The impact on radial injury of sheathless versus conventional access for transradial interventions: a randomized trial
Dirk Jan van der Heijden1, ; Maarten A.H. van Leeuwen2, ; Stijn L. Brinckman3, ; Maribel I. Madera Cambero4, ; Tamara Aipassa5, ; Priya Vart6, ; Robert-Jan M van Geuns7, ; Niels van Royen8, ;
1. Department of Cardiology, Haaglanden Medical Center, The Hague, the Netherlands, Netherlands 2. Department of Cardiology, Isala Heart Center, Zwolle, the Netherlands 3. Department of Cardiology, Tergooi Hospital, Blaricum, the Netherlands 4. Department of Cardiology, Tergooi Hospital, Blaricum, the Netherlands 5. Department of Cardiology, Radboud University Medical Center, Nijmegen, the Netherlands 6. Department of Health Evidence, section Biostatistics, Radboud Institute for Health Sciences Radboud University Medical center, Nijmegen, the Netherlands 7. Department of Cardiology, Radboud University Medical Center, Nijmegen, the Netherlands 8. Department of Cardiology, Radboud University Medical Center, Nijmegen, the Netherlands
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Recent studies reported a high rate of transradial access (TRA) induced vascular injury which leads to chronic intimal thickening and is associated with radial artery spasm (RAS) and radial artery occlusion (RAO)1–3. It is likely to be caused by radial artery puncture, sheath introduction and sheath friction caused by radial artery inner diameter-sheath outer diameter (RAID/SOD) mismatch. However, using Optical Coherence Tomography (OCT), post procedural radial artery (RA) damage was also found in the proximal part of the RA, where the vessel has a larger diameter and radial artery internal diameter/sheath outer diameter (RAID/SOD) mismatch is less likely to be the cause of vascular damage. One of the possible mechanisms is intimal damage caused by the space between the guidewire and the,catheter tip which shaves the vessel wall (“razor” effect, figure 1) 4.