Coronary artery aneurysms in acute coronary syndrome: case series, review, and proposed management strategy.

Coronary artery aneurysm (CAA) is an uncommon clinical finding, with an incidence varying from 1.5%-4.9% in adults, and is usually considered a variant of coronary artery disease (CAD). CAA identified in the context of acute coronary syndrome (ACS) represents a unique management challenge, particularly if the morphology of the CAA is suspected to have provoked the acute clinical syndrome. CAA is associated with thrombus formation due to abnormal laminar flow, as well as abnormal platelet and endothelial-derived pathophysiologic factors within the CAA. Once formed, mural thrombus may potentiate the deposition of additional thrombus within aneurysmal segments. Percutaneous revascularization of CAA has been associated with complications including distal embolization of thrombus, no-reflow phenomenon, stent malapposition, dissection, and rupture. Presently, there are no formal guidelines to direct the management of CAA in patients presenting with ACS; controversies exist whether conservative, surgical, or catheter-based management should be pursued. In this manuscript, we present an extensive review of the existing literature and associated clinical guidelines, and propose a management algorithm for patients with this complex clinical scenario. Armed with this perspective, therapeutic decisions may be tailored to synthesize patient factors and preferences, individualized clinical assessment, and existing American Heart Association/American College of Cardiology guidelines for management of ACS.

The effects of intra-arterial vasodilators on radial artery size and spasm: implications for contemporary use of trans-radial access for coronary angiography and percutaneous coronary intervention.

BACKGROUND: Transradial access (TRA) offers advantages including decreased vascular complications, reduced length of hospital stay, and reduced cost. The size of the radial artery (RA) limits the equipment that can be used via TRA. Intra-arterial (IA) vasodilators prevent and treat RA spasm, yet are not uniformly used in TRA and their effect on the absolute size of the RA remains unknown. METHODS AND MATERIALS: 121 patients undergoing TRA for cardiac catheterization were included. 78 patients underwent RA angiography prior to administration of IA vasodilators ('no vasodilator' group), 43 patients underwent radial angiography after administration of an IA verapamil and nitroglycerin cocktail ('vasodilator' group). Quantitative angiography was used to compare the RA diameters. RESULTS: Clinical characteristics were similar between the groups, except that patients in the 'no vasodilator' cohort were taller (1.67 ± 0.1 m vs. 1.73 ± 0.1 m, p=0.002), and heavier (84.9 ± 18.2 kg vs. 75 ± 17.1 kg, p=0.003). In the 'vasodilator' group the proximal RA diameter was larger (2.29 ± 0.47 mm vs. 2.09 ± 0.41 mm, p=0.02) as was the narrowest segment (1.83 ± 0.56 mm vs 1.39 ± 0.43, p<0.0001) compared to the 'no vasodilator' group. At the RA origin, 79.4% of those in the 'vasodilator' group were larger than a 6 Fr guide catheter, compared to 51.4% in the 'no vasodilator' group (p=0.004). At the narrowest segment a higher percentage of RAs in the 'vasodilator' group were larger than a 5 Fr guide catheter (65.1% vs 26.9%, p<0.001) and a 6 Fr catheter (34.9% vs 10.3%, p=0.001). CONCLUSION: IA vasodilators increase pre-procedural RA diameter in patients undergoing cardiac catheterization via TRA. This increase in diameter has important implications for procedural planning. SUMMARY FOR TABLE OF CONTENTS: Boyer et al. performed a blinded controlled clinical trial investigating the effects of intra-arterial vasodilators on radial artery size and spasm during cardiac catheterization. The study demonstrates that intra-arterial vasodilators significantly increased the radial artery size throughout the entire course of the vessel and significantly decreased the amount of radial artery spasm. The authors conclude that these findings support the use of intra-arterial vasodilators during cardiac catheterization and have important implications for emerging technologies such as larger bore sheathless radial procedures.

Saphenous vein graft intervention: a review.

Saphenous vein grafts are prone to degeneration and occlusion. Vein graft disease continues to be a significant problem in maintaining long-term benefits after coronary artery bypass surgery. The neointimal hyperplasia and aggressive atherosclerosis that occur in saphenous vein grafts make interventions particularly challenging due to plaque embolization and the no-reflow phenomenon. This review discusses the pathophysiology of vein graft disease and the various percutaneous strategies that have been applied to manage vein grafts. We review the issues surrounding stent selection and various approaches to embolic protection devices. Finally, we discuss the technical steps that optimize success in treating this challenging patient subset.

Interleukin-17 as a molecular target in immune-mediated arthritis: immunoregulatory properties of genetically modified murine dendritic cells that secrete interleukin-4.

OBJECTIVE: Our previous studies have shown that murine dendritic cells (DCs) genetically modified to express interleukin-4 (IL-4) reduce the incidence and severity of murine collagen-induced arthritis. The present studies were performed to assess the immunoregulatory mechanisms underlying this response, by assessing the effects of IL-4 DCs on cytokine production by subsets of T helper cells. METHODS: Male DBA mice ages 6-8 weeks old were immunized with type II collagen. Splenic T cells obtained during the initiation phase and the end stage of arthritis were cultured with IL-4 DCs or untransduced DCs in the presence of collagen rechallenge. Interferon-gamma (IFNgamma) and IL-17 responses were measured. Antibodies to IL-4, IL-12, and IL-23, and recombinant IL-4, IL-12, and IL-23 were used to further study the regulation of T cell cytokine production by IL-4 DCs. RESULTS: Splenic T cells obtained during the initiation phase of arthritis produced less IL-17 when cultured in the presence of IL-4 DCs, despite their production of increased quantities of other proinflammatory cytokines (IFNgamma and tumor necrosis factor). T cell IL-17 production after collagen rechallenge was not inhibited by a lack of IL-23, since IL-4-mediated suppression of IL-17 was not reconstituted by IL-23, an otherwise potent inducer of IL-17 production by T cells. Although IL-4 DCs can produce increased quantities of IL-12 and IFNgamma, suppression of IL-17 production by IL-4 DCs was independent of both. While IL-17 production by T cells obtained during the initiation phase of arthritis was regulated by IL-4 DCs, IL-17 production by T cells obtained during end-stage arthritis was not altered. CONCLUSION: Our data suggest that IL-4 DCs exert a therapeutic effect on collagen-induced arthritis by targeting IL-17. IL-17 suppression by IL-4 DCs is robust and is not reversed by IL-23. Timing might be important in IL-17-targeted therapy, since IL-17 production by T cells obtained during end-stage arthritis did not respond to suppression by IL-4 DCs.