In Part I of this article, the definitions, prevalence, and clinical presentation of chronic total occlusions (CTOs) were reviewed, the histopathology of CTOs was examined, efforts to replicate human CTOs with experimental models were appraised, and the clinical relevance and rationale for CTO revascularization were evaluated. 1 In Part II, we summarize the technical approach to and outcomes after percutaneous coronary intervention (PCI) of occluded coronary arteries, describe the novel devices and drugs approved and undergoing investigation for CTO recanalization, and conclude with practical perspectives on managing the patient with 1 or more chronic coronary occlusions.

This model predicted the probability of successful guidewire crossing within 30 min very well and can be applied for difficulty grading.

R emarkable progress in the percutaneous management of coronary artery disease has been achieved over the last decade. The scaffolding properties of coronary stents have resulted in percutaneous coronary intervention (PCI) becoming a predictable procedure, with reduced rates of acute closure and late restenosis compared with balloon angioplasty alone. 1,2 More recently, the site-specific delivery of antiproliferative agents from drug-eluting stents has been demonstrated to markedly attenuate vascular responses leading to neointimal hyperplasia, further reducing the occurrence of clinical and angiographic restenosis to Ͻ10% in most patients. 3,4 PCI in patients with acute coronary syndromes and acute myocardial infarction (AMI) has also been proven to save lives, reduce rates of myocardial infarction (MI), and enhance quality of life compared with alternative treatment modalities. [5][6][7] With these advances in perspective, it is often stated that successful recanalization of chronic total occlusions (CTOs) of native coronary arteries represents the "last frontier" of PCI. This statement is made in deference to the fact that CTOs represent the most technically challenging lesion subset that interventional cardiologists face, with procedural success rates considerably lower than those achieved in nonoccluded coronary vessels or acutely occluded arteries. Moreover, no consensus exists with regard to the definition of CTO, the factors related to procedural failure and/or complications, and the optimal technical approach. Indeed, until recently, the clinical benefits of PCI in CTOs had not been demonstrated.An international panel of 47 physicians from 9 countries was therefore convened in New York City for 2 days in January 2004, the purpose of which was to reach consensus on the current state of the art of CTO angioplasty (see Appendix in the online-only Data Supplement for a complete participant list). This goal was approached through a series of didactic lectures, roundtable discussions, breakout focus groups, and the performance of 14 live case demonstrations of CTO angioplasty by many of the world's most skilled operators in this subspecialty. The present report represents a synthesis of the findings from this meeting and also incorporates a literature review from the field of CTO intervention. Topics covered in Part I of this review include definitions, prevalence, and clinical presentation of CTOs; the anatomy and histopathology of coronary occlusions; experimental CTO models; and the clinical relevance and rationale for CTO revascularization. Part II will review the technical approach to and clinical outcomes after percutaneous intervention of CTOs and describe the novel devices and drugs approved and undergoing investigation for CTO recanalization.

Background-The influences of antiplatelet therapy discontinuation on the risk of stent thrombosis and long-term clinical outcomes after drug-eluting stent implantation have not yet been addressed adequately. Methods and Results-In an observational study in Japan, 2-year outcomes were assessed in 10 778 patients undergoing sirolimus-eluting stent implantation. Data on status of antiplatelet therapy during follow-up were collected prospectively. Incidences of definite stent thrombosis were 0.34% at 30 days, 0.54% at 1 year, and 0.77% at 2 years. Thienopyridine use was maintained in 97%, 62%, and 50% of patients at 30 days, 1 year, and 2 years, respectively. Patients who discontinued both thienopyridine and aspirin had a significantly higher rate of stent thrombosis than those who continued both in the intervals of 31 to 180 days, 181 to 365 days, and 366 to 548 days after stent implantation (1.76% versus 0.1%, PϽ0.001; 0.72% versus 0.07%, Pϭ0.02; and 2.1% versus 0.14%, Pϭ0.004, respectively). When discontinuation of aspirin was taken into account, patients who discontinued thienopyridine only did not have an excess of stent thrombosis in any of the time intervals studied. Adjusted rates of death or myocardial infarction at 24 months were 4.1% for patients taking thienopyridine and 4.1% for patients not taking thienopyridine (Pϭ0.99) in the 6-month landmark analysis. Conclusions-Discontinuation of both thienopyridine and aspirin, but not discontinuation of thienopyridine therapy only, was associated with an increased risk of stent thrombosis. Landmark analysis did not suggest an apparent clinical benefit of thienopyridine use beyond 6 months after sirolimus-eluting stent implantation. (Circulation. 2009;119:987-995.)