TY - JOUR T1 - 5 Effect of remote ischaemic preconditioning on coronary artery function in patients with stable coronary artery disease JF - Heart JO - Heart SP - A3 LP - A4 DO - 10.1136/heartjnl-2018-BCIS.5 VL - 104 IS - Suppl 1 AU - David S Corcoran AU - Robin Young AU - MD Pio Cialdella AU - Peter McCartney AU - Amrit Bajrangee AU - Barry Hennigan AU - Damien Collison AU - David Carrick AU - Aadil Shaukat AU - Richard Good AU - Stuart Watkins AU - Margaret McEntegart AU - Jonathan Watt AU - Paul Welsh AU - Naveed Sattar AU - Alex McConnachie AU - Keith G Oldroyd AU - Colin Berry Y1 - 2018/01/01 UR - http://heart.bmj.com/content/104/Suppl_1/A3.2.abstract N2 - Background Remote ischaemic preconditioning (RIPC) is a cardioprotective intervention invoking intermittent ischaemia in a tissue remote from the heart. Its mechanisms are incompletely understood. We hypothesised that RIPC might enhance coronary vasodilatation by an endothelium-dependent mechanism.Methods We performed a prospective, randomised, sham-controlled, blinded clinical trial. Patients with stable coronary artery disease undergoing elective angiography were randomised 1:1 to RIPC or sham. Endothelial-dependent and –independent function was assessed with intracoronary (ic) acetylcholine (ACh) and ic nitrate, respectively. Coronary luminal diameter was assessed by QCA. Primary outcome: between-group difference in mean% change in coronary luminal diameter following ACh.Results Following angiography, 60/75 patients (mean ±SD age 57.5±8.5 years; 80% male) were eligible and completed the protocol (n=30 RIPC, n=30 sham). The mean% change in coronary luminal diameter was −13.3±22.3% and −2.0±17.2% in the sham and RIPC groups respectively (difference 11.32%, 95% CI: 1.2 to 21.4, p=0.032) (figure 1). This remained significant with age and sex as covariates (difference 11.01%, 1.01–21.0, p=0.035).Abstract 5 Figure 1 Endothelial-dependent and independent function testing results. ACh=acetylcholine, GTN=glyceryl trinitrateConclusions RIPC attenuates the extent of vasoconstriction induced by intracoronary acetylcholine infusion, and this endothelium-dependent mechanism may contribute to its cardioprotective effects. ER -