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J Am Coll Cardiol, 2003; 41:23-30
© 2003 by the American College of Cardiology Foundation
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Pharmacologic plaque passivation for the reduction of recurrent cardiac events in acute coronary syndromes

V. Stephen Monroe, MD*, Richard A. Kerensky, MD, FACC*, Enrique Rivera, MD*, Karen M. Smith, MD, FACC* and Carl J. Pepine, MD, MACC*,*

* Division of Cardiovascular Medicine, University of Florida College of Medicine, Gainesville, Florida, USA



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  		Figure 1 Metabolism of collagen and elastin in the plaque’s fibrous cap. The vascular smooth muscle cell synthesizes the extracellular matrix protein, collagen, and elastin from amino acids. In the unstable plaque, interferon-gamma (IFN-{gamma}) secreted by activated T cells may inhibit collagen synthesis, interfering with maintenance and repair of the collagenous framework of the fibrous cap. The activated macrophage secretes proteases that can break down both collagen and elastin to peptides and, eventually, amino acids. Breakdown of these structural molecules of the extracellular matrix can weaken the fibrous cap, rendering it more susceptible to rupture and precipitation of an acute coronary syndrome. IFN-{gamma} secreted by the T lymphocytes can, in turn, activate the macrophage. Plaques also contain other activators of macrophages, including tumor necrosis factor-alpha (TNF-{alpha}), macrophage colony-stimulating factor (M-CSF), and macrophage chemoattractant protein-1 (MCP-1), among others. IL = interleukin. (Reprinted from Libby P, et al. Am J Cardiol 2000;86 Suppl:3J–9J. Copyright 2000, with permission from Excerpta Medica Inc., and reproduced with permission from the American Heart Association. Libby P, et al. Molecular bases of the acute coronary syndromes. Circulation 1995;91:2844–50.)

 


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  		Figure 2 Evolution of lipid fractions between admission and time of randomization to placebo or pravastatin (time 0) and after six weeks of therapy in patients with acute myocardial infarction or unstable angina. *p < 0.05; **p = 0.01 vs. admission; {dagger}p = 0.01 vs. placebo; and {ddagger}p = 0.01 vs. time 0. HDL = high-density lipoprotein; LDL = low-density lipoprotein. (Reproduced with permission from Lippincott Williams and Wilkins. Dupuis J, Tardif JC, Cernacek P, et al. Cholesterol reduction rapidly improves endothelial function after acute coronary syndromes. The RECIFE trial. Circulation 1999;99:3227–33.)

 


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  		Figure 3 Time course of the primary outcome and its major components. MI = myocardial infarction. (Reprinted with permission from Elsevier Science. Lancet 1997;349:1429–35.)

 


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  		Figure 4 A clinical efficacy summary: low-molecular-weight heparin (LMWH) vs. unfractionated heparin (UFH). ESSENCE = Efficacy and Safety of Subcutaneous Enoxaparin in Non–Q-wave Coronary Events trial; FRAXIS = FRAXiparine in Ischemic Syndromes trial; FRIC = FRagmin In unstable Coronary artery disease trial; MI = myocardial infarction; NS = not significant; RRR = relative risk reduction; TIMI = Thrombolysis In Myocardial Infarction. (Adapted [with permission from Thieme Publishers, 2002] from Semin Thromb Hemost 1999;25 Suppl 3:113–21 [Figure 3]).

 


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  		Figure 5 Percutaneous coronary intervention: 30-day clinical outcome with enoxaparin. MI = myocardial infarction. (Reproduced with permission from Lippincott Williams and Wilkins. Collet JP, Montelscot G, Lisbon L, et al. Percutaneous coronary intervention after subcutaneous enoxaparin pretreatment in patients with unstable angina. Circulation 2001;103:658–62.)

 


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  		Figure 6 The Trial on Reversing Endothelial Dysfunction (TREND) investigated the effects of six months of treatment with the ACE inhibitor quinapril on a target coronary artery segment (<40% diameter stenosis) in patients who underwent nonsurgical interventions for >50% stenosis in one to two other segments. At baseline, the endothelium-dependent vasodilator acetylcholine elicited a paradoxical vasoconstriction; quinapril resulted in a significant improvement in the response to acetylcholine (p < 0.014 vs. placebo). (Reprinted from Pepine JC, et al. Improved endothelial function with angiotensin-converting enzyme inhibitors. Am J Cardiol 2002;79:29–32. Copyright 2002, with permission from Excerpta Medica Inc.)

 




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