Introduction Marathon running is presumed to improve cardiovascular risk, but health benefits of high volume running are unknown. High-resolution coronary computed tomography angiography and cardiac risk factor assessment were completed in women with long-term marathon running histories to compare to sedentary women with similar risk factors. Methods Women who had run at least one marathon per year for 10–25 yr underwent coronary computed tomography angiography, 12-lead ECG, blood pressure and heart rate measurement, lipid panel, and a demographic/health risk factor survey. Sedentary matched controls were derived from a contemporaneous clinical study database. CT scans were analyzed for calcified and noncalcified plaque prevalence, volume, stenosis severity, and calcium score. Results Women marathon runners (n = 26), age 42–82 yr, with combined 1217 marathons (average 47) exhibited significantly lower coronary plaque prevalence and less calcific plaque volume. The marathon runners also had less risk factors (smoking, hypertension, and hyperlipidemia); significantly lower resting heart rate, body weight, body mass index, and triglyceride levels; and higher high-density lipoprotein cholesterol levels compared with controls (n = 28). The five women runners with coronary plaque had run marathons for more years and were on average 12 yr older (65 vs 53) than the runners without plaque. Conclusion Women marathon runners had minimal coronary artery calcium counts, lower coronary artery plaque prevalence, and less calcified plaque volume compared with sedentary women. Developing coronary artery plaque in long-term women marathon runners appears related to older age and more cardiac risk factors, although the runners with coronary artery plaque had accumulated significantly more years running marathons.

BACKGROUND:Long-term marathon running improves many cardiovascular risk factors, and is presumed to protect against coronary artery plaque formation. This hypothesis, that long-term marathon running is protective against coronary atherosclerosis, was tested by quantitatively assessing coronary artery plaque using high resolution coronary computed tomographic angiography (CCTA) in veteran marathon runners compared to sedentary control subjects.METHODS:Men in the study completed at least one marathon yearly for 25 consecutive years. All study subjects underwent CCTA, 12-lead electrocardiogram, measurement of blood pressure, heart rate, and lipid panel. A sedentary matched group was derived from a contemporaneous CCTA database of asymptomatic healthy individuals. CCTAs were analyzed using validated plaque characterization software.RESULTS:Male marathon runners (n = 50) as compared with sedentary male controls (n = 23) had increased total plaque volume (200 vs. 126 mm3, p < 0.01), calcified plaque volume (84 vs. 44 mm3, p < 0.0001), and non-calcified plaque volume (116 vs. 82 mm3, p = 0.04). Lesion area and length, number of lesions per subject, and diameter stenosis did not reach statistical significance.CONCLUSION:Long-term male marathon runners may have paradoxically increased coronary artery plaque volume.

BACKGROUND:A growing number of patients suffer from peripheral artery disease (PAD). Current therapies are often limited by the extent of vascular pathology and the occurrence of restenosis after angioplasty. The stimulatory effect of growth factor administration on collateral vessel formation (arteriogenesis) has evolved as a potential new treatment for this patient group. Granulocyte-macrophage colony-stimulating factor (GM-CSF) was shown to stimulate arteriogenesis in small-animal models and in a pilot study in patients with coronary artery disease. Although a recent clinical study demonstrated disappointing results after subcutaneous GM-CSF application in patients with PAD, we hypothesized that intra-arterial cytokine application using implantable infusion pumps might well stimulate arteriogenesis in a large-species model of peripheral vascular disease. We also aimed to compare continuous and intermittent infusion regimens and to validate experimental and clinically available measurements of collateral artery growth.METHODS:Twenty-four pigs underwent unilateral occlusion of the right femoral artery and received either GM-CSF continuously, GM-CSF intermittently, or phosphate-buffered saline (PBS). After 1 week, collateral conductance was determined under maximal vasodilatation with adenosine and by using a pump-driven extracorporal shunt system.RESULTS:Conductance showed a significant stimulatory effect of GM-CSF on arteriogenesis (collateral conductance [mL/min/mm Hg]: PBS, 37.7 +/- 5.4; GM-CSF continuous, 69.2 +/- 12.5; GM-CSF intermittent, 71.5 +/- 11.1). Flow measurements under reactive hyperemia were consistent with these results (flow occluded/non-occluded hind limb: PBS, 40.5% +/- 9.1%; GM-CSF continuous, 48.9% +/- 3.9%; GM-CSF intermittent, 48.7% +/- 4.4%). Measurements of ankle/brachial indices were not sensitive enough to detect the differences in collateral growth between the three groups.CONCLUSION:These results demonstrate the proarteriogenic properties of GM-CSF in larger animal species, revealing comparable efficacy of continuous and intermittent intra-arterial infusion. Furthermore, we provide evidence that implantable pumps offer a possible means for the intra-arterial application of growth factors. Intra-arterial application of GM-CSF might be a future treatment option for vascular occlusive disease. Finally, we show that in the peripheral circulation, pressure measurements alone have a low sensitivity to determine the effects of proarteriogenic therapy compared with flow or combined flow-pressure measurements.

OBJECTIVES:The present study assesses clinical outcomes in patients from the Potential Angina Class Improvement From Intramyocardial Channels (PACIFIC) trial of percutaneous transmyocardial revascularization (PTMR) who had previously been considered "no-option," but who subsequently underwent percutaneous coronary intervention (PCI) for continuing symptoms.BACKGROUND:Patients with advanced symptomatic coronary artery disease who are not candidates for coronary artery bypass grafting (CABG) or PCI comprise an important group, for which no established treatment is currently available. These patients have been described as having "no option," and are currently targeted for various experimental therapies. One such proposed therapy, PTMR, was recently examined in the PACIFIC trial. A subgroup of patients in this trial subsequently underwent PCI, although to initially qualify for the study they had previously been considered as unsuitable for PCI and as having "no option." The therapeutic benefit of PCI for patients of this type is unknown.METHODS:A retrospective analysis was performed on data obtained from all subjects of the PACIFIC study who underwent PCI within the 12-month follow-up period.RESULTS:Ten subjects originally randomized to PTMR and 11 subjects from the medical treatment group underwent PCI. Most had undergone at least one prior PCI and at least one CABG, and there was a high prevalence of cardiovascular risk factors. Despite excellent immediate procedural success, PCI resulted in only modest, statistically nonsignificant increases in mean exercise duration, small improvements in angina status, and no significant improvements in quality of life.CONCLUSIONS:These data suggest that PCI provides only marginal-if any-symptomatic benefit in these patients.

Over 1 million percutaneous coronary interventions (PCI) and a half million surgical coronary artery bypass grafting procedures (CABG) are performed in the United States annually for treatment of coronary artery disease. With recent advances in anti-restenosis strategies, the number of PCIs is expected to increase dramatically. Still, these therapies treat relatively discrete coronary lesions. However, there is a relatively large number of patients for whom traditional therapies are not optimal, either because there are diffuse coronary artery lesions, because there are chronic total occlusions, or because, in the instance of bypass surgery, creating proximal or distal anastomoses is problematic. We review three strategies in various stages of development aimed at treating patients not optimally served by traditional forms of revascularization: transmyocardial laser revascularization, angiogenic therapies, and direct ventricle-to-coronary artery bypass.

Transmyocardial laser revascularization (TMR or TMLR) is a surgical therapy developed to treat patients with debilitating, medically refractory angina pectoris due to epicardial coronary artery disease that is not amenable to treatment using the traditional methods of percutaneous coronary intervention (PCI) or coronary artery bypass graft surgery (CABG). This technique can also be applied percutaneously [percutaneous myocardial revascularization (PMR) or direct myocardial revascularization (DMR)]. The original hypotheses which motivated development of TMR were that: (i) oxygenated blood could flow directly from the left ventricle and perfuse the myocardium; and (ii) such artificially created channels would remain patent. However, experimental data have refuted both hypotheses. In the face of early reports of marked clinical benefits in terms of relief of anginal symptoms, alternate hypotheses to explain the mechanism have been pursued, including TMR-associated neoangiogenesis and cardiac denervation. Clinically, numerous reports of reduction in frequency and severity of anginal symptoms, improved exercise tolerance and improved quality of life have appeared from nonblind registry-type studies as well as nonblind randomized clinical trials of TMR or PMR versus continued medical therapy. TMR was not associated with a significant improvement in survival compared with medical therapy alone in randomized trials. For example, the prospective, randomized Angina Treatments-Lasers and Normal Therapies in Comparison (ATLANTIC) trial found a 1-year mortality of 5% in 92 TMR-treated patients and 10% in 90 patients treated with medication only. No proof of improved myocardial blood flow in hearts of treated patients is currently available. The first randomized study of PMR was the Potential Angina Class Improvement From Intramyocardial Channels (PACIFIC) trial which found significantly greater improvements in anginal symptoms and exercise tolerance with PMR plus medical therapy, compared with medical therapy alone. The preliminary results of two double-blind studies with PMR/DMR have been presented but have not yet been published in full. Whereas PMR-treated patients did significantly better than sham-treated control groups after 6 months in the Blinded Evaluation of Laser Intervention Electively For angina pectoris (BELIEF) trial, there was no difference after 1 year between DMR-treated patients and those treated with medication only in the DMR In Regeneration of Endomyocardial Channels Trial (DIRECT). Different devices used for revascularization in these two trials may explain the disparity in the results, and therefore the efficacy and tolerability of each device should be judged upon data collected with that particular device.

Transmyocardial laser revascularization (TMR or TMLR) is a surgical therapy developed to treat patients with debilitating, medically refractory angina pectoris due to epicardial coronary artery disease that is not amenable to treatment using the traditional methods of percutaneous coronary intervention (PCI) or coronary artery bypass graft surgery (CABG). This technique can also be applied percutaneously [percutaneous myocardial revascularization (PMR) or direct myocardial revascularization (DMR)]. The original hypotheses which motivated development of TMR were that: (i) oxygenated blood could flow directly from the left ventricle and perfuse the myocardium; and (ii) such artificially created channels would remain patent. However, experimental data have refuted both hypotheses.

American College of Cardiology/Society for Cardiac Angiography and Interventions Clinical Expert Consensus Document on Cardiac Catheterization Laboratory Standards A Report of the American College of Cardiology Task Force on Clinical Expert Consensus Documents Endorsed by the American Heart Association and the Diagnostic and Interventional Catheterization Committee of the Council on Clinical Cardiology of the AHA

A number of mechanical adjuncts to intracoronary stenting are now available to the interventional cardiologist. These devices have assisted in the development of a safer and more effective stenting practice. Intravascular ultrasound-guided stenting has been shown to reduce the rate of subacute thrombosis and subsequent restenosis. It allows a greater appreciation of lesion structure and severity so that an appropriate intervention strategy can be devised. Debulking techniques may allow the optimal deployment of stents so that restenosis is reduced; however, the results of large randomized studies are still awaited. The use of thrombectomy and distal embolization protection devices is emerging as a safer alternate to stenting alone in difficult patient subsets, such as those with thrombus-laden lesions and degenerated vein grafts. Doppler and pressure wires may be useful in determining optimal stent deployment and predict subsequent patient outcomes. An understanding of the indications and limitations of these devices is of increasing importance to the interventional cardiologist as the coming decade threatens to yield an impressive array of high-tech innovations.

This document has been developed as a Clinical Expert Consensus Document (CECD), combining the resources of the American College of Cardiology (ACC) and the Society for Cardiac Angiography and Interventions (SCA&I). It is intended to provide a perspective on the current state of cardiac

Catheterization and Cardiovascular InterventionsVolume 53, Issue 2 p. 281-286 Society News American College of Cardiology/Society for Cardiac Angiography and Interventions clinical expert consensus document on cardiac catheterization laboratory standards: Summary of a report of the American College of Cardiology Task Force on clinical expert consensus documents † ‡ Thomas M. Bashore MD, FACC, ISCAI, Corresponding Author Thomas M. Bashore MD, FACC, ISCAI thomas.bashore@duke.edu Cardiac Catheterization Laboratory, Duke University Medical Center, Durham, North CarolinaCardiac Catheterization Laboratory, Duke University Medical Center, Box 3012, Durham, NC 27710Search for more papers by this authorEric R. Bates MD, FACC, Eric R. Bates MD, FACC University of Michigan, Ann Arbor, MichiganSearch for more papers by this authorMorton J. Kern MD, FACC, ISCAI, Morton J. Kern MD, FACC, ISCAI St. Louis University Hospital, St. Louis, MissouriSearch for more papers by this authorPeter B. Berger MD, FACC, ISCAI, Peter B. Berger MD, FACC, ISCAI Mayo Clinic, Rochester, MinnesotaSearch for more papers by this authorWarren K. Laskey MD, FACC, ISCAI, Warren K. Laskey MD, FACC, ISCAI University of Maryland, Baltimore, MarylandSearch for more papers by this authorDavid A. Clark MD, FACC, ISCAI, David A. Clark MD, FACC, ISCAI Monterey, CaliforniaSearch for more papers by this authorMartin P. O'Laughlin MD, FACC, ISCAI, Martin P. O'Laughlin MD, FACC, ISCAI Duke Medical Center, Durham, North CarolinaSearch for more papers by this authorJack T. Cusma PhD, Jack T. Cusma PhD Mayo Clinic, Rochester, MinnesotaSearch for more papers by this authorStephen Oesterle MD, FACC, ISCAI, Stephen Oesterle MD, FACC, ISCAI Massachusetts General Hospital, Boston, MassachusettsSearch for more papers by this authorGregory J. Dehmer MD, FACC, ISCAI, Gregory J. Dehmer MD, FACC, ISCAI University of North Carolina, Chapel Hill, North CarolinaSearch for more papers by this authorJeffrey J. Popma MD, FACC, ISCAI, Jeffrey J. Popma MD, FACC, ISCAI Brigham and Women's Hospital, Boston, MassachusettsSearch for more papers by this author Thomas M. Bashore MD, FACC, ISCAI, Corresponding Author Thomas M. Bashore MD, FACC, ISCAI thomas.bashore@duke.edu Cardiac Catheterization Laboratory, Duke University Medical Center, Durham, North CarolinaCardiac Catheterization Laboratory, Duke University Medical Center, Box 3012, Durham, NC 27710Search for more papers by this authorEric R. Bates MD, FACC, Eric R. Bates MD, FACC University of Michigan, Ann Arbor, MichiganSearch for more papers by this authorMorton J. Kern MD, FACC, ISCAI, Morton J. Kern MD, FACC, ISCAI St. Louis University Hospital, St. Louis, MissouriSearch for more papers by this authorPeter B. Berger MD, FACC, ISCAI, Peter B. Berger MD, FACC, ISCAI Mayo Clinic, Rochester, MinnesotaSearch for more papers by this authorWarren K. Laskey MD, FACC, ISCAI, Warren K. Laskey MD, FACC, ISCAI University of Maryland, Baltimore, MarylandSearch for more papers by this authorDavid A. Clark MD, FACC, ISCAI, David A. Clark MD, FACC, ISCAI Monterey, CaliforniaSearch for more papers by this authorMartin P. O'Laughlin MD, FACC, ISCAI, Martin P. O'Laughlin MD, FACC, ISCAI Duke Medical Center, Durham, North CarolinaSearch for more papers by this authorJack T. Cusma PhD, Jack T. Cusma PhD Mayo Clinic, Rochester, MinnesotaSearch for more papers by this authorStephen Oesterle MD, FACC, ISCAI, Stephen Oesterle MD, FACC, ISCAI Massachusetts General Hospital, Boston, MassachusettsSearch for more papers by this authorGregory J. Dehmer MD, FACC, ISCAI, Gregory J. Dehmer MD, FACC, ISCAI University of North Carolina, Chapel Hill, North CarolinaSearch for more papers by this authorJeffrey J. Popma MD, FACC, ISCAI, Jeffrey J. Popma MD, FACC, ISCAI Brigham and Women's Hospital, Boston, MassachusettsSearch for more papers by this author First published: 31 May 2001 https://doi.org/10.1002/ccd.1166Citations: 6 † Endorsed by the Diagnostic and Interventional Catheterization Committee of the Council on Clinical Cardiology, American Heart Association ‡ Task Force Members: Robert A. O'Rourke, MD, FACC, Chair, Jonathan Abrams, MD, FACC, Mark A. Hlatky, MD, FACC, Eric R. Bates, MD, FACC, Judith S. Hochman, MD, FACC, Bruce R. Brodie, MD, FACC, Sanjiv Kaul, MBBS, FACC, Pamela S. Douglas, MD, FACC Cynthia M. Tracy, MD, FACC, Gabriel Gregoratos, MD, FACC, David D. Waters, MD, FACC, William L. Winters, Jr., MD, MACC AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume53, Issue2June 2001Pages 281-286 SCAI Member Sign in RelatedInformation

In-stent restenosis (ISR), when treated with balloon angioplasty (PTCA) alone, has an angiographic recurrence rate of 30%-85%. Ablating the hypertrophic neointimal tissue prior to PTCA is an attractive alternative, yet the late outcomes of such treatment have not been fully determined. This multicenter case control study assessed the angiographic and clinical outcomes of 157 consecutive procedures in 146 patients with ISR at nine institutions treated with either PTCA alone (n = 64) or excimer laser assisted coronary angioplasty (ELCA, n = 93)) for ISR. Demographics were similar except more unstable angina at presentation in ELCA-treated patients (74.5% vs. 63.5%; P = 0.141). Lesions selected for ELCA were longer (16.8 +/- 11.2 mm vs. 11.2 +/- 8.6 mm; P < 0.001), more complex (ACC/AHA type C: 35.1% vs. 13.6%; P < 0.001), and with compromised antegrade flow (TIMI flow < 3: 18.9% vs. 4.5%; P = 0.008) compared to PTCA-treated patients. ELCA-treated patients had similar rate of procedural success [93 (98.9% vs. 62 (98.4%); P = 1.0] and major clinical complications [1 (1.1%) vs. 1 (1.6%); P = 1.0]. At 30 days, repeat target site coronary intervention was lower in ELCA-treated patients (1.1% vs. 6.4% in PTCA-treated patients; P = 0.158), but not significantly so. At 1 year, ELCA-treated patients had similar rate of major cardiac events (39.1% vs. 45.2%; P = 0.456) and target lesion revascularization (30.0% vs. 32.3%; P = 0.646). These data suggest that ELCA in patients with complex in-stent restenosis is as safe and effective as balloon angioplasty alone. Despite higher lesion complexity in ELCA-treated patients, no increase in event rates was observed. Future studies should evaluate the relative benefit of ELCA over PTCA alone for the prevention of symptom recurrence specifically in patients with complex in-stent restenosis.

Background —Intracoronary γ- and β-radiation have reduced restenosis in animal models. In the clinical setting, the effectiveness of β-emitters has not been studied in a broad spectrum of patients, particularly those receiving stents. Methods and Results —A prospective, randomized, sham-controlled study of intracoronary radiotherapy with the β-emitting 32 P source wire, using a centering catheter and automated source delivery unit, was conducted. A total of 105 patients with de novo (70%) or restenotic (30%) lesions who were treated by stenting (61%) or balloon angioplasty (39%) received 0 (control), 16, 20, or 24 Gy to a depth of 1 mm in the artery wall. Angiography at 6 months showed a target site late loss index of 11±36% in radiotherapy patients versus 55±30% in controls ( P <0.0001). A low late loss index was seen in stented and balloon-treated patients and was similar across the 16, 20, and 24 Gy radiotherapy groups. Restenosis (≥50%) rates were significantly lower in radiotherapy patients at the target site (8% versus 39%; P =0.012) and at target site plus adjacent segments (22% versus 50%; P =0.018). Target lesion revascularization was needed in 5 radiotherapy patients (6%) and 6 controls (24%; P <0.05). Stenosis adjacent to the target site and late thrombotic events reduced the overall clinical benefit of radiotherapy. Conclusions —β-radiotherapy with a centered 32 P source is safe and highly effective in inhibiting restenosis at the target site after stent or balloon angioplasty. However, minimizing edge narrowing and late thrombotic events must be accomplished to maximize the clinical benefit of this modality.

Background-Intracoronary gamma- and beta-radiation have reduced restenosis in animal models. In the clinical setting, the effectiveness of beta-emitters has not been studied in a broad spectrum of patients, particularly those receiving stents.Methods and Results-A prospective, randomized, sham-controlled study of intracoronary radiotherapy with the beta-emitting P-32 source wire, using a centering catheter and automated source delivery unit, was conducted. A total of 105 patients with de novo (70%) or restenotic (30%) lesions who were treated by stenting (61%) or balloon angioplasty (39%) received 0 (control), 16, 20, or 24 Gy to a depth of 1 mm in the artery wall. Angiography at 6 months showed a target site late loss index of 11+/-36% in radiotherapy patients versus 55+/-30% in controls (P<0.0001). A low late loss index was seen in stented and balloon-treated patients and was similar across the 16, 20, and 24 Gy radiotherapy groups. Restenosis (greater than or equal to 50%) rates were significantly lower in radiotherapy patients at the target site (8% versus 39%; P=0.012) and at target site plus adjacent segments (22% versus 50%; P=0.018). Target lesion revascularization was needed in 5 radiotherapy patients (6%) and 6 controls (24%; P<0.05). Stenosis adjacent to the target site and late thrombotic events reduced the overall clinical benefit of radiotherapy.Conclusions-beta-radiotherapy with a centered P-32 source is safe and highly effective in inhibiting restenosis at the target site after stent or balloon angioplasty. However, minimizing edge narrowing and late thrombotic events must be accomplished to maximize the clinical benefit of this modality.

Twenty-two years have elapsed since Andreas Gruentzig, MD, performed the first coronary angioplasty [(1,2)][1]. During that period, coronary angioplasty and its related procedures have evolved into a highly specialized cognitive and technical discipline, and the expectation of quality in coronary

OBJECTIVES This study was designed to evaluate the composition and quantity of particulate debris resulting from vein graft intervention.BACKGROUND Distal embolization and "no reflow" are frequent and important complications resulting from angioplasty of diseased saphenous vein grafts. Little is known about the composition and quantity of embolic particulate debris associated with vein graft intervention, and no intervention has been shown to protect against its clinical consequences.METHODS A catheter system, designed to contain, retrieve and protect against distal embolization of this material, was evaluated during 27 percutaneous interventional saphenous vein graft procedures. Clinical, angiographic and pathologic analyses were performed.RESULTS The duration of distal graft occlusion required to allow intervention and subsequent debris removal was 150 +/- 54 s, decreasing as experience was gained. Thrombolysis in Myocardial Infarction trial (TIMI) flow grade increased from 2.6 +/- 0.8 to 3.0 +/- 0.0. Creatine kinase (CK) rose above normal in three patients (11.1%) exceeding 3x normal in one (3.7%) resulting in the diagnosis of non-myocardial infarction. Particulate material was identified following 21 of 23 procedures suitable for analysis. Particle size was 204 +/- 57 mu m in the major axis and 83 +/- 22 mu m in the minor axis. Particles consisted predominantly of soft acellular atheromatous material, such as that typically found under a fibrous cap. Semiquantitative analysis suggested that the quantity of particulate material was less following stenting than following balloon dilation.CONCLUSIONS Particulate matter is commonly present following routine angioplasty and stenting of saphenous Vein grafts. Containment, retrieval and analysis of this particulate debris are all feasible. Comparison to prior clinical experience is limited by small sample size. However, to the extent that these particles may contribute to distal embolization, no-reflow and infarction, such a system may contribute to the reduction of complications following vein graft intervention. (C) 1999 by the American College of Cardiology.

In January 1997, experts from the United States, Europe, and Japan gathered at Stanford University to review their collective experience with intracoronary and noncoronary stenting and to identify and prioritize issues requiring further clinical investigation. This report summarizes the discussions that took place during this stent summit. Knowledge of stent-tissue interaction from animal and human pathologic specimens was reviewed in the context of evolving stent designs. The relative merits of coil and slotted tubular stent designs were discussed. Stent deployment routines, including self-expansion, balloon expansion, and high-pressure delivery were debated. The potential for covered stents and coated stents was explored. Problems surrounding the routine deployment of stents were identified: small vessel disease, long lesions, bifurcation stenoses, vein graft disease, ostial disease, left main stenoses, and intrastent restenosis. The value of intravascular ultrasound, as an adjunct to stenting, was explored and debated. An algorithm for “provisional stenting” based on ultrasound criteria was developed. Noncoronary stenting of the aorta, iliacs, and carotids were discussed. Clinical applications that may lead to randomized clinical trials were identified. (Am Heart J 1998;136:578-99.)

Background —The validity of quantitative coronary angiography (QCA) after stent placement has been questioned because the optical density of a metallic stent, added to the density of a contrast-filled lumen, could affect border definition. Methods and Results —We deployed 3.0- and 4.0-mm Palmaz-Schatz, Wiktor, Multilink, NIR, and InStent stents in precision-cast phantoms. Central lumens of 2.0 mm were created. There was no difference between the “true” diameters of any stented lumen by both QCA and quantitative ultrasonic (QCU) measurement poststenting. QCA systematic error (SE) varied from 0.01 for the Wiktor stents to 0.14 mm for the Palmaz-Schatz stents; the random error (RE) was 0.03 to 0.14 mm. QCU SE varied from 0.05 to 0.11 mm, and RE ranged from 0.01 to 0.07 mm. At the next stage, 4.0-mm Wiktor and Palmaz-Schatz stents were deployed into the phantom lumens; 1.5-, 2.0-, 2.5- and 3.0-mm lumens were created inside the stents. QCA and QCU measurements of 1.5- to 2.5-mm residual lumens were overestimated by 0.1 to 0.3 mm. In the 3.0-mm residual lumen within the Wiktor stent, QCA underestimated the luminal size by −0.1 mm. There was no QCA inaccuracy for a 3.0-mm lumen within the Palmaz-Schatz stent. In patients, in 25 stented segments in both the Palmaz-Schatz and Wiktor groups, there was no difference between QCA and QCU diameters. Conclusions —QCU is sufficiently precise for the assessment of the coronary lumen after stenting. QCA can be used as an accurate method of poststent assessment, except when a very mild recurrence within a highly opaque stent is measured. In that instance, QCA may underestimate the luminal diameter.