Dear Readers,

This issue of the Journal of Invasive Cardiology contains numerous original clinical research studies and related commentaries. We start the issue with a submission from Dr. Marco Costa and colleagues representing investigators from the SECURE Registry. Costa et al. describe their results in using sirolimus-eluting stents in the treatment of complex bypass graft disease. They demonstrated that in-hospital outcomes for the treatment of grafts with sirolimus-eluting stents were similar to those achieved in native vessel lesions, and 8-month clinical and IVUS evaluation in a small subset of patients also showed comparable results in these high-risk patients. Dr. James Hermiller has provided a commentary to accompany this article, reiterating the increased efficacy that has been realized with the introduction of drug-eluting stents in the treatment of vein graft disease.

Treatment options for bypass graft disease, such as repeat CABG and percutaneous revascularization, are limited and provide disappointing outcomes.^1-4 Patients undergoing repeat CABG have over a four times greater rate of mortality compared to patients undergoing their first surgery.¹ The benefits of percutaneous revascularization with stent implantation, though superior to balloon angioplasty, are limited by a high incidence of procedural complications such as thrombosis and distal embolization, and unsatisfactory long-term reocclusion rates.^2-4

Large randomized trials have confirmed the long-term safety and efficacy of SES implanted in native coronary arteries.^5,6 However, SES have not been evaluated for the treatment of bypass graft disease. The aims of this study are to determine the feasibility and safety of using SES to treat high-risk patients with bypass graft disease.

Methods

Despite the promise of new transcatheter technologies, 400,000 coronary artery bypass (CABG) surgeries are performed each year in the United States, the vast majority incorporating saphenous vein grafts (SVG) as conduits.¹ Soon after implantation and exposure to systemic pressure, SVGs undergo intense intimal hyperplasia, followed by accelerated and progressive atherosclerosis.² In comparison to native vessel disease, SVG plaques have a poorly-defined cap, are bulkier, more diffuse and more friable, and have larger amounts of overlying thrombus. During the first year after bypass surgery, 10–15% of vein grafts fail, by 10 years 40–50% are closed, and of those that remain patent, half have significant obstructive disease.^3,4

Percutaneous coronary intervention is an established method of nonsurgical coronary revascularization, accounting for more than 1,500,000 annual procedures worldwide.¹ Despite technical advancements in recent years, with coronary stenting being the most important, restenosis remains the major problem that hampers the procedure’s efficacy. Angiographic restenosis rates following stent implantation is reported to be 15–20% in ideal lesions (BENESTENT I), but may occur in over 30–60% of patients with diabetes or with complex lesion anatomy (small vessels, long or bifurcation lesions).^2–5

Percutaneous coronary intervention (PCI) is central to the management of patients with coronary artery disease. Vascular access is most commonly achieved via the femoral artery by inserting a vascular access sheath. To reduce the risk of acute stent thrombosis, patients receive heparin. However, anticoagulation increases the risk of significant bleeding and hematoma formation at the time of sheath removal,¹ and therefore either sheath removal is delayed for ~4 hours until the anticoagulant effects of heparin have worn off, or a vascular closure device is used. Vascular closure devices can be costly, thus delayed sheath removal is the preferred option in most centers.

Coronary stenting has significantly improved the angiographic and clinical outcomes in vessels with a reference diameter (RD) > 3 mm.^1–5 However, several randomized trials have shown conflicting results when comparing coronary stenting with standard balloon angioplasty (PTCA) for small vessels.^6–11 Nearly 50% of all percutaneous interventions are performed in vessels with a RD < 3.0 mm,¹² a setting related to a higher incidence of early and late adverse outcomes.^13,14

The emerging use of drug-eluting stents (DES) has markedly decreased the incidence of restenosis, both with sirolimus–eluting stents (SES) and paclitaxel-eluting stents (PES).^15–18 More recently, several multi-center randomized trials evaluated the efficacy of DES for the treatment of vessels with reference diameters ? 3.0 mm and have shown a significant reduction in both restenosis and clinical events.^19–21

Stent placement in coronary arteries larger than 3 mm in diameter has been proven to be superior to conventional balloon angioplasty (PTCA) in reducing the risk of restenosis and major adverse cardiac events (MACE). Subsequent improvements in stenting technique and antithrombotic regimen have dramatically reduced the incidence of stent thrombosis.¹ This has resulted in an exponential rise in the number of stent-related procedures and has extensively broadened the indications for stenting.

A major advance in the use of heparin has been the development of low-molecular weight heparins (LMWH), which inhibit both the action (anti-IIa effect) and the generation (anti-Xa effect) of thrombin.^1,2 Because of their ease of administration and possible clinical superiority, the use of LMWH has increased substantially in recent years, particularly in patients presenting with acute coronary syndromes.^3–5 As such, an increasing number of patients referred for angiography and possible percutaneous coronary intervention (PCI) are presenting to the cardiac catheterization laboratory having received subcutaneous LMWH at various intervals from the time of subcutaneous injection.^6–8 Because of the pharmacokinetics of LMWH (less binding to plasma proteins and greater anti-Xa inhibition compared with unfractionated heparin), it has been suggested that monitoring the level of anticoagulation with standard and readily available tests based predominantly on a

Primary percutaneous transluminal coronary angioplasty (PTCA) has been consistently demonstrated to be superior to thrombolytic therapy and is currently the recommended therapy for myocardial infarction (MI).¹ However, no-reflow phenomenon develops in up to 10–15% of MI interventions.² The occurrence of no-reflow is associated with a high incidence of death and adverse events.^2–5

It is estimated that as many as 20% of Americans ? 65 years old and 50% ? 75 years old have peripheral arterial disease (PAD), a total approaching 14–16 million Americans.^1-4 With our rapidly increasing elderly population, it is likely that the incidence of PAD and diabetes mellitus (DM) will continue to grow. Critical limb ischemia (CLI) is the end-stage of lower extremity PAD in which severe obstruction of blood flow results in ischemic rest pain, ulcers and a significant risk for limb loss. CLI is responsible for an estimated 220,000–240,000 amputations yearly in the United States and Europe, and is a source of significant mortality, morbidity, disability and social and economic costs.^4–9 The annual costs of CLI have recently been estimated to be > $10 billion for the United States alone.⁴