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Simple, cheap and easy to perform, remote ischaemic conditioning (RIC) appeared a very appealing way to improve outcomes in patients with myocardial infarction (MI).
However, in a Hot Line presentation yesterday, Professor Hans Erik Bøtker (Aarhus University Hospital, Aarhus, Denmark) reported neutral results from the large, randomised CONDI-2/ERIC-PPCI trial–an international multicentre study led by Prof. Bøtker and Professor Derek Hausenloy (Hatter Institute, University College London, London, UK) as Co-Principal Investigators.
“Although there have been tremendous improvements in outcomes for patients with MI, mortality reduction seems to have plateaued and post-MI heart failure has not decreased to the extent that we have expected in ST-segment elevation MI (STEMI),” says Prof. Bøtker. “Primary percutaneous coronary intervention (PPCI) has radically increased the chances of short-term recovery but we now need to find ways to reduce reperfusion damage and subsequent hospitalisations for heart failure. Inducing temporary ischaemia in tissue remote from the heart with RIC may stimulate activation of an endogenous pathway to protect against reperfusion damage. Indeed, in proof-of-concept investigations, we found that RIC improved myocardial salvage and reduced myocardial infarct size.1”
Prof. Bøtker continues, “With the CONDI-2/ERIC-PPCI trial, we wanted to see the effect of reducing infarct size on patient outcomes.” Over 5,000 patients with STEMI at centres across Denmark, UK, Spain and Serbia were randomised to receive standard treatment or RIC prior to PPCI. RIC was achieved in the arm using an automated cuff device programmed to deliver four cycles of 5-minute inflation (to 200 mmHg) and 5-minute deflation prior to PPCI. The primary endpoint was combined cardiac death and hospitalisation for heart failure at 12 months. Secondary endpoints included the individual components of the primary endpoint and major adverse cardiovascular and cerebral events.
RIC had no effect on the primary endpoint or on any of the secondary endpoints.
“We also found no effect of RIC on the use of implantable cardioverter defibrillators within 12 months or on troponin release in a subgroup of 2,600 patients,” says Prof. Bøtker. “Finally, we had expected that patients with the largest infarcts would benefit the most from RIC, which was what we had seen in our proof-of-concept study, but that did not turn out to be the case in the outcomes trial.”
Speculating about why RIC did not work, Prof. Bøtker suggests it may be because the efficacy of modern revascularisation therapy outweighs potential improvements with RIC because infarct size is low. “Although we did not identify a specific interaction, novel antiplatelet therapies may have an inherent cardioprotective effect that was not seen with therapies used at the time of the proof-of-concept studies,” he also notes. “This was a robustly designed, sufficiently powered trial and so our conclusion has to be that RIC does not improve clinical cardiac outcomes at 12 months in ischaemic patients undergoing PPCI.”
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