Introduction: Remote ischemic conditioning (RIC) is a non-invasive therapeutic strategy that uses brief cycles of inflation and deflation of a blood pressure cuff to reduce ischemia-reperfusion injury during acute ST-elevation myocardial infarction (STEMI). The primary objective of this systematic review was to determine if RIC initiated prior to catheterization increases myocardial salvage index, defined as the proportion of area at risk of the left ventricle salvaged by treatment following emergent percutaneous coronary intervention (PCI) for STEMI. Secondary outcomes included infarct size and major adverse cardiovascular events. Methods: Electronic searches of PubMed, Ovid MEDLINE, EMBASE and Cochrane Central Register of Controlled Trials were conducted and reference lists were hand-searched. Randomized controlled trials comparing PCI with and without RIC for patients with STEMI published in English were included. Two reviewers independently screened abstracts, assessed quality of the studies, and extracted data. Data were pooled using random-effects models and reported as risk ratios (RR) with 95% confidence intervals (CIs). Results: Nine RCTs were included with a combined total of 999 patients (RIC+PCI = 534, PCI = 465). The myocardial salvage index was higher in the RIC+PCI group at 3 and 30 days; mean difference 0.09 (95% CI: 0.04, 0.15) and 0.12 (95% CI: 0.03, 0.21), respectively. Infarct size was reduced in the RIC+PCI group at 3 and 30 days; mean difference -3.82 (95% CI: -8.15, 0.51) and -4.00 (95% CI: -7.07, -0.93), respectively. There was no statistical difference with respect to death and re-infarction, however there was a reduction in heart failure with RIC+PCI at 6 months; RR: 0.43 (95% CI: 0.19, 0.99). Conclusion: RIC is emerging as a promising adjunctive treatment to PCI for the prevention of reperfusion injury in STEMI patients. Ongoing, multicenter clinical trials will help elucidate the effect of RIC on clinical outcomes such a hospitalization, heart failure and mortality.

Limb remote ischemic conditioning (LRIC) provides a physiologic strategy for harnessing the body’s endogenous protective capabilities against injury induced by ischemia–reperfusion in the central nervous system. The aim of the present study was to determine if LRIC played a role in protecting the retina from ischemia–reperfusion injury. A total of 81 adult male Sprague-Dawley rats were randomly assigned to sham and ischemia/reperfusion with or without remote LRIC arms. The retinal ischemic model was generated through right middle cerebral artery occlusion (MCAO) and pterygopalatine artery occlusion for 60 min followed by 1, 3, and 7 days of subsequent reperfusion. LRIC was conducted immediately following MCAO by tightening a tourniquet around the upper thigh and releasing for three cycles. Paraffin sections were stained with hematoxylin and eosin in order to quantify the number of cells in retinal ganglion cells (RGCs) layer throughout the duration of the study. Cellular expression of glial fibrillary acidic protein (GFAP) was detected and examined through immunohistochemistry. Protein expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) was also analyzed by Western blot techniques. Our study demonstrated that the loss of cells in RGC layer was attenuated by LRIC treatment at 3 and 7 days following reperfusion (P < 0.05). Immunohistochemistry studies depicted a gradual increase (P < 0.05) in GFAP levels from day 1 through day 7 following ischemia and subsequent reperfusion, whereas LRIC reduced GFAP levels at 1, 3, and 7 days postreperfusion. In addition, LRIC increased the expression of Nrf2 and HO-1 at day 1 and 3 following ischemia/reperfusion. This particular study is the first remote conditioning study applicable to retinal ischemia. Our results strongly support the position that LRIC may be used as a noninvasive neuroprotective strategy, which provides retinal protection from ischemia–reperfusion injury through the upregulation of antioxidative stress proteins, such as Nrf2 and HO-1.