Coronary Artery Disease: Faxon DP

Bonow RO, Carabello BA, Chatterjee K, de Leon AC, Faxon DP, Freed MD, Gaasch WH, Lytle BW, Nishimura RA, O'Gara PT, O'Rourke RA, Otto CM, Shah PM, Shanewise JS, Nishimura RA, Carabello BA, Faxon DP, Freed MD, Lytle BW, O'Gara PT, O'Rourke RA, Shah PM, Anonymous00383. · No affiliation provided · J Am Coll Cardiol. · Pubmed #18848134 No free full text.

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Bonow RO, Carabello BA, Chatterjee K, de Leon AC, Faxon DP, Freed MD, Gaasch WH, Lytle BW, Nishimura RA, O'Gara PT, O'Rourke RA, Otto CM, Shah PM, Shanewise JS, Nishimura RA, Carabello BA, Faxon DP, Freed MD, Lytle BW, O'Gara PT, O'Rourke RA, Shah PM, Anonymous00383. · No affiliation provided · J Am Coll Cardiol. · Pubmed #18848134 No free full text.

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King SB, Aversano T, Ballard WL, Beekman RH, Cowley MJ, Ellis SG, Faxon DP, Hannan EL, Hirshfeld JW, Jacobs AK, Kellett MA, Kimmel SE, Landzberg JS, McKeever LS, Moscucci M, Pomerantz RM, Smith KM, Vetrovec GW, Creager MA, Hirshfeld JW, Holmes DR, Newby LK, Weitz HH, Merli G, Piña I, Rodgers GP, Tracy CM, Anonymous00143, Anonymous00144, Anonymous00145. · No affiliation provided · J Am Coll Cardiol. · Pubmed #17601554 No free full text.

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Anonymous00180, King SB, Aversano T, Ballard WL, Beekman RH, Cowley MJ, Ellis SG, Faxon DP, Hannan EL, Hirshfeld JW, Jacobs AK, Kellett MA, Kimmel SE, Landzberg JS, McKeever LS, Moscucci M, Pomerantz RM, Smith KM, Vetrovec GW, Creager MA, Holmes DR, Newby LK, Weitz HH, Merli G, Piña I, Rodgers GP, Tracy CM. · No affiliation provided · Circulation. · Pubmed #17592076 links to  free full text

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Anonymous00282, Anonymous00283, Anonymous00284, Anonymous00285, Bonow RO, Carabello BA, Kanu C, de Leon AC, Faxon DP, Freed MD, Gaasch WH, Lytle BW, Nishimura RA, O'Gara PT, O'Rourke RA, Otto CM, Shah PM, Shanewise JS, Smith SC, Jacobs AK, Adams CD, Anderson JL, Antman EM, Faxon DP, Fuster V, Halperin JL, Hiratzka LF, Hunt SA, Lytle BW, Nishimura R, Page RL, Riegel B. · No affiliation provided · Circulation. · Pubmed #16880336 links to  free full text

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Anonymous00282, Anonymous00283, Anonymous00284, Anonymous00285, Bonow RO, Carabello BA, Kanu C, de Leon AC, Faxon DP, Freed MD, Gaasch WH, Lytle BW, Nishimura RA, O'Gara PT, O'Rourke RA, Otto CM, Shah PM, Shanewise JS, Smith SC, Jacobs AK, Adams CD, Anderson JL, Antman EM, Faxon DP, Fuster V, Halperin JL, Hiratzka LF, Hunt SA, Lytle BW, Nishimura R, Page RL, Riegel B. · No affiliation provided · Circulation. · Pubmed #16880336 links to  free full text

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Eagle KA, Guyton RA, Davidoff R, Edwards FH, Ewy GA, Gardner TJ, Hart JC, Herrmann HC, Hillis LD, Hutter AM, Lytle BW, Marlow RA, Nugent WC, Orszulak TA, Antman EM, Smith SC, Alpert JS, Anderson JL, Faxon DP, Fuster V, Gibbons RJ, Gregoratos G, Halperin JL, Hiratzka LF, Hunt SA, Jacobs AK, Ornato JP, Anonymous00232, Anonymous00233, Anonymous00234. · No affiliation provided · J Am Coll Cardiol. · Pubmed #15337239 No free full text.

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Klocke FJ, Baird MG, Lorell BH, Bateman TM, Messer JV, Berman DS, O'Gara PT, Carabello BA, Russell RO, Cerqueira MD, St John Sutton MG, DeMaria AN, Udelson JE, Kennedy JW, Verani MS, Williams KA, Antman EM, Smith SC, Alpert JS, Gregoratos G, Anderson JL, Hiratzka LF, Faxon DP, Hunt SA, Fuster V, Jacobs AK, Gibbons RJ, Russell RO, Anonymous00288, Anonymous00289, Anonymous00290. · No affiliation provided · J Am Coll Cardiol. · Pubmed #14522503 No free full text.

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Klocke FJ, Baird MG, Lorell BH, Bateman TM, Messer JV, Berman DS, O'Gara PT, Carabello BA, Russell RO, Cerqueira MD, St John Sutton MG, DeMaria AN, Udelson JE, Kennedy JW, Verani MS, Williams KA, Antman EM, Smith SC, Alpert JS, Gregoratos G, Anderson JL, Hiratzka LF, Faxon DP, Hunt SA, Fuster V, Jacobs AK, Gibbons RJ, Russell RO, Anonymous00249, Anonymous00250, Anonymous00251. · No affiliation provided · Circulation. · Pubmed #12975245 links to  free full text

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Gibbons RJ, Abrams J, Chatterjee K, Daley J, Deedwania PC, Douglas JS, Ferguson TB, Fihn SD, Fraker TD, Gardin JM, O'Rourke RA, Pasternak RC, Williams SV, Gibbons RJ, Alpert JS, Antman EM, Hiratzka LF, Fuster V, Faxon DP, Gregoratos G, Jacobs AK, Smith SC, Anonymous00182, Anonymous00183. · No affiliation provided · Circulation. · Pubmed #12515758 links to  free full text

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Eagle KA, Berger PB, Calkins H, Chaitman BR, Ewy GA, Fleischmann KE, Fleisher LA, Froehlich JB, Gusberg RJ, Leppo JA, Ryan T, Schlant RC, Winters WL, Gibbons RJ, Antman EM, Alpert JS, Faxon DP, Fuster V, Gregoratos G, Jacobs AK, Hiratzka LF, Russell RO, Smith SC, Anonymous00237. · No affiliation provided · Circulation. · Pubmed #11889023 links to  free full text

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Smith SC, Dove JT, Jacobs AK, Kennedy JW, Kereiakes D, Kern MJ, Kuntz RE, Popma JJ, Schaff HV, Williams DO, Gibbons RJ, Alpert JP, Eagle KA, Faxon DP, Fuster V, Gardner TJ, Gregoratos G, Russell RO, Smith SC, Anonymous00159, Anonymous00160. · No affiliation provided · J Am Coll Cardiol. · Pubmed #11419905 No free full text.

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Smith SC, Dove JT, Jacobs AK, Kennedy JW, Kereiakes D, Kern MJ, Kuntz RE, Popma JJ, Schaff HV, Williams DO, Gibbons RJ, Alpert JP, Eagle KA, Faxon DP, Fuster V, Gardner TJ, Gregoratos G, Russell RO, Smith SC, Anonymous00100, Anonymous00101. · Committee Members. · Circulation. · Pubmed #11413094 links to  free full text

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Bokhari SW, Faxon DP. · Section of Cardiology, University of Chicago Pritzker School of Medicine, Chicago, Illinois, USA. · Rev Cardiovasc Med. · Pubmed #15580159 No free full text.

Abstract: Renal artery stenosis (RAS) is a common condition associated with hypertension and renal insufficiency. The high prevalence of RAS patients with coronary and lower extremity vascular disease has been well established. Fibromuscular dysplasia in young females and atherosclerosis in patients over the age of 55 are the most common causes. Poorly controlled hypertension refractory to medical therapy, worsening of renal function, and flash pulmonary edema may point to underlying RAS. Duplex ultrasonography and magnetic resonance angiography have largely replaced captopril scanning for RAS screening. However, renal angiography still remains the gold standard to diagnose RAS. Treatment options include medical therapy, angioplasty, and surgery. In general, patients with a stenosis greater than 50%, a translesional systolic pressure gradient greater than 15 mm Hg, and difficult-to-control hypertension and/or worsening renal insufficiency are candidates for renal revascularization. Percutaneous transluminal revascularization has evolved to become the preferred revascularization therapy because it is a less invasive and more cost-effective alternative to surgery and is associated with high technical success, as well as a low complication rate. The natural history of RAS is to progress over time, leading to renal artery occlusion, loss of renal mass, worsening of renal function, and, ultimately, end-stage renal disease. It is therefore important to aggressively screen, recognize, and treat the entity early in its course.

Naghavi M, Libby P, Falk E, Casscells SW, Litovsky S, Rumberger J, Badimon JJ, Stefanadis C, Moreno P, Pasterkamp G, Fayad Z, Stone PH, Waxman S, Raggi P, Madjid M, Zarrabi A, Burke A, Yuan C, Fitzgerald PJ, Siscovick DS, de Korte CL, Aikawa M, Airaksinen KE, Assmann G, Becker CR, Chesebro JH, Farb A, Galis ZS, Jackson C, Jang IK, Koenig W, Lodder RA, March K, Demirovic J, Navab M, Priori SG, Rekhter MD, Bahr R, Grundy SM, Mehran R, Colombo A, Boerwinkle E, Ballantyne C, Insull W, Schwartz RS, Vogel R, Serruys PW, Hansson GK, Faxon DP, Kaul S, Drexler H, Greenland P, Muller JE, Virmani R, Ridker PM, Zipes DP, Shah PK, Willerson JT. · The Center for Vulnerable Plaque Research, University of Texas-Houston, The Texas Heart Institute, and President Bush Center for Cardiovascular Health, Memorial Hermann Hospital, Houston, USA. · Circulation. · Pubmed #14557340 links to  free full text

Abstract: Atherosclerotic cardiovascular disease results in >19 million deaths annually, and coronary heart disease accounts for the majority of this toll. Despite major advances in treatment of coronary heart disease patients, a large number of victims of the disease who are apparently healthy die suddenly without prior symptoms. Available screening and diagnostic methods are insufficient to identify the victims before the event occurs. The recognition of the role of the vulnerable plaque has opened new avenues of opportunity in the field of cardiovascular medicine. This consensus document concludes the following. (1) Rupture-prone plaques are not the only vulnerable plaques. All types of atherosclerotic plaques with high likelihood of thrombotic complications and rapid progression should be considered as vulnerable plaques. We propose a classification for clinical as well as pathological evaluation of vulnerable plaques. (2) Vulnerable plaques are not the only culprit factors for the development of acute coronary syndromes, myocardial infarction, and sudden cardiac death. Vulnerable blood (prone to thrombosis) and vulnerable myocardium (prone to fatal arrhythmia) play an important role in the outcome. Therefore, the term "vulnerable patient" may be more appropriate and is proposed now for the identification of subjects with high likelihood of developing cardiac events in the near future. (3) A quantitative method for cumulative risk assessment of vulnerable patients needs to be developed that may include variables based on plaque, blood, and myocardial vulnerability. In Part I of this consensus document, we cover the new definition of vulnerable plaque and its relationship with vulnerable patients. Part II of this consensus document will focus on vulnerable blood and vulnerable myocardium and provide an outline of overall risk assessment of vulnerable patients. Parts I and II are meant to provide a general consensus and overviews the new field of vulnerable patient. Recently developed assays (eg, C-reactive protein), imaging techniques (eg, CT and MRI), noninvasive electrophysiological tests (for vulnerable myocardium), and emerging catheters (to localize and characterize vulnerable plaque) in combination with future genomic and proteomic techniques will guide us in the search for vulnerable patients. It will also lead to the development and deployment of new therapies and ultimately to reduce the incidence of acute coronary syndromes and sudden cardiac death. We encourage healthcare policy makers to promote translational research for screening and treatment of vulnerable patients.

Mak KH, Faxon DP. · Department of Cardiology, National Heart Centre, Singapore, Singapore. · Eur Heart J. · Pubmed #12804923 links to  free full text

Abstract: With the increasing prevalence, diabetes is rapidly growing into a global public health problem. Cardiovascular disease is a major consequence of this chronic condition, and a critical issue facing physicians worldwide today is choice of coronary revascularization procedures in treating these patients. Since the Bypass Angioplasty Revascularization Investigation (BARI) alert in 1995, there have been several reports on subgroup analysis of clinical trials and registries concerning revascularization among patients with diabetes. Although randomized control studies comparing percutaneous and surgical revascularization procedures in this high-risk group of patients are lacking, this article provides the background for the excess risk and reviews the findings of these investigations. Current strategies to improve outcomes in patients with diabetes undergoing coronary revascularization procedures are discussed.

Durairaj A, Mehra A, Singh RP, Faxon DP. · Division of Cardiology, University of Southern California School of Medicine, Los Angeles, California, USA. · Cardiol Rev. · Pubmed #11174906 No free full text.

Abstract: Coronary artery disease remains the leading cause of morbidity and mortality in the Western world. The initial approach to treatment involves risk factor modification in an attempt to halt or slow the progression of disease. Treatment of symptomatic disease aims at reducing myocardial oxygen demand with medical therapy. When this fails, revascularization to restore blood supply by percutaneous coronary intervention or coronary artery bypass grafting is often necessary. Advances in medical technology have both increased the success rate and lowered the morbidity and mortality of these 2 procedures. However, a significant number of patients have diffuse coronary artery disease, absent conduits after previous bypass surgery, small distal vessels, and comorbidities that may preclude either procedure. In a recent analysis of 500 consecutive patients at a tertiary referral center, approximately 12% of these patients fell into this category (1). With the widespread use of revascularization, it is likely that the number of patients who will not be suitable for revascularization in the future will increase significantly. Therapeutic angiogenesis is an exciting new method of improving blood supply to an ischemic segment of the myocardium to provide symptomatic relief to a large and growing population of patients.

O'Rourke RA, Brundage BH, Froelicher VF, Greenland P, Grundy SM, Hachamovitch R, Pohost GM, Shaw LJ, Weintraub WS, Winters WL, Forrester JS, Douglas PS, Faxon DP, Fisher JD, Gregoratos G, Hochman JS, Hutter AM, Kaul S, Wolk MJ. · No affiliation provided · Circulation. · Pubmed #10880426 links to  free full text

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Hodis HN, Mack WJ, Azen SP, Lobo RA, Shoupe D, Mahrer PR, Faxon DP, Cashin-Hemphill L, Sanmarco ME, French WJ, Shook TL, Gaarder TD, Mehra AO, Rabbani R, Sevanian A, Shil AB, Torres M, Vogelbach KH, Selzer RH, Anonymous00288. · Atherosclerosis Research Unit, Keck School of Medicine, Los Angeles, CA 90033, USA. · N Engl J Med. · Pubmed #12904518 links to  free full text

Abstract: BACKGROUND: In postmenopausal women with coronary artery disease, conjugated equine estrogen with or without continuous administration of medroxyprogesterone acetate has failed to slow the progression of atherosclerosis. Whether 17beta-estradiol (the endogenous estrogen molecule) alone or administered sequentially with medroxyprogesterone acetate can slow the progression of atherosclerosis is unknown. METHODS: We conducted a double-blind, placebo-controlled trial in 226 postmenopausal women (mean age, 63.5 years) who had at least one coronary-artery lesion. Participants were randomly assigned to usual care (control group), estrogen therapy with micronized 17beta-estradiol alone (estrogen group), or 17beta-estradiol plus sequentially administered medroxyprogesterone acetate (estrogen-progestin group). In all patients the low-density lipoprotein (LDL) cholesterol level was reduced to a target of less than 130 mg per deciliter. The primary outcome was the average per-participant change between base-line and follow-up coronary angiograms in the percent stenosis measured by quantitative coronary angiography. RESULTS: After a median of 3.3 years of follow-up, the mean (+/-SE) change in the percent stenosis in the 169 participants who had a pair of matched angiograms was 1.89+/-0.78 percentage points in the control group, 2.18+/-0.76 in the estrogen group, and 1.24+/-0.80 in the estrogen-progestin group (P=0.66 for the comparison among the three groups). The mean difference in the percent stenosis between the estrogen group and the control group was 0.29 percentage point (95 percent confidence interval, -1.88 to 2.46), and the mean difference between the estrogen-progestin group and the control group was -0.65 (95 percent confidence interval, -2.87 to 1.57). CONCLUSIONS: In older postmenopausal women with established coronary-artery atherosclerosis, 17beta-estradiol either alone or with sequentially administered medroxyprogesterone acetate had no significant effect on the progression of atherosclerosis.

Berger PB, Velianou JL, Aslanidou Vlachos H, Feit F, Jacobs AK, Faxon DP, Attubato M, Keller N, Stadius ML, Weiner BH, Williams DO, Detre KM, Anonymous00242. · Division of Cardiovascular Disease, Mayo Clinic, Rochester, Minnesota 55905, USA. · J Am Coll Cardiol. · Pubmed #11691521 No free full text.

Abstract: OBJECTIVES: We sought to compare survival after coronary artery bypass graft (CABG) and percutaneous transluminal coronary angioplasty (PTCA) in high-risk anatomic subsets. BACKGROUND: Compared with medical therapy, CABG decreases mortality in patients with three-vessel disease and two-vessel disease involving the proximal left anterior descending artery (LAD), particularly if left ventricular (LV) dysfunction is present. How survival after PTCA and CABG compares in these high-risk anatomic subsets is unknown. METHODS: In the Bypass Angioplasty Revascularization Investigation (BARI), 1,829 patients with multivessel disease were randomized to an initial strategy of PTCA or CABG between 1988 and 1991. Stents and IIb/IIIa inhibitors were not utilized. Since patients in BARI with diabetes mellitus had greater survival with CABG, separate analyses of patients without diabetes were performed. RESULTS: Seven-year survival among patients with three-vessel disease undergoing PTCA and CABG (n = 754) was 79% versus 84% (p = 0.06), respectively, and 85% versus 87% (p = 0.36) when only non-diabetics (n = 592) were analyzed. In patients with three-vessel disease and reduced LV function (ejection fraction <50%), seven-year survival was 70% versus 74% (p = 0.6) in all PTCA and CABG patients (n = 176), and 82% versus 73% (p = 0.29) among non-diabetic patients (n = 124). Seven-year survival was 87% versus 84% (p = 0.9) in all PTCA and CABG patients (including diabetics) with two-vessel disease involving the proximal LAD (n = 352), and 78% versus 71% (p = 0.7) in patients with two-vessel disease involving the proximal LAD with reduced LV function (n = 72). CONCLUSION: In high-risk anatomic subsets in which survival is prolonged by CABG versus medical therapy, revascularization by PTCA and CABG yielded equivalent survival over seven years.

Wu C, Hannan EL, Walford G, Faxon DP. · University at Albany, State University of New York, Albany, New York, USA. · Ann Thorac Surg. · Pubmed #18805151 No free full text.

Abstract: BACKGROUND: Limited contemporary information is available on outcomes for patients with unprotected left main coronary artery (LMCA) disease who are revascularized. METHODS: We examined the relative frequency, severity of illness, and outcomes of stenting and coronary artery bypass graft (CABG) surgery for treating unprotected LMCA disease in New York between January 1, 2000 and December 31, 2004. A total of 16,336 (98.7%) patients who underwent CABG surgery and 212 (1.3%) who underwent stenting were included in this study. RESULTS: Stent patients had higher preprocedural severity of illness (eg, they were older, more likely to be female, and had more comorbidities). A total of 135 stent patients were matched to 135 CABG patients on baseline characteristics identified by a propensity model as predictors of type of procedure received. At the end of follow-up on December 31, 2004, the respective 2-year survival rates were 94.1% and 82.0% (hazard ratio = 0.32, p = 0.005) for the 135 pairs of matched CABG and stent patients. The respective 2-year rates for freedom from subsequent revascularization were 93.7% and 62.7% (hazard ratio = 0.15, p < 0.001). In the drug-eluting stent era between October 1, 2003 and December 31, 2004, the same trends in mortality (hazard ratio = 0.73, p = 0.69) and repeat revascularization (hazard ratio = 0.10, p = 0.03) were observed among the 56 pairs of matched CABG and drug-eluting stent patients. CONCLUSIONS: Most patients with LMCA disease who needed coronary revascularization received CABG surgery; stent patients were sicker. This study found that surgery patients experienced lower risk of long-term death and repeat revascularization. However, more studies comparing these procedures are needed, especially in the drug-eluting stent era.

Holper EM, Brooks MM, Kim LJ, Detre KM, Faxon DP, Anonymous00019. · Department of Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA. · Am J Cardiol. · Pubmed #17631069 No free full text.

Abstract: This study evaluated the effect of heart failure (HF) and ejection fraction (EF) at baseline on long-term cardiac mortality in patients undergoing coronary revascularization and investigated the effect of diabetes mellitus (DM) on mortality. We evaluated long-term outcomes of patients without HF, HF and a preserved EF, and HF and a decreased EF who underwent revascularization with percutaneous transluminal coronary angioplasty or coronary artery bypass graft surgery after enrollment in the Bypass Angioplasty Revascularization Investigation (BARI) trial. Ten years after initial revascularization, cumulative rates of freedom from cardiac death were 90% in patients without HF, 75% in patients with HF and a preserved EF, and 59% in patients with HF and a decreased EF (p <0.001, 3-way comparison). In diabetic patients with HF and a preserved EF, there was a significant increase in cardiac mortality compared with patients without HF (p <0.001); however, this relation was not seen in patients without DM. In conclusion, patients with HF and a preserved EF have increased mortality over 10 years compared with those without HF. Only in patients with DM did HF with preserved EF confer additional risk.

Hong TE, Faxon DP. · Section of Cardiology, University of Chicago Pritzker School of Medicine, Chicago, Illinois, USA. · Rev Cardiovasc Med. · Pubmed #16379018 No free full text.

Abstract: Buerger's disease (thromboangiitis obliterans) is a small- and medium-vessel vasculitis that predominantly involves the distal extremities. Coronary involvement in Buerger's disease is very unusual and rarely reported. We describe the unusual coronary angiogram findings of a 61-year-old Caucasian male with Buerger's disease who underwent cardiac catheterization for preoperative cardiac risk stratification prior to a carotid endarterectomy. Following the case presentation, we review the pathology, pathogenesis, and diagnostic criteria for Buerger's disease, and also include a review of the existing literature on coronary involvement in Buerger's disease.

Bokhari SW, Bokhari ZW, Zell JA, Lee DW, Faxon DP. · University of Chicago-Pritzker School of Medicine, Illinois 60637, USA. · Coron Artery Dis. · Pubmed #15818084 No free full text.

Abstract: BACKGROUND: Numerous studies have shown a relationship between hyperhomocysteinemia, atherothrombosis and cardiovascular mortality. However, an association between hyperhomocysteinemia and the extent of coronary artery disease (CAD) remains controversial whereas its relationship with left ventricular systolic function has not been established. METHODS: One hundred and fifty-seven patients with angiographically defined CAD were included. The relationships between hyperhomocysteinemia, severity of CAD and left ventricular systolic function were studied. Left ventricular systolic function was determined primarily by ventriculography. The severity of CAD was determined through coronary angiography using the Gensini score and the number of vessels with > or = 50% stenosis. RESULTS: The mean fasting plasma homocysteine level was 13.4 mumol/l+/-0.5 SE. Elevated levels of homocysteine correlated significantly with increased severity of CAD both by the Gensini scores (r-value = 0.344, P < 0.0005) and the total number of diseased vessels (r-value = 0.387, P < 0.0005). The patients with hyperhomocysteinemia were found to have significantly reduced left ventricular ejection fraction (r-value = -0.382, P < 0.0005). A multivariate regression analysis revealed homocysteine level to be an independent predictor of left ventricular systolic function. In addition, adjusted analysis revealed hyperhomocysteinemia to be associated with global left ventricular dysfunction. CONCLUSION: In patients with CAD, homocysteine levels correlate independently with left ventricular systolic function. The mechanism of this association between homocysteine and left ventricular systolic function is unknown but may be due to a direct effect of homocysteine on myocardial function separate from its effects on coronary atherosclerosis.

Glaser R, Selzer F, Faxon DP, Laskey WK, Cohen HA, Slater J, Detre KM, Wilensky RL. · University of Pennsylvania, Philadelphia, PA 19104, USA. · Circulation. · Pubmed #15623544 links to  free full text

Abstract: BACKGROUND: With the reduction in restenosis rates by drug-eluting stents, there is new controversy concerning the optimal management of incidental, nontarget lesions identified during percutaneous coronary intervention (PCI). Such lesions have been treated conservatively because of risk of restenosis but now are being considered for PCI to prevent plaque instability. However, the impact of incidental stenoses on future cardiac events remains unknown. METHODS AND RESULTS: We performed a retrospective cohort study to determine the rate and features of clinical plaque progression using the National Heart, Lung, and Blood Institute Dynamic Registry of consecutive patients undergoing PCI at multiple centers in 1997 to 1998 and 1999. Of 3747 PCI patients, 216 (5.8%) required additional nontarget lesion PCI for clinical plaque progression at 1 year. Fifty-nine percent presented with new unstable angina, and 9.3% presented with nonfatal myocardial infarction. Patients with multivessel coronary artery disease during original PCI were more likely to require nontarget lesion PCI during follow-up (adjusted odds ratio, 1.72 [95% CI, 1.18 to 2.52] for 2 vessels; adjusted odds ratio, 3.37 [95% CI, 2.32 to 4.89] for 3 vessels). Angiographic review showed that the majority (86.9%) of lesions requiring subsequent PCI were < or =60% in severity during original PCI, with the mean lesion stenosis 41.8+/-20.8% at the time of the initial PCI and 83.9+/-13.9% during the recurrent event. CONCLUSIONS: Approximately 6% of PCI patients will have clinical plaque progression requiring nontarget lesion PCI by 1 year. Greater coronary artery disease burden confers a significantly higher risk for clinical plaque progression.