Saphenous vein graft percutaneous coronary intervention via radial artery access: safe and effective with reduced hospital length of stay.

BACKGROUND: Although percutaneous coronary intervention (PCI) via radial artery access confers many advantages over the femoral artery, PCI to saphenous vein grafts (SVG) is commonly performed via the femoral route. We compared outcomes in patients undergoing SVG PCI from the radial and femoral routes. METHODS: We performed a retrospective analysis of patients who underwent SVG PCI between January 2006 and December 2010 in 2 large interventional centers in the United Kingdom. All radial and femoral operators selected for this analysis performed high-volume (>200 PCIs per year) procedures via either vascular route. RESULTS: Of 305 patients (260 males) who underwent SVG PCI, 208 (68.2%) had the procedure completed from the femoral route and 97 (32.8%) radially. There was no difference between groups in fluoroscopy time (femoral vs radial 1095 vs 1125 seconds, P nonsgnificant), but radiation doses were greater (43.87 ± 2.83 Gy/cm(2) vs 56.92 ± 4.52 Gy/cm(2), P = .012) as was body mass index in the radial group (27.99 ± 0.33 vs 29.05 ± 0.42, P = .048). Three femoral access patients had vascular access complications, whereas the radial route group had none. There were no differences in no flow/slow flow (femoral 3.86% vs radial 2.54%, P nonsignificant). The mean length of hospital stay was significantly shorter in the radial access cohort (1.09 vs 2.09 days, P < .001). Three patients converted from radial to femoral artery, whereas one converted from femoral to radial after technical failure to complete the procedure. CONCLUSION: Saphenous vein graft PCI can be safely and effectively performed via radial artery access with comparable fluoroscopy times but not radiation doses. Of clinical significance, use of the radial artery access was associated with decreased hospital stay and arterial complications. These data suggest that a routine radial approach for SVG PCI is feasible and could offer clinical and economic benefits.

Outcomes following PCI in patients with previous CABG: a multi centre experience.

BACKGROUND: Limited data is available to guide operators as to the optimal revascularisation strategy in patients with previous CABG representing with angina. METHOD: Retrospective analysis of 161 patients with prior CABG undergoing PCI in two centres between September 2005 and April 2008. RESULTS: 161 patients (132 male, 68 ± 8 years) underwent PCI at 126 ± 65 months after index CABG. Clinical presentation of recurrent ischaemia was stable in 59.7% and as an acute coronary syndrome in 40.3% of patients. Mean follow-up after PCI was 13.5 ± 4.8 months. About 62.7% of patients underwent native vessel PCI, 32.9% had a graft only PCI, and 4.4% having a combination of both. Drug eluting stents were used in 84.9% of cases. There was one cardiac death and one case of redo CABG during follow-up. Mean CCS angina class decreased from 2.87 to 0.67 (P < 0.0001) in the follow-up group. About 13.6 % of all patients had a MACE at follow up. This was higher in the graft PCI group (21.6% vs. 8.9%, P = 0.048). About 12.4% of the total cohort underwent repeat PCI although 30% of these required PCI for a de-novo lesion. TVR rate was significantly higher in patients undergoing graft PCI than native vessel PCI (15% vs. 4.9%, P = 0.031). Graft PCI was an independent predictor (HR 3.73, 1.27-10.87 [95%CI], P = 0.016) of MACE in these patients. CONCLUSION: PCI significantly improved angina in these patients with low overall rates of TVR. However TVR rate was significantly higher in patients undergoing graft PCI than those undergoing native vessel PCI.

Direct vasoactive properties of thienopyridine-derived nitrosothiols.

Thienopyridines (ticlopidine, clopidogrel, and prasugrel) require in vivo metabolism to exhibit a critical thiol group in the active form that binds to the P2Y12 platelet receptor to inhibit platelet activation. We hypothesized that formation of thienopyridine-derived nitrosothiols (ticlopidine-SNO, clopidogrel-SNO, and prasugrel-SNO) occurs directly from the respective parent drug. Pharmaceutical-grade thienopyridine (ticlopidine, clopidogrel chloride, clopidogrel sulfate, clopidogrel besylate, or prasugrel) was added to nitrite in aqueous solution to form the respective thienopyridine-SNO (Th-SNO). An isolated aortic ring preparation was used to test vasoactivity of the Th-SNO derivatives. Increasing nitrite availability resulted in increased Th-SNO formation for all drugs (other than ticlopidine). Th-SNO induced significant endothelium-independent relaxation of preconstricted aortic rings. Clopidogrel-chloride-SNO displayed rapid-release kinetics in a chemical environment, which was reflected by immediate and transient vasorelaxation when compared with the SNO derivatives of the other thienopyridines. Accounting for differences in yield, clopidogrel-chloride-SNO exhibited the greatest propensity to immediately relax vascular tissue. Th-SNO derivatives exhibit nitrovasodilator properties by supplying NO that can directly activate vascular soluble guanylate cyclase to induce vasorelaxation. Differences in SNO yield and vasoactivity exist between thienopyridine preparations that might be important to our understanding of the direct pharmacological effectiveness of thienopyridines on vascular and platelet function.

Direct formation of thienopyridine-derived nitrosothiols--just add nitrite!

Thienopyridines (ticlopidine, clopidogrel and prasugrel) are pro-drugs that require metabolism to exhibit a critical thiol group in the active form that binds to the P2Y12 receptor to inhibit platelet activation and prevent thrombus formation in vivo. We investigated whether these thienopyridines participate in S-nitrosation (SNO) reactions that might exhibit direct anti-platelet behaviour. Optimum conditions for in vitro formation of thienopyridine-SNO formation were studied by crushing ticlopidine, clopidogrel or prasugrel into aqueous solution and adding sodium nitrite, or albumin-SNO. Ozone-based chemiluminescence techniques were utilised to specifically detect NO release from the SNO produced. Effect on agonist-induced platelet aggregation was monitored using light transmittance in a 96 well microplate assay. Pharmaceutical grade preparations of ticlopidine, clopidogrel and prasugrel were found to exhibit significant free thiol and formed SNO derivatives directly from anionic nitrite in water under laboratory conditions without the need for prior metabolism. Thienopyridine-SNO formation was dependent on pH, duration of mixing and nitrite concentration, with prasugrel-SNO being more favourably formed. The SNO moiety readily participated in trans-nitrosation reactions with albumin and plasma. Prasugrel-SNO showed significantly better inhibition of platelet aggregation compared with clopidogrel-SNO, however when compared on the basis of SNO concentration these were equally effective (IC50=7.91 ± 1.03 v/s 10.56 ± 1.43 µM, ns). Thienopyridine-derived SNO is formed directly from the respective base drug without the need for prior in vivo metabolism and therefore may be an important additional contributor to the pharmacological effectiveness of thienopyridines not previously considered.