Effect Of Remote Ischemic Preconditioning Research Articles

Adrenomedullin serves a role in the humoral pathway of delayed remote ischemic preconditioning via a hypoxia-inducible factor-1α-associated mechanism.

Remote ischemic preconditioning (RIPC) is a minimally invasive method that provides protection by reducing injury to the heart, kidneys, brain and other tissues or organs. RIPC may improve the outcome in patients undergoing surgery. Although the role of RIPC has been studied, the results remain controversial. It is difficult to confirm whether RIPC has a kidney protective effect and the understanding of the preconditioning signal pathway involved remains unclear. In the present study, the effect of RIPC in urology was evaluated. The protection against renal damage was assessed by investigating the potential mediator, hypoxia-inducible factor-1α (HIF-1α), and the functional adrenomedullin (ADM) pathway. Male Sprague-Dawley (SD) rats were used in the present study. The animal model of kidney damage induced by ischemia reperfusion (IR) was used to investigate the protective effect of the acute and delayed phase RIPC. Furthermore, the protective effects of RIPC mediated by a HIF-1α-ADM pathway were assessed. The indexes of renal function and oxidative damage indicators were measured by Cr, BUN, mALB, β2-MG, MPO, MDA and SOD assays, and the expression of HIF-1α and ADM were detected by western blot analysis, immunohistochemistry and ELISA assays. Tubular score, determined using hematoxylin and eosin staining, was used to evaluate renal tissue damage. Applying RIPC prevented IR-induced renal dysfunction and oxidative damage by decreasing Cr, BUN, mALB, β2-MG, MPO, MDA levels and increasing SOD activity. Findings showed that delayed RIPC had an improved effect compared with acute treatment. Delayed RIPC also upregulated the expression of HIF-1α and ADM, indicating that the protective effect of the delayed RIPC may be associated with a HIF-1α-ADM-mediated mechanism. The effect of the delayed RIPC to reduce IR-induced renal damage and increase ADM expression was enhanced by HIF-1α agonists DMOG and BAY 85–3934, whereas the effect was whittled by HIF-1α antagonists YC-1 and 2-MeOE2. Furthermore, receiving ADM also offered protection to the kidney in comparison with the IR+Vehicle group. These findings suggest that RIPC prevents IR-mediated renal damage by HIF-1α via an ADM humoral pathway. In the present study, RIPC provided an effective renal protection. ADM could also offer protection regulated by HIF-1α in renal tissue. However, the mechanism of ADM as a protective factor in RIPC requires further research.

Remote Ischemic Preconditioning has a Cardioprotective Effect in Children in the Early Postoperative Phase: A Meta-Analysis of Randomized Controlled Trials.

In this updated meta-analysis, we assessed the cardioprotective effect of remote ischemic preconditioning (RIPC) in pediatric patients undergoing congenital heart surgery. A total of 9 randomized controlled trials (RCTs) involving 793 pediatric patients under 18years old were identified. RIPC obviously reduced the release of troponin I at 6h after surgery [standard mean difference (SMD) -0.59, 95% confidence interval (CI) -1.14 to -0.04; p = 0.03], mitigated the inotropic scores within 4-6h (SMD -0.43, 95% CI -0.72 to -0.14; p = 0.004) and within 12 h (SMD -0.26, 95% CI -0.50 to -0.02; p = 0.03) and shortened the ventilator support time (SMD -0.28, 95% CI -0.49 to -0.07; p = 0.01) as well as the duration of intensive care unit (ICU) stay (SMD -0.21, 95% CI -0.35 to -0.06; p = 0.004). Our meta-analysis determined that RIPC had cardioprotective effects in the early postoperative phase. Additional RCTs focused on the cardiac benefits from RIPC in pediatric patients are warranted.

Effects of remote ischemic preconditioning on contrast induced nephropathy after percutaneous coronary intervention in patients with acute coronary syndrome.

Objective:The aim of this study was to explore the clinical effects of remote ischemic preconditioning (RIPC) on contrast-induced nephropathy after percutaneous coronary intervention (PCI) in patients with acute coronary syndrome (ACS).Patients and Methods:The study was a single-center, prospective, randomized, controlled study. A total of 161 patients with ACS and the rate of estimate glomerular filtration (eGFR) 15 to 70 mL/min/1.73 m2 undergoing PCI were randomly assigned to RIPC group (induced by 4 times of 5-minute inflations of a blood pressure cuff to 200 mmHg around the upper arm, followed by 5-min intervals of reperfusion at 1 hour before PCI therapy) or control group (an uninflated cuff around the arm). Successful completion of the PCI eventually included 107 cases of patients, including 50 cases in the RIPC group and 57 cases in the control group. The level of serum creatinine (Scr), CystatinC (CysC), blood neutrophil gelatinase-associated lipocalin (NGAL), eGFR were measured in all patients at 6 am before the day of PCI, and 4-hour NGAL, 24-hour CysC, 72-hour Scr, and eGFR after PCI in the 2 groups. The incidence of major adverse events in the kidney (including the incidence of CIN, the need for dialysis, or renal replacement therapy after using contrast agent) and the composite endpoint of cardiovascular events were recorded at 6 months after PCI.Results:There were no statistically significant differences in baseline indicators between the 2 groups. Scr, CysC, and blood NGAL levels and the incidence of CIN in patients with RIPC group were significantly lower than those form the control group after PCI (P < .05), but there were no significant differences between the average value of eGFR and occurrence of Major cardiovascular events in the postoperative 6 months (P > .05).Conclusions:RIPC can reduce PCI-related CIN and protect renal function in patients with ACS. The benefits of these patients by RIPC may be related to the reduction of the NGAL and CysC.

Effect of Remote Ischemic Preconditioning on Maximal Exercise Tolerance in Young Adults

Effect of Remote Ischemic Preconditioning on Maximal Exercise Tolerance in Young Adults

Effect of remote ischemic preconditioning on myocardial injury after off-pump coronary artery bypass graft: unicentric randomized trial

Effect of remote ischemic preconditioning on myocardial injury after off-pump coronary artery bypass graft: unicentric randomized trial

Protection of Coronary Circulation by Remote Ischemic Preconditioning: An Intriguing Research Frontier

Ischemic preconditioning is a protective phenomenon, by which brief ischemic stimuli in a vascular bed are able to counteract the damage from a longer subsequent ischemia. Preconditioning may also confer protection from ischemia to distal tissues and organs. In this case, ischemic preconditioning is known as remote ischemic preconditioning (RIPC). RIPC can be safely and easily reproduced in clinical settings. Indeed, over the past years, its protective actions have been tested in various clinical settings, including cardiac surgery and elective percutaneous coronary interventions. However, translational studies on RIPC have provided conflicting results on reduction of mortality. Recently, studies in humans have investigated the effects of RIPC on coronary circulation, showing that RIPC could have a protective effect on coronaries. This recent area of research may offer innovative insights for designing translational studies on RIPC, unveiling new mechanisms by which RIPC protects the heart. The aims of the present manuscript are to summarize the available clinical evidence on RIPC efficacy for cardioprotection and to review studies assessing the effects of RIPC on coronary circulation in humans.

Remote Ischemic Preconditioning Ameliorates Acute Kidney Injury due to Contrast Exposure in Rats through Augmented O-GlcNAcylation.

Remote ischemic preconditioning (RIPC) is an adaptive response, manifesting when local short-term ischemic preconditioning reduces damage to adjacent or distant tissues or organs. O-linked β-N-acetylglucosamine (O-GlcNAc) glycosylation of intracellular proteins denotes a type of posttranslational modification that influences multiple cytoplasmic and nuclear protein functions. Growing evidence indicates that stress can induce an acute increase in O-GlcNAc levels, which can be cytoprotective. The current study aimed to determine whether RIPC can provide renoprotection against contrast-induced acute kidney injury (CI-AKI) by augmenting O-GlcNAc signaling. We established a stable model of CI-AKI using 5/6 nephrectomized rats exposed to dehydration followed by iohexol injection via the tail vein. We found that RIPC increased UDP-GlcNAc levels through the hexosamine biosynthetic pathway as well as global renal O-GlcNAcylation. RIPC-induced elevation of O-GlcNAc signaling ameliorated CI-AKI based on the presence of less tubular damage and apoptosis and the amount of reactive oxygen species. In addition, the use of alloxan, an O-GlcNAc transferase inhibitor, and azaserine, a glutamine fructose-6-phosphate amidotransferase inhibitor, neutralized the protective effect of RIPC against oxidative stress and tubular apoptosis. In conclusion, RIPC attenuates local oxidative stress and tubular apoptosis induced by contrast exposure by enhancing O-GlcNAc glycosylation levels; this can be a potentially useful approach for lowering the risk of CI-AKI.

The effects of remote ischaemic preconditioning on coronary artery function in patients with stable coronary artery disease

BackgroundRemote ischaemic preconditioning (RIPC) is a cardioprotective intervention invoking intermittent periods of ischaemia in a tissue or organ remote from the heart. The mechanisms of this effect are incompletely understood. We hypothesised that RIPC might enhance coronary vasodilatation by an endothelium-dependent mechanism. MethodsWe performed a prospective, randomised, sham-controlled, blinded clinical trial. Patients with stable coronary artery disease (CAD) undergoing elective invasive management were prospectively enrolled, and randomised to RIPC or sham (1:1) prior to angiography. Endothelial-dependent vasodilator function was assessed in a non-target coronary artery with intracoronary infusion of incremental acetylcholine doses (10−6, 10−5, 10−4mol/l). Venous blood was sampled pre- and post-RIPC or sham, and analysed for circulating markers of endothelial function. Coronary luminal diameter was assessed by quantitative coronary angiography. The primary outcome was the between-group difference in the mean percentage change in coronary luminal diameter following the maximal acetylcholine dose (Clinicaltrials.gov identifier: NCT02666235). Results75 patients were enrolled. Following angiography, 60 patients (mean±SD age 57.5±8.5years; 80% male) were eligible and completed the protocol (n=30 RIPC, n=30 sham). The mean percentage 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– 21.4, p=0.032). This remained significant when age and sex were included as covariates (difference 11.01%, 95%CI: 1.01– 21.0, p=0.035). There were no between-group differences in endothelial-independent vasodilation, ECG parameters or circulating markers of endothelial function. ConclusionsRIPC attenuates the extent of vasoconstriction induced by intracoronary acetylcholine infusion. This endothelium-dependent mechanism may contribute to the cardioprotective effects of RIPC.

Assessing renal changes after remote ischemic preconditioning (RIPC) of the upper extremity using BOLD imaging at 3T.

Acute kidney injury (AKI) is an important risk factor for a number of adverse outcomes including end-stage renal disease and cardiovascular morbidity and mortality. Whilst many clinical situations that can induce AKI are known-e.g. drug toxicity, contrast agent exposure or ischemia during surgery-targeted preventive or therapeutic measures are still lacking. As to renoprotective strategies, remote ischemic preconditioning (RIPC) is one of the most promising novel approaches and has been examined by a number of clinical trials. The aim of this study was to use blood oxygenation level-dependent (BOLD) MRI as a surrogate parameter to assess the effect of RIPC in healthy volunteers. In this IRB-approved, prospective study, 40 healthy volunteers were stratified with 20 undergoing an RIPC procedure (i.e. RIPC group) with a transient ischemia of the right arm, and 20 undergoing a sham procedure. Before and after the procedure, both kidneys of all participants were scanned using a 12-echo mGRE sequence for functional BOLD imaging at 3T. For each volunteer, 180 ROIs were placed in the cortex and the medulla of the kidneys. Ultimately, R2* values, which have an inverse correlation with the oxygenation level of tissue, were averaged for the RIPC and control groups. Following intervention, mean R2* values significantly decreased in the RIPC group in both the cortex (18.6±2.3 vs. 17.5±1.7Hz; p=0.0047) and medulla (34±5.2 vs. 32.2±4.2Hz; p=0.0001). However, no significant differences were observed in the control group. RIPC can be non-invasively assessed in healthy volunteers using BOLDMRI at 3T, demonstrating a higher oxygen content in kidney tissue. This study presents a first-in-man trial establishing a quantifiable readout of RIPC and its effects on kidney physiology. BOLD measurements may advance clinical trials in further evaluating RIPC for future clinical care.

Coronary flow response to remote ischemic preconditioning is preserved in old cardiac patients.

The effect of remote ischemic preconditioning (RIPC) on coronary flow in elderly cardiac patients has not been investigated yet. Thus, we aimed to study the change of coronary flow subsequent to RIPC in old patients with heart diseases and to identify its main correlates. Ninety-five elderly patients (aged ≥ 65years) accessing cardiac rehabilitation ward underwent transthoracic ultrasound evaluation of peak diastolic flow velocity of left anterior descending artery. Measurements of coronary flow velocity were performed on baseline and after an RIPC protocol (three cycles of 5min ischemia of right arm alternating 5min reperfusion). Differences between subjects with coronary flow velocity change over or equal the 75° percentile (high-responders) and subjects with a coronary flow velocity change under the 75° percentile (low-responders) were assessed. In enrolled elderly heart patients, coronary flow velocity significantly augmented from baseline after RIPC [0.23m/s (0.18-0.28) vs 0.27m/s (0.22-0.36); p < 0.001 by Wilcoxon test]. High-responders to RIPC were significantly younger and in better functional status than low-responders. Heart failure resulted as the main variable associated with impairment of RIPC responsiveness (R 2 = 0.202; p = 0.002)]. Our sample of old cardiac patients presented a significant median increment of coronary flow velocity after RIPC. The magnitude of the observed change of coronary flow velocity was comparable to that previously described in healthy subjects. The coronary response to RIPC was attenuated by heart failure. Further research should define whether such RIPC responsiveness is associated with cardioprotection and carries prognostic implications.

GW28-e0791 Acute Hemodynamic Effects of Remote Ischemic Preconditioning on the Coronary Occlusive pressure and Coronary Collateral Blood Flow

GW28-e0791 Acute Hemodynamic Effects of Remote Ischemic Preconditioning on the Coronary Occlusive pressure and Coronary Collateral Blood Flow

Remote Ischemic Preconditioning in Neurological Death Organ Donors: The RIPNOD Prospective Randomized Clinical Trial

Remote ischemic preconditioning (RIPC) is a phenomenon induced by brief periods of ischemia that protects remote organs from prolonged ischemia. Effect of RIPC on organs recovered from neurologic-death donors (NDD) is unknown.

Effects of remote ischemic preconditioning in patients with concentric myocardial hypertrophy: A randomized, controlled trial with molecular insights

BackgroundEfficacy of remote ischemic preconditioning (RIPC) for cardioprotection in cardiac surgery is controversial. We aimed to evaluate the clinical and molecular effects of RIPC on the concentrically hypertrophied myocardium. MethodsSeventy-two aortic stenosis patients receiving aortic valve replacement (AVR) under sevoflurane anesthesia were randomly allocated to RIPC (3cycles of 5-min inflation [300mmHg] and deflation on the left arm) or control (deflated cuff placement) group. The primary endpoints were 24-h area under the curve (AUC) for serum creatine kinase (CK)-MB and troponin (Tn)-T levels. The secondary endpoints were myocardial activation of cell signaling pathways, including reperfusion injury salvage kinases (RISK), signal transducer and activator of transcription (STAT), nitric oxide synthase (NOS), and apoptosis related molecules, obtained from right atrial tissue before and after cardiopulmonary bypass (CPB). ResultsThere were no intergroup differences in 24-h AUCs of CK-MB and Tn-T. Phosphorylations of RISK pathway molecules were not enhanced by RIPC before and after CPB. Phosphorylation of STAT5 was significantly lower in the RIPC group before and after CPB. Phosphorylations of STAT3 and endothelial NOS were not enhanced by RIPC before and after CPB. Expression level of cleaved caspases-3/caspase-3 was significantly higher in the RIPC group before CPB. ConclusionsRIPC did not provide clinical benefits or activate protective signaling in patients with concentric left ventricular hypertrophy undergoing AVR.

Remote Ischemic Preconditioning Decreases the Magnitude of Hepatic Ischemia-Reperfusion Injury on a Swine Model of Supraceliac Aortic Cross-Clamping

Temporary hepatic ischemia is inevitable during open aortic surgery when supraceliac clamping is necessary, as in thoracoabdominal or pararenal aneurysms. Remote ischemic preconditioning (RIPC) has been described as a potential protective means against ischemia-reperfusion injury (IRI) in various tissues including the liver. The aim of this experimental study was to detect the effect of RIPC on liver IRI in a model of supraceliac aortic cross-clamping. An animal study was performed. Four groups of 6 swines each were examined: the control (sham) group, the ischemia-reperfusion (IR) group, and 2 remote ischemic preconditioning groups (RIPC I and RIPC II group). In the IR group, the animals underwent a complete cessation of the splanchnic arterial circulation for 30min by a concomitant occlusion of the supraceliac and the infrarenal aorta. In the RIPC groups, a remote preconditioning was applied before the splanchnic ischemia. This consisted of a temporary occlusion of the infrarenal aorta for 15min followed by 15min of reperfusion (RIPC I group), and 3 cycles of 5min similar ischemia, followed by 5min of reperfusion each (RIPC II group). All animals were followed for 24hr after the ischemia (reperfusion period). The liver ischemia-reperfusion injury was assessed by examining specific serum biomarkers indicating the magnitude of metabolic injury from selective blood samples of the hepatic circulation. In particular, the following parameters were examined: C-reactive protein, interleukin 6, tumor necrosis factor a, ferritin, and L-arginine. All parameters were affected in the IR group as compared to the sham group. Both RIPC groups developed a less serious change as compared to the IR group, in all examined parameters. In an animal study of splanchnic ischemia produced in a way to this produced during a supraceliac aortic aneurysm open repair, the remote ischemic preconditioning seemed to attenuate the effect of hepatic ischemia-reperfusion injury. Remote ischemic preconditioning produced with short bouts of ischemia of the lower body by temporary clamping of the infrarenal aorta might be used as a means of decreasing the detrimental effects of hepatic ischemia-reperfusion injury after supraceliac aortic cross-clamping. This was found in a swine model of suprarenal AAA open repair by studying the variance of certain biological biomarkers in selective blood samples retrieved from the hepatic vein.

Effect of Remote Ischemic Preconditioning on Troponin I in CABG.

BackgroundElective open heart surgery is associated with troponin release in some cases due to myocyte necrosis.ObjectivesThe aim of this study was to measure cardiac troponin I (cTnI) preoperatively in elective CABG after remote ischemic preconditioning.MethodsTwenty-eight patients were selected for elective CABG. They were randomized to receive remote ischemic preconditioning (induced by three 5-min cycles of inflation with a pneumatic tourniquet and 5-min deflation between inflation episodes as reperfusion).OutcomesPrimary outcomes were cardiac troponin I levels at 6 and 24 hours after the procedure, and the secondary outcomes included creatine phosphokinase, lactate dehydrogenase, and serum creatinine levels. Hemodynamic changes were evaluated between the treatment and control groups.ResultsCardiac troponin I at 6 hours after preconditioning was significantly lower compared to the control group (P = 0.036), and after 24 hours, there was still a significant difference between the two groups (P < 0.05).ConclusionsRemote ischemic preconditioning reduces ischemic biomarkers during coronary artery bypass graft and attenuates procedure-related cardiac troponin I release and eventually reduces cardiovascular events such as myocardial infarction, chest pain, and hemodynamic changes after cardiac surgery.

Remote ischemic preconditioning does not prevent acute mountain sickness after rapid ascent to 3,450 m.

P = 0.496 for LLS; P = 0.320 for AMS-C score) of AMS. RIPC also had no significant effect on SPAP [maximum after 10 h at high altitude; RIPC: 33 (SD 8) mmHg; controls: 37 (SD 7) mmHg; P = 0.19]. This study indicates that RIPC, performed immediately before passive ascent to 3,450 m, does not attenuate AMS and the magnitude of high-altitude pulmonary hypertension.NEW & NOTEWORTHY Remote ischemic preconditioning (RIPC) has been reported to improve neurologic and pulmonary outcome following an acute ischemic or hypoxic insult, yet the effect of RIPC for protecting from high-altitude diseases remains to be determined. The present study shows that RIPC, performed immediately before passive ascent to 3,450 m, does not attenuate acute mountain sickness and the degree of high-altitude pulmonary hypertension. Therefore, RIPC cannot be recommended for prevention of high-altitude diseases.

Remote ischemic preconditioning protects liver ischemia-reperfusion injury by regulating eNOS-NO pathway and liver microRNA expressions in fatty liver rats

Ischemic preconditioning (IPC) is a strategy to reduce ischemia-reperfusion (I/R) injury. The protective effect of remote ischemic preconditioning (RIPC) on liver I/R injury is not clear. This study aimed to investigate the roles of RIPC in liver I/R in fatty liver rats and the involvement of endothelial nitric oxide synthase-nitric oxide (eNOS-NO) pathway and microRNA expressions in this process. A total of 32 fatty rats were randomly divided into the sham group, I/R group, RIPC group and RIPC+I/R group. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and nitric oxide (NO) were measured. Hematoxylin-eosin staining was used to observe histological changes of liver tissues, TUNEL to detect hepatocyte apoptosis, and immunohistochemistry assay to detect heat shock protein 70 (HSP70) expression. Western blotting was used to detect liver inducible NOS (iNOS) and eNOS protein levels and real-time quantitative polymerase chain reaction to detect miR-34a, miR-122 and miR-27b expressions. Compared with the sham and RIPC groups, serum ALT, AST and iNOS in liver tissue were significantly higher in other two groups, while serum NO and eNOS in liver tissue were lower, and varying degrees of edema, degeneration and inflammatory cell infiltration were found. Cell apoptosis number was slightly lower in the RIPC+I/R group than that in I/R group. Compared with the sham group, HSP70 expressions were significantly increased in other three groups (all P<0.05). Compared with the sham and RIPC groups, elevated miR-34a expressions were found in I/R and RIPC+I/R groups (P<0.05). MiR-122 and miR-27b were found significantly decreased in I/R and RIPC+I/R groups compared with the sham and RIPC groups (all P<0.05). RIPC can reduce fatty liver I/R injury by affecting the eNOS-NO pathway and liver microRNA expressions.

Effect of Remote Ischemic Preconditioning on Intestinal Ischemia-Reperfusion Injury in Adults Undergoing On-Pump CABG Surgery: A Randomized Controlled Pilot Trial

Cardiopulmonary bypass (CPB) surgery commonly threatens the heart and remote organs with ischemia-reperfusion injury. Transient episodes of ischemia to nonvital tissue, known as remote ischemic preconditioning (RIPC), is thought to help local and remote vital organs to withstand subsequent ischemic insults. Prospective, randomized, double-blinded control trial. Tertiary referral academic teaching hospital. Thirty patients undergoing elective CPB surgery INTERVENTION: RIPC was achieved via three 5-minute cycles of upper limb ischemia using a blood pressure cuff or control (sham cuff). Primary outcome was the occurrence of intestinal injury, as measured by an increase in intestinal fatty acid binding protein (I-FABP). Secondary outcomes included incidence of gastrointestinal complications and duration of intensive care unit (ICU) stay. RIPC did not affect serum IFABP levels at the end of surgery and on the first postoperative day (p = 0.697 and p = 0.461, respectively). For all patients, mean I-FABP levels significantly increased at the end of surgery and decreased to under baseline levels on the first postoperative day (from a mean [± standard deviation] baseline value of 764 ± 492 pg/mL to 2,002 ± 974 pg/mL and decreased to 568 ± 319 pg/mL, p < 0.001). All patients remained clinically absent of gastrointestinal complications until hospital discharge. Duration of ICU stay was not correlated with I-FABP levels at the end of surgery. Neither duration of CPB nor duration of aortic clamping significantly correlated with postoperative I-FABP levels. These findings suggest that RIPC does not affect intestinal injury in patients undergoing CPB surgery. In patients undergoing cardiac surgery, intestinal injury appears to be moderate and transient without any clinical relevant complication.

Remote Ischemic Preconditioning and Clinical Outcomes in On-Pump Coronary Artery Bypass Grafting: A Meta-Analysis of 14 Randomized Controlled Trials.

The purpose of this article is to perform the first pooled analysis on remote ischemic preconditioning (RIPC) used for the improvement of clinical outcomes of patients only undergoing on-pump coronary artery bypass grafting (CABG) in randomized controlled trials (RCTs). A systematic search was performed using PubMed, the Cochrane Library, and the Web of Science to identify studies that described the effect of RIPC on postoperative mortality in patients only undergoing on-pump CABG. The outcomes included postoperative mortality, postoperative morbidity (including incidence of myocardial infarction, atrial fibrillation, stroke, acute kidney injury, and renal replacement therapy), mechanical ventilation (MV), intensive care unit length of stay (ICU LOS), and hospital length of stay (HLOS). A total of 14 RCTs (2830 participants) were included. Our meta-analysis found that RIPC failed to reduce the postoperative mortality in patients only undergoing on-pump CABG compared with control individuals (odds ratio, 0.81; 95% confidence interval, [0.40, 1.64]; P = 0.55; I2 = 25%). Moreover, there were no differences in postoperative morbidity, ICU LOS, and HLOS between the two groups. However, MV in the RIPC group was shorter than that in control individuals (standard mean difference, -0.41; 95% confidence interval, [-0.80, -0.01]; P = 0.04; I2 = 73%). The present meta-analysis found that RIPC failed to improve most of clinical outcomes in patients only undergoing on-pump CABG; however, MV was reduced. Adequately powered trials are warranted to provide more evidence in the future.

Effect of terminal warm reperfusion (hot shot) and remote ischemic preconditioning, either separately or combined, on myocardial recovery in adult cardiac surgery

BackgroundReperfusion injury is a major contributor to morbidity and mortality after cardiac surgery. Among the myocardial protective modalities, terminal warm reperfusion (hot shot) and remote ischemic pre-conditioning techniques were found to protect myocardial function and improve better postoperative outcomes. The aim of this study was to compare the effect of terminal hot shot cardioplegia, the effect of remote ischemic preconditioning and the effect of both techniques on myocardial recovery after adult cardiac surgery. MethodsOne hundred forty-five patients were divided into four groups comparing hot shot group, remote ischemic preconditioning group, combined hot shot and remote ischemic preconditioning group and the control group. The data collected included preoperative demographic and clinical characteristics, intraoperative data and postoperative short term outcome including inhospital mortality. ResultsPatients of the combined group were found to have significantly better outcome including fewer ventricular arrhythmias, less intra-operative need of intra-aortic balloon pump, low cardiac output, and less length of ICU stay. The in-hospital mortality showed a significant difference between the 4 groups. Among patients without hot shot, the incidence of postoperative temporary epicardial pacing was higher and decreased in patients underwent hot shot and remote ischemic preconditioning but didn't reach a statistical significance. ConclusionsBoth remote ischemic preconditioning and terminal hot shot reperfusion before removal of the aortic cross clamping improved outcome of on-pump adult cardiac surgery patients. There was a significant effect on the in-hospital mortality and there were fewer incidences of arrhythmias and less requirement for postoperative inotropic support with this technique.