Final results of the randomised evaluation of short-term dual antiplatelet therapy in patients with acute coronary syndrome treated with a new-generation stent (REDUCE trial).

AIMS: The optimal duration of DAPT in ACS patients treated with DES is still unclear. Therefore, the aim of the current study was to investigate a short versus a standard 12-month DAPT regimen in ACS patients undergoing new-generation DES implantation. METHODS AND RESULTS: REDUCE was a prospective, open-label, multicentre, investigator-initiated study that randomised 1,496 ACS patients after treatment with the COMBO stent to either three (n=751) or 12 months (n=745) of DAPT. The primary study endpoint was a composite of all-cause mortality, myocardial infarction, stent thrombosis, stroke, target vessel revascularisation and bleeding at 12 months. No difference was observed in the demographic and clinical characteristics between the two groups, except for gender (p=0.01). At one-year follow-up, non-inferiority of three- versus 12-month DAPT in the primary endpoint was met (8.2% vs 8.4%, pnon-inferiority<0.001). The similar outcome between the two groups was confirmed at two-year follow-up (11.6% vs 12.1%, p=0.76), with no significant difference in overall mortality (3.1% vs 2.2%, p=0.27), cardiac mortality (1.8% vs 1.1%, p=0.28), stent thrombosis (1.6% vs 0.8%, p=0.16) and major bleeding (3.3% vs 4.0%, p=0.46). CONCLUSIONS: The results show that, among ACS patients treated with the COMBO stent, three months is non-inferior to 12 months of DAPT. However, given the numerically higher rates of mortality and ST in the three-month DAPT group, one-year DAPT should still be recommended in ACS until more information becomes available. A three-month DAPT strategy should be considered only if clinically mandated.

Dietary fish oil replacement with palm or poultry oil increases fillet oxidative stability and decreases liver glutathione peroxidase activity in barramundi (Lates calcarifer).

Complete dietary fish oil replacement with palm or poultry oil in barramundi (Lates calcarifer) had no detrimental effects on growth or hepatosomatic index of juvenile fish up to an average size of ~50 g. However, it significantly decreased the omega-3 (n-3) long-chain polyunsaturated fatty acid content of the fish muscle (fillet) lipids. This was particularly true for eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) which are recognised for their health beneficial effects in the human diet. As a result of their decreased EPA and DHA content, the peroxidation index of the muscle lipids was also decreased. This was associated with increased simulated retail storage shelf life as indicated by decreased thiobarbituric acid reactive substances in muscle samples from fish fed the palm or poultry oil-based diets. Concomitantly, glutathione peroxidase (GPx) activity, but not glutathione S-transferase (GST) activity or reduced glutathione concentration, was significantly reduced in the liver of barramundi fed the palm or poultry oil-based diets as compared with the fish fed the fish oil-based diet. Furthermore, GPx and GST activity were very low in muscle, much lower than in gastrointestinal tract, liver or swim bladder. Therefore, we propose that liver GPx activity may be a good predictor of fillet shelf life in barramundi and other fish species.

Nature of the slow relaxation of smooth muscle induced by a EP2 receptor agonist with a non-prostanoid structure.

The remarkably slow onset/offset of relaxation of guinea-pig isolated trachea induced by a 'non-prostanoid' EP2 receptor agonist, (o-(o-benzyloxy)-cinnamyl)-cinnamic acid (coded (L)-9), was investigated. (L)-9 kinetics was slightly faster on mouse trachea and considerably faster on rabbit vena cava. In each case, reversal of (L)-9 relaxation by the selective EP2 antagonist ACA-23 was rapid and similar to other EP2 agonists (e.g. ONO-AE1-259). On guinea-pig aorta, in the presence of extensive EP2 receptor blockade, (L)-9 inhibited TP agonist-induced contraction more slowly than TP antagonists of similar affinity. The slower kinetics of (L)-9 appear to correlate with greater adventitial/submucosal barriers and thicker smooth muscle layers in the tissues examined. It is proposed that interactions of (L)-9 with EP2 and TP receptors are not rate-limiting, rather diffusion to and from the centre of the muscle mass is retarded by the high lipophilicity of (L)-9 (logP=6.69; ONO-AE1-259=3.95).