LAUSR

We thank Dr Elbadawi et al for their interest in and insightful comments on our article. They correctly identify the concerns regarding the validity of myocardial salvage index based on myocardium at risk (MaR) from cardiac magnetic resonance (CMR) imaging in studies of myocardial conditioning considering previous studies reporting a smallerMaR in the intervention groups. They alsomention general concerns about determining MaR from CMR summarized by Wince and Kim. This review focuses on MaR in T2-weighted CMR, which also was the method used in the above-mentioned earlier conditioning studies and it may be appropriate to detect hypothetical pitfalls resulting from a possibly unreliable MaR. It is worth emphasizing that we used cine contrast-enhanced steady-state free precession in our study which is distinct from T2-weighted CMR. However, we argue that the findings of smaller MaR in the intervention groups in the studies byCrimi et al,White et al. , and Thuny et al. should be regarded as observations with largely undetermined causes. The objective of these studies was not to evaluate the effect of the intervention on MaR, and thus, any conclusions in that direction might be overhasty. It might of course very well be so that the smaller MaR actually was a result from the intervention, but one cannot exclude that the smaller MaR was a result from possible imbalances of factors such as localization of culprit lesion (proximal vs distal), distribution of collaterals, and heterogeneity of compromised coronary flow up until the point of coronary angiography. Some of these factors are difficult to detect or measure but have the power to dramatically affect variables such as MaR. Furthermore, several studies of cardioprotection in patients with ST-elevation myocardial infarction have not observed a reduced MaR in the intervention group. In addition, the validity of MaR determined by contrast-enhanced steady-state free precession has been confirmed in a recent meta-analysis, which showed that MaR was not affected by cardioprotection treatment. Hence, we find no solid basis to interpret our observation of a larger MaR in the intervention group as a result of anything else than an imbalance of the distribution of proximal left anterior descending artery occlusions between the 2 study groups. To further determine thepossible impact of remote ischemic conditioning onMaR, a properly designed study focusing on this variable as primary outcome would need to be performed. We agree with Dr Elbadawi et al. that forthcoming large sample trials with clinical end points will provide important answers on the future directions of remote ischemic conditioning.