
© 1997 American Heart Association, Inc.

Articles

When to Start Cholesterol-Lowering Therapy in Patients With Coronary Heart Disease

A Statement for Healthcare Professionals From the American Heart Association Task Force on Risk Reduction

Scott M. Grundy, MD, PhD, Chair; Gary J. Balady, MD; Michael H. Criqui, MD; Gerald Fletcher, MD; Philip Greenland, MD; Loren F. Hiratzka, MD; Nancy Houston-Miller, BSN, RN; Penny Kris-Etherton, PhD, RD; Harlan M. Krumholz, MD; John LaRosa, MD; Ira S. Ockene, MD; Thomas A. Pearson, MD; James Reed, MD; Sidney C. Smith, Jr, MD; Reginald Washington, MD

Key Words: AHA Medical/Scientific Statements • diet • cholesterol • prevention • drugs

	Introduction

Top Introduction General Approach Timeliness of Approach Summary References

 
Strong evidence denotes benefit from reducing serum cholesterol levels in patients with established coronary heart disease (CHD).¹ Treatment to decrease recurrent coronary events and reduce total mortality can be called secondary prevention. Support for aggressive cholesterol-lowering therapy as a component of secondary prevention comes from meta-analysis of earlier secondary prevention trials² and from recent large clinical trials.^{3 4 5} Among the latter, the Scandinavian Simvastatin Survival Study (4S),³ in which hypercholesterolemic patients with CHD received simvastatin therapy, documented a 34% reduction in major coronary events, a 42% decrease in coronary mortality, and a 30% reduction in total mortality. Investigators in the Cholesterol and Recurrent Events (CARE) study⁵ likewise observed significant benefits when pravastatin was given to CHD patients with average serum cholesterol levels. Several other trials^{6 7 8} in which angiographic end points were used show that cholesterol-lowering therapy retards progression of coronary atherosclerosis; a decrease in acute thrombolic events in coronary arteries was also noted. The summed results of these different categories of trials justify aggressive cholesterol management in most patients with CHD.

The National Cholesterol Education Program (NCEP)¹ calls for intensive cholesterol-lowering therapy in patients with any form of clinical atherosclerotic disease, specifically, acute myocardial infarction or angina pectoris, coronary artery angioplasty, peripheral arterial disease, abdominal aortic aneurysm, symptomatic carotid artery disease, or a history of coronary artery bypass graft. These patients carry a fivefold to sevenfold elevated risk for developing new or recurrent CHD and thus need intensive risk reduction. Despite the proven benefit of cholesterol-lowering therapy in patients with CHD, many patients—up to two thirds—receive no therapy to lower LDL cholesterol levels (National Heart, Lung, and Blood Institute; unpublished data; 1995). These patients are being deprived of valuable treatment that will decrease the likelihood of their having recurrent thrombotic events. A majority have LDL cholesterol concentrations well above optimal levels. The 4S and CARE trials^{3 5} clearly document risk reduction as soon as 2 years after starting cholesterol-reducing therapy; some angiographic trials suggest even earlier benefit from cholesterol-lowering therapy.^{4 7} Consequently, aggressive cholesterol management should be started as soon as the diagnosis of clinical atherosclerotic disease is established.

According to current guidelines, the goal of therapy in patients with clinical atherosclerotic disease, including CHD, is to decrease LDL cholesterol to 100 mg/dL. This level is considered optimal for patients with CHD by the NCEP Expert Panel,¹ the American Heart Association Secondary Prevention Panel,⁹ and the American College of Cardiology.^{9 10} The consensus opinion on the optimal target goal for LDL cholesterol in patients with atherosclerotic disease is supported on both theoretical and experimental grounds, including clinical trials.^{3 4 5 6 7 8}

Before starting LDL-lowering therapy at any level, a baseline should be established to ensure better monitoring of therapeutic results. At least two or preferably three fasting lipoprotein measurements¹¹ provide the most accurate baseline. Sampling can be done on consecutive days. Several studies^{12 13 14 15} suggest that plasma lipoprotein measurements made immediately upon admission to the hospital for acute coronary events provide a reasonable estimate of baseline cholesterol levels. These values can be used to alert physicians to patients who are possible candidates for cholesterol-lowering drugs. However, metabolic stability is required before initiating cholesterol-lowering drug therapy in patients who have had a recent coronary event. Sometimes during an acute event the LDL cholesterol level falls below the true baseline; it should return to baseline after a few weeks. The same holds true for patients undergoing surgical revascularization; their lipid and lipoprotein levels should be evaluated 2 to 3 months after surgery.¹⁶ If laboratory values (eg, liver function test) are abnormal in the period surrounding an acute event, a 6-week waiting period to allow for a return to normal metabolic function is prudent. If cholesterol-reducing agents are started while a patient is metabolically unstable, evaluation for possible drug toxicity can be compromised. On the other hand, if the patient is metabolically stable at discharge, consideration can be given to starting drug therapy. Before starting drugs in patients with high levels of lipids and lipoproteins, however, secondary causes of hypercholesterolemia—hypothyroidism, nephrotic syndrome, and obstructive liver disease—should be ruled out.

	General Approach

Top Introduction General Approach Timeliness of Approach Summary References

 
Immediate institution of nonpharmaceutical therapy is warranted in all patients with CHD and LDL cholesterol levels >100 mg/dL. Nonpharmaceutical therapy includes a maximal reduction in daily intake of saturated fats (to 7% of total calories) and cholesterol (to <200 mg/d), weight loss in persons who are overweight, and physical activity appropriate for cardiac status.¹ Individualized dietary therapy by a registered dietitian or other qualified nutritional professional will often improve dietary adherence. Maximal dietary therapy typically reduces LDL cholesterol levels by 15 to 25 mg/dL.¹ In addition to dietary change, cardiac rehabilitation programs are valuable for instituting optimal physical activity. Maximal dietary therapy should be started and continued even when cholesterol-lowering drugs are used; dietary therapy enhances drug actions and helps reduce risk for recurrent events through other mechanisms.

If the baseline LDL cholesterol level in patients with CHD is >130 mg/dL, cholesterol-lowering drug therapy is often needed in addition to maximal nonpharmaceutical therapy to achieve the target LDL cholesterol level of 100 mg/dL. Withholding drug therapy in an effort to reach target LDL level with the nonpharmaceutical approach is not necessary. The major drugs used for LDL reduction are statins, bile acid sequestrants, and nicotinic acid. Large clinical trials have documented that these agents are safe in the vast majority of patients.^{3 4 5 17 18 19} The choice and dose of drug depends on the baseline LDL cholesterol level as well as lipoprotein patterns. If LDL cholesterol is only slightly above 130 mg/dL, low doses of drug combined with dietary change may be sufficient to reach the target LDL level. Greater LDL elevations will require more aggressive drug therapy. In patients with definite hypercholesterolemia, combined drug therapy, eg, statin plus sequestrant, may be needed to achieve the LDL level of 100 mg/dL. If the LDL cholesterol concentration declines to 100 to 129 mg/dL on single-drug therapy, the physician must consider efficiency, cost, and side effects before prescribing a second drug to obtain an LDL level 100 mg/dL.¹

If the baseline LDL cholesterol level in patients with CHD ranges from 100 to 129 mg/dL, maximal dietary therapy alone can be tried for 6 weeks. If LDL does not decrease to <100 mg/dL with diet alone, clinical judgment will be needed to determine whether to initiate drug therapy.¹ Many patients with CHD and a baseline LDL cholesterol level ranging from 100 to 129 mg/dL have a low HDL cholesterol level (<35 mg/dL). In such patients, nicotinic acid can be considered for first-line therapy because of its potential for increasing HDL.¹ Alternatively, a statin can be used to reduce LDL cholesterol levels to well below 100 mg/dL.²⁰ The aim is to produce an extra low LDL cholesterol level to offset the increased risk associated with low HDL.

	Timeliness of Approach

Top Introduction General Approach Timeliness of Approach Summary References

 
Many patients with CHD and other chronic atherosclerotic diseases will be identified first as outpatients in the primary care setting. In such cases the primary care physician appropriately takes responsibility for initiating cholesterol-reducing therapy. The time has come to make such therapy routine in patients with atherosclerotic disease. Clinical trials have proved the benefit and safety of cholesterol lowering in patients with established atherosclerotic disease, particularly CHD; this fact should eliminate any hesitancy on the part of the primary care physician about starting cholesterol management, whether nonpharmaceutical or drug therapy. Consultation with a cardiovascular specialist before initiating cholesterol-lowering therapy is not necessary. However, referral to a cardiovascular specialist may be useful for developing an overall strategy for management in patients with chronic forms of atherosclerotic disease. Referrals to a lipid specialist may be helpful when the goals of lipid-lowering therapy are not readily attained.

Other candidates for cholesterol-reducing therapy are first identified when they experience an acute coronary event, ie, unstable angina or myocardial infarction. Many of these patients will immediately come under the care of a cardiovascular specialist. Because cholesterol-lowering therapy appears to be highly efficacious for reducing risk for recurrent coronary syndromes, its initiation at the time of discharge from the hospital can be considered, provided the patient is metabolically stable. As mentioned above, if LDL cholesterol is 130 mg/dL at time of discharge, a cholesterol-reducing drug can reasonably be started simultaneously with nonpharmaceutical therapy. On the other hand, if LDL cholesterol is <130 mg/dL at discharge, the LDL level should be reevaluated after 6 weeks of maximal dietary therapy.

One important issue concerns responsibility for initiating cholesterol-lowering therapy in the setting of acute coronary events. Divided responsibility often leads to no therapy at all. The following approach seems reasonable: The cardiovascular specialist or attending physician should be responsible for starting some form of cholesterol-lowering therapy in patients upon discharge from the hospital after acute coronary events. Failure to do so can convey a message to the patient's follow-up physician that cholesterol management is not necessary. The cardiovascular specialist thus should ensure that appropriate therapy is initiated and maintained. Interaction between the cardiovascular specialist and primary care physician will further assure that cholesterol management is initiated and continued and that the patient is monitored for drug toxicity.

	Summary

Top Introduction General Approach Timeliness of Approach Summary References

 
At present a large number of patients with atherosclerotic disease are not receiving aggressive cholesterol-lowering therapy. Consequently they are being deprived of a cost-effective, risk-reducing treatment. Every physician who treats patients with clinical atherosclerotic disease should become fully informed about the results of cholesterol-lowering trials in patients at high risk. All physicians who care for high-risk patients should take responsibility for cholesterol management, including primary care physicians and cardiovascular specialists. Highly effective and generally safe drugs for cholesterol lowering are available. The benefits of therapy for reducing recurrent CHD and prolonging life are considerable. There is no justification for unduly delaying institution of therapy for the majority of patients. The many advantages of nonpharmaceutical therapy call for its use in almost all patients, but drug treatment should not be postponed if the target for LDL cholesterol lowering (100 mg/dL) is unlikely to be achieved in the near term by a nonpharmaceutical approach alone. The view that patients with CHD or other forms of atherosclerotic disease do not receive substantial clinical benefits from aggressive cholesterol-lowering therapy is no longer warranted. Intensive cholesterol reduction, initiated immediately, has the potential to significantly reduce both morbidity and mortality. Cholesterol-lowering therapy thus should become a routine part of clinical management to reduce risk of future coronary events and to prolong life in patients with CHD or other forms of atherosclerotic disease.

	Footnotes

 
"When to Start Cholesterol-Lowering Therapy in Patients With Coronary Heart Disease" was approved by the American Heart Association Science Advisory and Coordinating Committee in November 1996.

A single reprint is available by calling 800-242-8721 (US only) or writing the American Heart Association, Public Information, 7272 Greenville Avenue, Dallas, TX 75231-4596. Ask for reprint No. 71-0105.

	References

Top Introduction General Approach Timeliness of Approach Summary References

 

1. National Cholesterol Education Program: Second Report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel II). Circulation.. 1994;89:1333-1445. [Medline] [Order article via Infotrieve]
   
2. Rossouw JE, Lewis B, Rifkind BM. The value of lowering cholesterol after myocardial infarction. N Engl J Med.. 1990;323:1112-1119. [Medline] [Order article via Infotrieve]
   
3. Scandinavian Simvastatin Survival Study Group. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet. 1994;344:1383-1389. [Medline] [Order article via Infotrieve]
   
4. Byington RP, Jukema JW, Salonen JT, Pitt B, Bruschke AV, Hoen H, Furberg CD, Mancini GB. Reduction in cardiovascular events during pravastatin therapy: pooled analysis of clinical events of the Pravastatin Atherosclerosis Intervention Program. Circulation.. 1995;92:2419-2425. [Medline] [Order article via Infotrieve]
   
5. Sacks FM, Pfeffer MA, Moye LA, Rouleau JL, Rutherford JD, Cole TG, Brown L, Warnica JW, Arnold JMO, Wun C-C, Davis BR, Braunwald E, for the Cholesterol and Recurrent Events Trial Investigators. The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. N Engl J Med.. 1996;335:1001-1009. [Abstract/Free Full Text]
   
6. Buchwald H, Varco RL, Matts JP, Long JM, Fitch LL, Campbell GS, Pearce MB, Yellin AE, Edmiston WA, Smink RD Jr, Sawin HS, Campos CT, Hansen BJ, Tune N, Karnegis JN, Sanmarco ME, Amplatz K, Castaneda-Zuniga WR, Hunter DW, Bissett JK, Weber FJ, Stevenson JW, Leon AS, Chalmers TC, the POSCH group. Effect of partial ileal bypass surgery on mortality and morbidity from coronary heart disease in patients with hypercholesterolemia: report of the Program on the Surgical Control of Hyperlipidemias (POSCH). N Engl J Med.. 1990;323:946-955. [Abstract]
   
7. Brown BG, Zhao X-Q, Sacco DE, Albers JJ. Lipid lowering and plaque regression: new insights into prevention of plaque disruption and clinical events in coronary disease. Circulation.. 1993;87:1781-1791. [Medline] [Order article via Infotrieve]
   
8. The Post Coronary Artery Bypass Graft Trial Investigators. The effect of aggressive lowering of low-density lipoprotein cholesterol levels and low-dose anticoagulation on obstructive changes in saphenous-vein coronary-artery bypass grafts. N Engl J Med.. 1997;336:153-162. [Abstract/Free Full Text]
   
9. Smith SC Jr, Blair SN, Criqui MH, Fletcher GF, Fuster V, Gersh BJ, Gotto AM, Gould KL, Greenland P, Grundy SM, Hill MN, Hlatky MA, Houston-Miller N, Krauss RM, LaRosa J, Ockene IS, Oparil S, Pearson TA, Rapaport E, Starke RD, the Secondary Prevention Panel. Preventing heart attack and death in patients with coronary disease. Circulation.. 1995;92:2-4.
   
10. 27th Bethesda Conference: Matching the Intensity of Risk Factor Management With the Hazard for Coronary Disease Events; September 14-15, 1995. J Am Coll Cardiol.. 1996;27:957-1047. [Medline] [Order article via Infotrieve]
    
11. LaRosa JC. Guidelines for detection and treatment of dyslipoproteinemia in adults. In: Rifkind BM, ed. Drug Treatment of Hyperlipidemia. New York, NY: Marcel Dekker; 1991:58.
    
12. Gore JM, Goldberg RJ, Matsumoto AS, Castelli WP, McNamara PM, Dalen JE. Validity of serum total cholesterol level obtained within 24 hours of acute myocardial infarction. Am J Cardiol.. 1984;54:722-725. [Medline] [Order article via Infotrieve]
    
13. Ahnve S, Angelin B, Edhag O, Berglund L. Early determination of serum lipids and apolipoproteins in acute myocardial infarction: possibility for immediate intervention. J Intern Med.. 1989;226:297-301. [Medline] [Order article via Infotrieve]
    
14. Carlsson R, Lindberg G, Westin L, Israelsson B. Serum lipids four weeks after acute myocardial infarction are a valid basis for lipid lowering intervention in patients receiving thrombolysis. Br Heart J.. 1995;74:18-20. [Abstract/Free Full Text]
    
15. Caggiula AW, Watson JE, Kuller LH, Olson MB, Milas NC, Berry M, Germanowski J. Cholesterol-lowering intervention program: effect of the step I diet in community office practices. Arch Intern Med.. 1996;156:1205-1213. [Abstract]
    
16. Pearson T, Rapaport E, Criqui M, Furberg C, Fuster V, Hiratzka L, Little W, Ockene I, Williams G. Optimal risk factor management in the patient after coronary revascularization: a statement for healthcare professionals from an American Heart Association Writing Group. Circulation.. 1994;90:3125-3133. [Medline] [Order article via Infotrieve]
    
17. The Lipid Research Clinics Coronary Primary Prevention Trial results, I: reduction in incidence of coronary heart disease. JAMA.. 1984;251:351-364. [Abstract]
    
18. The Lipid Research Clinics Coronary Primary Prevention Trial results, II: the relationship of reduction in incidence of coronary heart disease to cholesterol lowering. JAMA.. 1984;251:365-374. [Abstract]
    
19. Clofibrate and niacin in coronary heart disease. JAMA.. 1975;231:360-381. [Medline] [Order article via Infotrieve]
    
20. Oberman A, Kreisberg RA, Henkin Y. Principles and Management of Lipid Disorders: A Primary Care Approach. Baltimore, Md: Williams & Wilkins; 1992:256.
    

This article has been cited by other articles:

				A. M. Wessell, H. A. Liszka, P. J. Nietert, R. G. Jenkins, L. S. Nemeth, and S. Ornstein Achievable Benchmarks of Care for Primary Care Quality Indicators in a Practice-Based Research Network American Journal of Medical Quality, February 1, 2008; 23(1): 39 - 46. [Abstract] [PDF]

				American Diabetes Association Nutrition Recommendations and Interventions for Diabetes: A position statement of the American Diabetes Association Diabetes Care, January 1, 2008; 31(Supplement_1): S61 - S78. [Full Text] [PDF]

				S. Schneeweiss, A. R. Patrick, M. Maclure, C. R. Dormuth, and R. J. Glynn Adherence to Statin Therapy Under Drug Cost Sharing in Patients With and Without Acute Myocardial Infarction: A Population-Based Natural Experiment Circulation, April 24, 2007; 115(16): 2128 - 2135. [Abstract] [Full Text] [PDF]

				American Diabetes Association Nutrition Recommendations and Interventions for Diabetes-2006: A position statement of the American Diabetes Association. Diabetes Care, September 1, 2006; 29(9): 2140 - 2157. [Full Text] [PDF]

				Dyslipidemia Management in Adults With Diabetes Diabetes Care, January 1, 2004; 27(90001): s68 - 71. [Full Text] [PDF]

				M. Rauchhaus, A. L. Clark, W. Doehner, C. Davos, A. Bolger, R. Sharma, A. J. S. Coats, and S. D. Anker The relationship between cholesterol and survival in patients with chronic heart failure J. Am. Coll. Cardiol., December 3, 2003; 42(11): 1933 - 1940. [Abstract] [Full Text] [PDF]

				R. A. Kreisberg and A. Oberman Medical Management of Hyperlipidemia/Dyslipidemia J. Clin. Endocrinol. Metab., June 1, 2003; 88(6): 2445 - 2461. [Full Text] [PDF]

				T. A. Denton, G. C. Fonarow, K. A. LaBresh, and A. Trento Secondary prevention after coronary bypass: the American Heart Association "Get with the Guidelines" program Ann. Thorac. Surg., March 1, 2003; 75(3): 758 - 760. [Full Text] [PDF]

				M. J. Franz So Many Nutrition Recommendations--Contradictory or Compatible? Diabetes Spectr, January 1, 2003; 16(1): 56 - 63. [Full Text] [PDF]

				Management of Dyslipidemia in Adults With Diabetes Diabetes Care, January 1, 2003; 26(90001): s83 - 86. [Full Text] [PDF]

				A. Schomig, J. Mehilli, H. Holle, K. Hosl, D. Kastrati, J.u. Pache, M. Seyfarth, F.-J. Neumann, J. Dirschinger, and A. Kastrati Statin treatment following coronary artery stenting and one-year survival J. Am. Coll. Cardiol., September 4, 2002; 40(5): 854 - 861. [Abstract] [Full Text] [PDF]

				C. N. B. Merz, G. A. Mensah, V. Fuster, P. Greenland, and P. D. Thompson Task Force #5--the role of cardiovascular specialists as leaders in prevention: from training to champion J. Am. Coll. Cardiol., August 21, 2002; 40(4): 641 - 649. [Full Text] [PDF]

				J. Yarzebski, C. F. Bujor, R. J. Goldberg, F. Spencer, D. Lessard, and J. M. Gore A Community-Wide Survey of Physician Practices and Attitudes Toward Cholesterol Management in Patients With Recent Acute Myocardial Infarction Arch Intern Med, April 8, 2002; 162(7): 797 - 804. [Abstract] [Full Text] [PDF]

				M. J. Franz, J. P. Bantle, C. A. Beebe, J. D. Brunzell, J.-L. Chiasson, A. Garg, L. A. Holzmeister, B. Hoogwerf, E. Mayer-Davis, A. D. Mooradian, et al. Evidence-Based Nutrition Principles and Recommendations for the Treatment and Prevention of Diabetes and Related Complications Diabetes Care, January 1, 2002; 25(1): 148 - 198. [Full Text] [PDF]

				P. Amarenco Hypercholesterolemia, lipid-lowering agents, and the risk for brain infarction Neurology, September 1, 2001; 57(90002): S35 - 44. [Abstract] [Full Text]

				J. Yarzebski, F. Spencer, R. J. Goldberg, D. Lessard, and J. M. Gore Temporal Trends (1986-1997) in Cholesterol Level Assessment and Management Practices in Patients With Acute Myocardial Infarction: A Population-Based Perspective Arch Intern Med, June 25, 2001; 161(12): 1521 - 1528. [Abstract] [Full Text] [PDF]

				W. S. Aronow Treatment of Older Persons With Hypercholesterolemia With and Without Cardiovascular Disease J. Gerontol. A Biol. Sci. Med. Sci., March 1, 2001; 56(3): 138M - 145. [Abstract] [Full Text]

				G. C. Fonarow, W. J. French, L. S. Parsons, H. Sun, and J. A. Malmgren Use of Lipid-Lowering Medications at Discharge in Patients With Acute Myocardial Infarction : Data From the National Registry of Myocardial Infarction 3 Circulation, January 2, 2001; 103(1): 38 - 44. [Abstract] [Full Text] [PDF]

				H.B. Rubins, D. Collins, and S.J. Robins The VA HDL Intervention Trial: clinical implications Eur. Heart J., July 2, 2000; 21(14): 1113 - 1115. [PDF]

				S. M. Grundy Cholesterol-Lowering Therapy in Secondary Prevention: Remaining Issues J. Clin. Endocrinol. Metab., June 1, 2000; 85(6): 2092 - 2098. [Full Text]

				B. J. Ansell, K. E. Watson, and A. M. Fogelman An Evidence-Based Assessment of the NCEP Adult Treatment Panel II Guidelines JAMA, December 1, 1999; 282(21): 2051 - 2057. [Abstract] [Full Text] [PDF]

				S. M. Grundy Primary Prevention of Coronary Heart Disease : Integrating Risk Assessment With Intervention Circulation, August 31, 1999; 100(9): 988 - 998. [Full Text] [PDF]

				S. M. Grundy, J. I. Cleeman, B. M. Rifkind, L. H. Kuller, and for the Coordinating Committee of the National Cho Cholesterol Lowering in the Elderly Population Arch Intern Med, August 9, 1999; 159(15): 1670 - 1678. [Abstract] [Full Text] [PDF]

				D. Waters Cholesterol Lowering : Should It Continue to Be the Last Thing We Do? Circulation, June 29, 1999; 99(25): 3215 - 3217. [Full Text] [PDF]

				J. Dupuis, J.-C. Tardif, P. Cernacek, and P. Theroux Cholesterol Reduction Rapidly Improves Endothelial Function After Acute Coronary Syndromes : The RECIFE (Reduction of Cholesterol in Ischemia and Function of the Endothelium) Trial Circulation, June 29, 1999; 99(25): 3227 - 3233. [Abstract] [Full Text] [PDF]

				T. A. Jacobson, J. R. Schein, A. Williamson, and C. M. Ballantyne Maximizing the Cost-effectiveness of Lipid-Lowering Therapy Arch Intern Med, October 12, 1998; 158(18): 1977 - 1989. [Abstract] [Full Text] [PDF]

				R. N. Lemaitre, C. D. Furberg, A. B. Newman, S. B. Hulley, D. J. Gordon, J. S. Gottdiener, R. H. McDonald Jr, and B. M. Psaty Time Trends in the Use of Cholesterol-Lowering Agents in Older Adults: The Cardiovascular Health Study Arch Intern Med, September 14, 1998; 158(16): 1761 - 1768. [Abstract] [Full Text] [PDF]

				H. T. Westerveld, J. E. R. van Lennep, H. W. O. R. van Lennep, A.-H. Liem, J. A. J. de Boo, Y. T. van der Schouw, and D. W. Erkelens Apolipoprotein B and Coronary Artery Disease in Women : A Cross-sectional Study in Women Undergoing Their First Coronary Angiography Arterioscler. Thromb. Vasc. Biol., July 1, 1998; 18(7): 1101 - 1107. [Abstract] [Full Text] [PDF]

				S. M. Grundy Statin Trials and Goals of Cholesterol-Lowering Therapy Circulation, April 21, 1998; 97(15): 1436 - 1439. [Full Text] [PDF]

				T. R. Pedersen, A. G. Olsson, O. Færgeman, J. Kjekshus, H. Wedel, K. Berg, L. Wilhelmsen, T. Haghfelt, G. Thorgeirsson, K. Pyorala, et al. Lipoprotein Changes and Reduction in the Incidence of Major Coronary Heart Disease Events in the Scandinavian Simvastatin Survival Study (4S) Circulation, April 21, 1998; 97(15): 1453 - 1460. [Abstract] [Full Text] [PDF]

				A. M. Gotto Jr Cholesterol Management in Theory and Practice Circulation, December 16, 1997; 96(12): 4424 - 4430. [Abstract] [Full Text]

This Article Free upon publication Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Grundy, S. M. Articles by Washington, R. Search for Related Content PubMed PubMed Citation Articles by Grundy, S. M. Articles by Washington, R.