Catheter-Based Treatment of Coronary Artery Disease by David R. Holmes, and David O. Williams Circ Cardiovasc Interv Volume 1(1):60-73 August 1, 2008 Copyright © American Heart Association, Inc. All rights reserved.

Figure 1. Early equipment and procedural performance at the beginning of intervention. Figure 1. Early equipment and procedural performance at the beginning of intervention. A, An early balloon catheter, which usually required an 8F or a 9F guiding catheter. B, Typical measurements of coronary pressure gradients documenting improved hemodynamic after balloon deflation. Δp indicates change in pressure; AOP, aortic pressure; COP, colloid osmotic pressure; and CM contrast media. Reproduced from Grüntzig AR. PTCA technique with a double-lumen dilatation catheter. In Proceedings of the Workshop on Percutaneous Transluminal Coronary Angioplasty, National Institutes of Health, March 1980, pp 123-133. David R. Holmes, Jr, and David O. Williams Circ Cardiovasc Interv. 2008;1:60-73 Copyright © American Heart Association, Inc. All rights reserved.

Figure 2. The results of serial angiography after successful PTCA documenting the fact that most restenosis occurs within the first 3 to 6 months.15. Figure 2. The results of serial angiography after successful PTCA documenting the fact that most restenosis occurs within the first 3 to 6 months.15 David R. Holmes, Jr, and David O. Williams Circ Cardiovasc Interv. 2008;1:60-73 Copyright © American Heart Association, Inc. All rights reserved.

Figure 3. The concept of “bigger is better” arose with the observations that a crucial determinate of subsequent restenosis was the magnitude of initial improvement in angiographic result. Figure 3. The concept of “bigger is better” arose with the observations that a crucial determinate of subsequent restenosis was the magnitude of initial improvement in angiographic result. That was found to be the case with balloon angioplasty directional coronary atherectomy and BMS. Left, Probability of restenosis after a procedure classified by postprocedure lumen diameter. Right, Actual restenosis rate.27 David R. Holmes, Jr, and David O. Williams Circ Cardiovasc Interv. 2008;1:60-73 Copyright © American Heart Association, Inc. All rights reserved.

Figure 4. A, Meta-analysis of DES for in-stent restenosis of BMS Figure 4. A, Meta-analysis of DES for in-stent restenosis of BMS. Treatment with DES improved target lesion revascularization. Figure 4. A, Meta-analysis of DES for in-stent restenosis of BMS. Treatment with DES improved target lesion revascularization. However, there were no significant differences in stent thrombosis (B) or the composite of death or infarction (C).48 Reproduced from Dibra et al48 with permission from the American College of Cardiology. Copyright 2007 American College of Cardiology. David R. Holmes, Jr, and David O. Williams Circ Cardiovasc Interv. 2008;1:60-73 Copyright © American Heart Association, Inc. All rights reserved.

Figure 5. Collaborative network meta-analysis of 38 trials Figure 5. Collaborative network meta-analysis of 38 trials.42 There was a dramatic reduction in target lesion revascularization with drug-eluting stents (A) but no significant decrease in death or myocardial infarction (B). Figure 5. Collaborative network meta-analysis of 38 trials.42 There was a dramatic reduction in target lesion revascularization with drug-eluting stents (A) but no significant decrease in death or myocardial infarction (B). PES indicates paclitaxel-eluting stent; SES, sirolimus-eluting stent; and HR, hazard ratio. Reproduced from Stettler et al42 with permission from Elsevier Ltd. Copyright 2007 Elsevier Ltd. David R. Holmes, Jr, and David O. Williams Circ Cardiovasc Interv. 2008;1:60-73 Copyright © American Heart Association, Inc. All rights reserved.

Figure 6. NHLBI Dynamic Registry of 6551 patients with off-label indications documenting no difference in adjusted risk of death or myocardial infarction in patients treated with DES but decreased target lesion revascularization. Figure 6. NHLBI Dynamic Registry of 6551 patients with off-label indications documenting no difference in adjusted risk of death or myocardial infarction in patients treated with DES but decreased target lesion revascularization. Reproduced from Marroquin et al41 with permission from The Massachusetts Medical Society. Copyright 2008 Massachusetts Medical Society. All rights reserved. David R. Holmes, Jr, and David O. Williams Circ Cardiovasc Interv. 2008;1:60-73 Copyright © American Heart Association, Inc. All rights reserved.

Figure 7. A, At 10 years, 2.0% of patients receiving a BMS in the study by Doyle et al53 had developed stent thrombosis. Figure 7. A, At 10 years, 2.0% of patients receiving a BMS in the study by Doyle et al53 had developed stent thrombosis. In this series, restenosis was not a benign event that occurred with increasing frequency over 10 years (B) and but rather was associated with unstable angina or acute myocardial infarction (MI) in 9% of patients (C). Adapted from Doyle et al53 with permission from the American Heart Association. Copyright 2007 American Heart Association. David R. Holmes, Jr, and David O. Williams Circ Cardiovasc Interv. 2008;1:60-73 Copyright © American Heart Association, Inc. All rights reserved.

Figure 8. Results of a matched cohort of patients with left main coronary artery disease treated with either DES or CABG documenting no significant difference in death (A) but still a difference in need for subsequent procedures (B). Figure 8. Results of a matched cohort of patients with left main coronary artery disease treated with either DES or CABG documenting no significant difference in death (A) but still a difference in need for subsequent procedures (B). Reproduced from Seung et al81 with permission from The Massachusetts Medical Society. Copyright 2008 Massachusetts Medical Society. All rights reserved. David R. Holmes, Jr, and David O. Williams Circ Cardiovasc Interv. 2008;1:60-73 Copyright © American Heart Association, Inc. All rights reserved.

Figure 9. Left, Composite documenting the effects of adjustment, showing 18-month rate of survival of unadjusted 3-vessel disease, with 93.7% for CABG and 93.4% for DES (P=NS). Figure 9. Left, Composite documenting the effects of adjustment, showing 18-month rate of survival of unadjusted 3-vessel disease, with 93.7% for CABG and 93.4% for DES (P=NS). Right, After adjustment, there was a slight increase in survival rate for CABG, from 93.7% to 94.0%, and a slight decrease in survival for DES, from 93.4% to 92.7%, but these slight changes resulted in statistical significance (P=0.03). Reproduced from Hannan et al83 with permission from The Massachusetts Medical Society. Copyright 2008 Massachusetts Medical Society. All rights reserved. David R. Holmes, Jr, and David O. Williams Circ Cardiovasc Interv. 2008;1:60-73 Copyright © American Heart Association, Inc. All rights reserved.

Figure 10. Systemic review of effectiveness of PCI and CABG using a total of 23 randomized clinical trials and a total of 9963 patients. Figure 10. Systemic review of effectiveness of PCI and CABG using a total of 23 randomized clinical trials and a total of 9963 patients. Adapted from Bravata et al88 with permission from the American College of Physicians. Copyright 2007 American College of Physicians. David R. Holmes, Jr, and David O. Williams Circ Cardiovasc Interv. 2008;1:60-73 Copyright © American Heart Association, Inc. All rights reserved.