Optimizing Percutaneous Coronary Intervention Outcomes
2005; Lippincott Williams & Wilkins; Volume: 111; Issue: 2 Linguagem: Inglês
10.1161/01.cir.0000153621.57449.8e
ISSN1524-4539
Autores Tópico(s)Acute Myocardial Infarction Research
ResumoHomeCirculationVol. 111, No. 2Optimizing Percutaneous Coronary Intervention Outcomes Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBOptimizing Percutaneous Coronary Intervention OutcomesThe Next Steps George W. Vetrovec, MD George W. VetrovecGeorge W. Vetrovec From the Division of Cardiology, Virginia Commonwealth University at Medical College of Virginia, Richmond. Originally published18 Jan 2005https://doi.org/10.1161/01.CIR.0000153621.57449.8ECirculation. 2005;111:125–126Death and myocardial infarction rates have been reduced significantly with the enhanced management of cardiovascular risk factors. That's the good news. Conversely, a significant risk for subsequent adverse ischemic events remains, particularly after acute coronary syndromes (ACS). This risk of recurrent ischemic events appears to be highest early after the ACS event, decreasing over time to that of chronic stable angina by 6 to 12 months. The cause of increased events is a composite of disease progression, especially in the culprit vessel in the absence of intervention, but it also involves nonculprit lesions that appear to have a variable risk of progression.See p 143Much has been learned about the potential risk of late recurrent events. Vulnerable plaques,1 often in multiple lesions and vessels, have been described in patients with ACS via different imaging modalities, including plaque rupture as seen on intravascular ultrasound, increased plaque temperature, angioscopic descriptions of plaque disruption with intracoronary thrombus,2,3 and morphological markers identified by coronary angiography. Associated with these morphological definitions of plaque instability have been the systemic patient markers of inflammation,4 best described by C-reactive protein,5 which is a significant predictor of late adverse ischemic events.Although all of the described markers have been associated with lesion instability, leading to an increased risk of late ischemic outcomes, the impact of therapeutic interventions has been harder to define. Late event rates appear to be related to lesion and clinical markers, suggesting the existence of a definable patient group with increased risk. The benefits of early percutaneous coronary intervention (PCI) for ACS accrue from decreasing early recurrent events attributable to the primary culprit lesion and from reducing the risk of late culprit lesion progression. Late restenosis of the primary lesion as well as disease progression in nonprimary (untreated) lesions, however, all contribute to an increased risk of late events. In this drug-eluting stent era with low restenosis rates, if secondary "at risk" lesions could be identified and treated at the time of the initial PCI, late outcomes should improve. Several questions remain: What is the magnitude of the risk of nonculprit lesion progression leading to late events? How can one easily identify at-risk nonsignificant lesions? Could prophylactic revascularization of noncritical lesions with drug-eluting stents lead to improved outcomes?In this issue of Circulation, Glaser et al6 partially address the above issues. They evaluated the relative risk of nonculprit lesion progression from the National Heart, Lung, and Blood Institute Dynamic Registry. In all, 5.8% of patients had late angiography documenting progressive disease in vessels not initially treated, and in the majority (87%) of cases late progressive lesions were not significantly stenotic on initial angiography. Nearly one third of the progressive lesions occurred in the primary target vessel and were equally distributed proximal or distal to the primary lesion. Furthermore, as the authors point out, because of the elimination of cases without follow-up angiography, the true incidence of progressive disease may have been higher. As opposed to restenosis, which rarely results in death or myocardial infarction, progressive lesion disease appears to possess the characteristics of an unstable plaque with the inherent risk of death or myocardial infarction. More than half of the patients presented with ACS. Thus, the risk of late progression, not surprisingly, is related to the initial clinical presentation, being more common in patients with ACS. A substudy population with available pre- and late angiography showed no clear angiographic predictors of future noncritical lesion instability. More underlying multivessel coronary artery disease was present in the progression group, however, and interestingly, statin use was also higher in the progression group, possibly reflecting greater suspected risk on the part of the practitioners.Do these data suggest that the concept of "prophylactic stenting" is flawed? No. To the contrary, these data support the principle that now that the restenosis rate is in the single digits,7 more attention must be aimed at preventing late adverse outcomes related to progressive disease. It appears that what the authors have identified is a high-risk population with more underlying significant disease, perhaps a greater resistance to usual risk management, and a higher rate of rapidly progressive, previously noncritical coronary disease, which increases the risk of late adverse unstable coronary events. Better ways are needed to risk-stratify nonsignificant coronary disease while better defining systemic patient risks such as inflammation. The goal is to define appropriate noncritical lesions for early selected revascularization, further supported by optimum adjunctive medical risk management. The consequence should be improved late outcomes.Examples of potential strategies include better defining the length of the primary lesion. In the article by Glaser and coworkers, the relatively high incidence of progression in the target vessel suggests that stenting may be too focal, accounting for the relatively high incidence of target vessel progression. Enhanced techniques to define potential unstable plaques also need to be refined. Although coronary angiography was not helpful in their study, historically angiography has been shown to define unstable coronary disease to a reasonable degree. In addition, Goldstein et al,8 using angiographic criteria, did demonstrate a predictive risk for multiple unstable lesions. Intravascular ultrasound also may specifically detect plaque fractures or other markers of lesion instability. Ocular coherence tomography and plaque temperature measurement have the potential to provide much more detailed definition of the plaque instability. In addition, growing evidence indicates that MRI may provide a noninvasive method to detect unstable plaque. The good news is that solutions should be forthcoming.In addition to local plaque behavior, another important area of focus is the systemic inflammatory response, which is predictive of late risk. This inflammatory response may be further enhanced by the PCI stent procedure itself. Thus, the primary treatment via producing a systemic inflammatory response may contribute to the later risk of progression. Statins, particularly high dose,9 appear to block plaque progression and to reduce inflammatory responses. Likewise, a recent report indicates that statins reduce the PCI-related inflammatory response. Therefore, better systemic risk management should further reduce the risk of late progression.10Can all of the risk be mediated by systemic therapy alone? This seems unlikely. Lipid-lowering trials11,12 in patients with stable angina in general require 12 to 18 months or longer before a significant reduction in coronary event rates is observed. During this interval, the primary and secondary lesions remain at risk. Thus, the use of stenting for the primary and appropriately selected secondary lesions with selected adjunctive medical therapy should provide the greatest late benefits.In summary, Glaser et al have significantly contributed to our understanding of the minimal risk of clinically important lesion progression after PCI treatment. Improved diagnostic tools should enhance identification of at-risk noncritical lesions. Coupled with better characterization of the inflammatory risk and the use of intensive statin and antiplatelet therapy, the combination of revascularization should enhance outcomes for all PCI patients, but particularly for those whose initial presentation is ACS. The initial use of one or two more stents could ultimately reduce total cost by preventing late hospitalizations with ACS. Thus, as we evolve in the drug-eluting stent era with low restenosis rates, greater attention needs to be placed on optimizing subacute and late outcomes by focusing on better management of the entire at-risk coronary vasculature. Success in reaching this goal will further improve patient outcomes.The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.FootnotesCorrespondence to Dr George W. Vetrovec, 1200 E Broad St, PO Box 980036, Richmond, VA 23298-0036. E-mail [email protected] References 1 Davies MJ. Stability and instability: two faces of coronary atherosclerosis. The Paul Dudley White Lecture 1995. Circulation. 1996; 94: 2013–2020.CrossrefMedlineGoogle Scholar2 Vetrovec GW, Cowley MJ, Overton H, Richardson DW. Intracoronary thrombus in syndromes of unstable ischemia. Am Heart J. 1981; 102: 1202–1208.CrossrefMedlineGoogle Scholar3 Ambrose JA, Winters SL, Stern A, Eng A, Teichholz LE, Gorlin R, Fuster V. Angiographic morphology and the pathogenesis of unstable angina pectoris. J Am Coll Cardiol. 1985; 5: 609–616.CrossrefMedlineGoogle Scholar4 Buja LM, Willerson JT. Role of inflammation in coronary plaque disruption. Circulation. 1994; 89: 503–505.CrossrefMedlineGoogle Scholar5 Morrow DA, Rifai N, Antman EM, Weiner DL, McCabe CH, Cannon CP, Braunwald E. C-reactive protein is a potent predictor of mortality independently of and in combination with troponin T in acute coronary syndromes: a TIMI 11A substudy. Thrombolysis in Myocardial Infarction. J Am Coll Cardiol. 1998; 31: 1460–1465.CrossrefMedlineGoogle Scholar6 Glaser R, Selzer F, Faxon D, Laskey W, Cohen H, Slater J, Detre K, Wilensky R. Clinical progression of incidental, asymptomatic lesions discovered during culprit vessel coronary intervention. Circulation. 2005; 111: 143–149.LinkGoogle Scholar7 Moses JW, Leon MB, Popma JJ, Fitzgerald PJ, Holmes DR, O'Shaughnessy C, Caputo RP, Kereiakes DJ, Williams DO, Teirstein PS, Jaeger JL, Kuntz RE; SIRIUS Investigators. Sirolimus-eluting stents versus standard stents in patients with stenosis in a native coronary artery. N Engl J Med. 2003; 349: 1315–1323.CrossrefMedlineGoogle Scholar8 Goldstein JA, Demetriou D, Grines CL, Pica M, Shoukfeh M, O'Neill WW. Multiple complex coronary plaques in patients with acute myocardial infarction. N Engl J Med. 2000; 343: 915–922.CrossrefMedlineGoogle Scholar9 Cannon CP, Braunwald E, McCabe CH, Rader DJ, Rouleau JL, Belder R, Joyal SV, Hill KA, Pfeffer MA, Skene AM; Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis in Myocardial Infarction 22 Investigators. Intensive versus moderate lipid lowering with statins after acute coronary syndromes. N Engl J Med. 2004; 350: 1495–1504.CrossrefMedlineGoogle Scholar10 Pasceri V, Patti G, Nusca A, Pristipino C, Richichi G, Di Sciascio G; ARMYDA Investigators. Randomized trial of atorvastatin for reduction of myocardial damage during coronary intervention: results from the ARMYDA (Atorvastatin for Reduction of MYocardial Damage during Angioplasty) study. Circulation. 2004; 110: 674–678.LinkGoogle Scholar11 Heart Protection Study Collaboration Group. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20 536 high-risk individuals: a randomised placebo-controlled trial. Lancet. 2002; 360: 7–22.CrossrefMedlineGoogle Scholar12 Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet. 1994; 344: 1383–1389.MedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By QUAN W, LU G, QI W, LI Y, SHEN Y and YUAN R (2008) Diagnostic value of magnetocardiography in patients with coronary heart disease and in-stent restenosis, Chinese Medical Journal, 10.1097/00029330-200801010-00005, 121:1, (22-26), Online publication date: 1-Jan-2008. KHAN M (2006) Angioplasty/Coronary Balloon Encyclopedia of Heart Diseases, 10.1016/B978-012406061-6/50011-4, (57-60), . Bogaty P and Brophy J (2006) Acute ischemic heart disease and interventional cardiology: a time for pause, BMC Medicine, 10.1186/1741-7015-4-25, 4:1, Online publication date: 1-Dec-2006. KHAN M (2006) Heart Attacks Encyclopedia of Heart Diseases, 10.1016/B978-012406061-6/50065-5, (397-431), . Lin C, Janero D and Garvey D (2005) Nitric oxide-based molecular strategies for restenosis therapy, Expert Opinion on Therapeutic Patents, 10.1517/13543776.15.5.483, 15:5, (483-495), Online publication date: 1-May-2005. January 18, 2005Vol 111, Issue 2 Advertisement Article InformationMetrics https://doi.org/10.1161/01.CIR.0000153621.57449.8EPMID: 15657386 Originally publishedJanuary 18, 2005 KeywordsEditorialsstentsischemialesionplaquePDF download Advertisement SubjectsAcute Coronary Syndromes
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