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DOI: 10.1055/s-2004-817691
Copyright © 2003 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel.: +1(212) 584-4662
Early Statin Therapy in Acute Coronary Syndromes
Publication History
Publication Date:
03 February 2004 (online)
ABSTRACT
Patients who survive an acute coronary syndrome of unstable angina or myocardial infarction are at much higher risk of a recurrent event within the following year than patients with stable coronary syndromes. Statin therapy is justified for many of these patients, not only for long-term benefit but also to reduce the risk of recurrent events within weeks of the primary event. The mechanisms that underlie this benefit are probably related to improvements in endothelial function, a decrease in vascular inflammation, and reduced prothrombotic factors. The effects of statins may be mediated by cholesterol reduction, cholesterol-independent effects (particularly decreasing isoprenoids), and mechanisms that are independent of inhibiting 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase. Observational studies consistently show an early reduction in mortality with statin therapy started before discharge from hospital after an acute coronary syndrome. Several randomized controlled trials also support an early benefit of risk reduction from statins started during the hospital admission for an acute coronary syndrome. Early statin therapy is also related to improved compliance and use of statins several years after a coronary event. Thus, early statin therapy may improve both early and long-term secondary prevention efforts.
KEYWORDS
Statins - acute coronary syndromes - lipids - nonlipid effects - observational studies - randomized controlled trials
REFERENCES
- 1 Waters D D, Hsue P Y. What is the role of intensive cholesterol lowering in the treatment of acute coronary syndromes?. Am J Cardiol . 2001; 88 7J-16J
- 2 Cannon C P, Weintraub W S, Demopoulos L A. et al . Comparison of early invasive and conservative strategies in patients with unstable coronary syndromes treated with the glycoprotein IIb/IIIa inhibitor tirofiban. N Engl J Med . 2001; 344 1879-1887
- 3 Braunwald E, Antman E M, Beasley J W. et al . ACC/AHA guideline update for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction- 2002; summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients With Unstable Angina). Circulation . 2002; 106 1893-1900
- 4 Ryan T J, Antman E M, Brooks N H. et al . 1999 update: ACC/AHA Guidelines for the Management of Patients With Acute Myocardial Infarction: Executive Summary and Recommendations: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Acute Myocardial Infarction). Circulation . 1999; 100 1016-1030
- 5 Libby P. Current concepts of the pathogenesis of the acute coronary syndromes. Circulation . 2001; 104 365-372
- 6 Falk E, Shah P K, Fuster V. Coronary plaque disruption. Circulation . 1995; 92 657-671
- 7 Bogaty P, Hackett D, Davies G, Maseri A. Vasoreactivity of the culprit lesion in unstable angina. Circulation . 1994; 90 5-11
- 8 Kinlay S, Ganz P. Relation between endothelial dysfunction and the acute coronary syndrome: implications for therapy. Am J Cardiol . 2000; 86 10J-14J
- 9 Tamai O, Matsuoka H, Itabe H, Wada Y, Kohno K, Imaizumi T. Single LDL apheresis improves endothelium-dependent vasodilatation in hypercholesterolemic humans Circulation . 1997; 95 76-82
- 10 Crisby M, Nordin-Fredriksson G, Shah P K, Yano J, Zhu J, Nilsson J. Pravastatin treatment increases collagen content and decreases lipid content, inflammation, metalloproteinases, and cell death in human carotid plaques: implications for plaque stabilization. Circulation . 2001; 103 926-933
- 11 Aikawa M, Rabkin E, Sugiyama S. et al . An HMG-CoA reductase inhibitor, cerivastatin, suppresses growth of macrophages expressing matrix metalloproteinases and tissue factor in vivo and in vitro. Circulation . 2001; 103 276-283
- 12 Aikawa M, Rabkin E, Okada Y. et al . Lipid lowering by diet reduces matrix metalloproteinase activity and increases collagen content of rabbit atheroma: a potential mechanism of lesion stabilization Circulation . 1998; 97 2433-2444
- 13 Aikawa M, Voglic S J, Sugiyama S. et al . Dietary lipid lowering reduces tissue factor expression in rabbit atheroma. Circulation . 1999; 100 1215-1222
- 14 Kinlay S, Libby P, Ganz P. Endothelial function and coronary artery disease. Curr Opin Lipidol . 2001; 12 383-389
- 15 Laufs U, Liao J K. Post-transcriptional regulation of endothelial nitric oxide synthase mRNA stability by Rho GTPase. J Biol Chem . 1998; 273 24266-24271
- 16 Lopez S, Peiretti F, Bonardo B, Juhan-Vague I, Nalbone G. Effect of atorvastatin and fluvastatin on the expression of plasminogen activator inhibitor type-1 in cultured human endothelial cells. Atherosclerosis . 2000; 152 359-366
- 17 Bourcier T, Libby P. HMG CoA reductase inhibitors reduce plasminogen activator inhibitor-1 expression by human vascular smooth muscle and endothelial cells. Arterioscler Thromb Vasc Biol . 2000; 20 556-562
- 18 Weitz-Schmidt G, Welzenbach K, Brinkmann V. et al . Statins selectively inhibit leukocyte function antigen-1 by binding to a novel regulatory integrin site. Nat Med . 2001; 7 687-692
- 19 Stenestrand U, Wallentin L. Early statin treatment following acute myocardial infarction and 1-year survival. JAMA . 2001; 285 430-436
- 20 Aronow H D, Topol E J, Roe M T. et al . Effect of lipid-lowering therapy on early mortality after acute coronary syndromes: an observational study. Lancet . 2001; 357 1063-1068
- 21 Heeschen C, Hamm C W, Laufs U, Snapinn S, Bohm M, White H D. Withdrawal of statins increases event rates in patients with acute coronary syndromes. Circulation . 2002; 105 1446-1452
- 22 Newby L K, Kristinsson A, Bhapkar M V. et al . Early statin initiation and outcomes in patients with acute coronary syndromes. JAMA . 2002; 287 3087-3095
- 23 Michels K B, Braunwald E. Estimating treatment effects from observational data: dissonant and resonant notes from the SYMPHONY trials. JAMA . 2002; 287 3130-3132
- 24 Arntz H R, Agrawal R, Wunderlich W. et al . Beneficial effects of pravastatin (+/-cholestyramine/niacin) initiated immediately after a coronary event (the randomized Lipid-Coronary Artery Disease [L-CAD] Study). Am J Cardiol . 2000; 86 1293-1298
- 25 Schwartz G G, Olsson A G, Ezekowitz M D. et al . Effects of atorvastatin on early recurrent ischemic events in acute coronary syndromes: the MIRACL study: a randomized controlled trial. JAMA . 2001; 285 1711-1718
- 26 Waters D D, Schwartz G G, Olsson A G. et al . Effects of atorvastatin on stroke in patients with unstable angina or non-Q-wave myocardial infarction: a Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) substudy. Circulation . 2002; 106 1690-1695
- 27 Kinlay S, Schwartz G G, Olsson A G. et al . High-dose atorvastatin enhances the decline in inflammatory markers in patients with acute coronary syndromes in the MIRACL study. Circulation . 2003; 108 1560-1566
- 28 Pearson T A, Laurora I, Chu H, Kafonek S. The lipid treatment assessment project (L-TAP): a multicenter survey to evaluate the percentages of dyslipidemic patients receiving lipid- lowering therapy and achieving low-density lipoprotein cholesterol goals. Arch Intern Med . 2000; 160 459-467
- 29 Fonarow G C, Gawlinski A, Moughrabi S, Tillisch J H. Improved treatment of coronary heart disease by implementation of a Cardiac Hospitalization Atherosclerosis Management Program (CHAMP). Am J Cardiol . 2001; 87 819-822
- 30 Muhlestein J B, Horne B D, Bair T L. et al . Usefulness of in-hospital prescription of statin agents after angiographic diagnosis of coronary artery disease in improving continued compliance and reduced mortality. Am J Cardiol . 2001; 87 257-261
- 31 Goldstein J A, Demetriou D, Grines C L, Pica M, Shoukfeh M, O'Neill W W. Multiple complex coronary plaques in patients with acute myocardial infarction. N Engl J Med . 2000; 343 915-922
- 32 Asakura M, Ueda Y, Yamaguchi O. et al . Extensive development of vulnerable plaques as a pan-coronary process in patients with myocardial infarction: an angioscopic study. J Am Coll Cardiol . 2001; 37 1284-1288