The no-reflow phenomenon is defined as a severe reduction in antegrade coronary flow in the absence of epicardial vessel obstruction.¹ The presence of no-reflow substantially increases the risk of major adverse clinical events (MACE) in percutaneous coronary artery interventions (PCI), particularly in saphenous vein grafts (SVG).^2,3 Mechanisms underlying no-reflow are not completely understood. Several hypotheses have been proposed, including microvascular spasm, in situ thrombosis and distal embolization. Distal protection devices are designed to prevent no-reflow by preventing the distal embolization of materials released during SVG PCI. Several clinical trials have shown that distal protection devices substantially reduced MACE in SVG PCI.^4–6 Webb et al.

Proximal left anterior descending artery (LAD) stenoses are considered to have special prognostic implications.¹ Medically treated patients with isolated proximal LAD stenosis have a significantly worse prognosis than patients with lesions in other locations.² Stenting is an accepted treatment with excellent short-term results, yet previous studies have shown that proximal LAD stenoses per se have higher rates of restenosis than stenoses in other coronary segments after angioplasty,³ as well as after stenting.^4,5

Percutaneous intervention of saphenous vein grafts is associated with approximately 20% risk of major adverse cardiovascular events secondary to decreased antegrade flow or “no-reflow” during the procedure.¹ The mechanism of this phenomenon is probably multifactorial and involves microvascular dysfunction and potentially platelet-mediated loss of capillary autoregulation. Since the typical vein graft lesion is friable with large plaque volume, it may be that embolization of thrombotic and atheromatous material during the intervention is the trigger that starts a cascade of events, leading to microvascular obstruction.² In addition to particulate obstruction, we have learned to recognize the importance of soluble mediators that may play a key role in this process.³

Since Robert Goetz first performed a single mammary artery bypass to the anterior descending artery in 1960, its evolution has been associated with unparalleled clinical benefit in terms of symptom relief and a favorable effect on mortality, particularly in diabetics and those with multivessel disease. In fact, there have been few, if any, treatment strategies in all of modern vascular medicine that rival the beneficial impact of the mammary artery anastamosis, specifically when used to treat disease involving the left anterior descending (LAD) coronary artery.^2–10

Myocardial injury after percutaneous coronary interventions has been recognized as a frequent and prognostically important event.¹ Multiple institutions have now reported follow-up studies of percutaneous revascularization, and the evidence supports a relation between the elevation of cardiac enzymes and poorer clinical outcomes during subsequent clinical evaluations.^1–4 Recent studies presented evidence that statin therapy before percutaneous coronary interventions (PCI) is associated with a marked improvement in short- and long-term prognosis.^5,6 Reduction in procedure-related myocardial injury has been proposed as one of the plausible mechanisms accounting for this survival benefit.^7,8

Transradial coronary percutaneous procedures are associated with reduced entry site complications compared to transfemoral or transbrachial techniques.^1–4 However, the transradial approach is technically more challenging and time-consuming,⁴ which explains its less widespread acceptance as compared to the transfemoral approach. Nonetheless, over the past ten years, considerable improvements have been achieved in catheter configuration and design, and a great variety of transradial-dedicated material is now available. The availability of specifically designed arterial sheaths and catheters has helped to promote a substantial increase in the transradial approach’s popularity over the past few years.

The recurrence of coronary in-stent restenosis has been significantly reduced by brachytherapy.^1–3 Patients treated with brachytherapy are characterized by poor outcomes in concomitant stent deployment, mainly because of late vessel thrombosis.^1,2,4 In the treatment of in-stent restenosis, additional stents may be required for either suboptimal results or residual flow-limiting dissections.^5,6 The risk of late vessel thrombosis has been overcome by prolongation of double antiplatelet therapy,⁷ however specific studies focusing on the influence of additional stenting on the recurrence of restenosis are lacking. The aim of our study was to evaluate the outcomes of patients with in-stent restenosis treated with brachytherapy and additional stenting, followed by prolonged antiplatelet therapy.

Methods

Coronary artery perforation (CP) is a rare and potentially life-threatening complication of percutaneous coronary intervention (PCI). CP has historically been reported to occur in 0.1–3.0% of PCI procedures.^1–5 Although CP can be caused by coronary wires and balloon angioplasty,⁶ they are more frequently reported in PCI using atheroablative devices, stenting and excimer laser coronary angioplasty.²

The number of percutaneous coronary interventions (PCI) performed worldwide is increasing. With the improvement of technology and interventional tools, the number of procedures is expected to further increase. As the range of equipment available to the interventional cardiologist evolves, together with necessary operator expertise, not only will the number of procedures increase, but interventionists will be treating patients with complex disease and more challenging coronary anatomy.

Within a decade of coronary artery bypass graft surgery, 50% of saphenous vein grafts fail, causing recurrent angina and acute coronary syndromes.¹ Because of the substantial risk associated with re-operation, percutaneous intervention is often preferred to further surgery in this population. However, percutaneous revascularization is hampered by a high incidence of acute complications, specifically, distal embolization and periprocedural myocardial infarction (MI).^2,3 Significant elevation in cardiac enzymes resulting from distal embolization is an independent predictor of late mortality.³ The advent of distal protection devices to capture embolic material has improved outcomes substantially by reducing the incidence of periprocedural MI.⁴ However, even with distal protection, non-Q-wave MI still occurs in approximately 10% of patients.^4,5