scholarly journals Hypothermia for Reduction of Myocardial Reperfusion Injury in Acute Myocardial Infarction: Closing the Translational Gap

2021 ◽  
Author(s):  
Mohamed El Farissi ◽  
Danielle C.J. Keulards ◽  
Jo M. Zelis ◽  
Marcel van ’t Veer ◽  
Frederik M. Zimmermann ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Infarct Size ◽  
Reperfusion Injury ◽  
Myocardial Reperfusion ◽  
Myocardial Reperfusion Injury ◽  
Current Status ◽  
Myocardial Salvage ◽  
Nonlinear Phenomena ◽  
Comprehensive Overview

Myocardial reperfusion injury—triggered by an inevitable inflammatory response after reperfusion—may undo a considerable part of the myocardial salvage achieved through timely percutaneous coronary intervention in patients with acute myocardial infarction. Because infarct size is strongly correlated to mortality and risk of heart failure, the importance of endeavors for cardioprotective therapies to attenuate myocardial reperfusion injury and decrease infarct size remains undisputed. Myocardial reperfusion injury is the result of several complex nonlinear phenomena, and for a therapy to be effective, it should act on multiple targets involved in this injury. In this regard, hypothermia remains a promising treatment despite a number of negative randomized controlled trials in humans with acute myocardial infarction so far. To turn the tide for hypothermia in patients with acute myocardial infarction, sophisticated solutions for important limitations of systemic hypothermia should continue to be developed. In this review, we provide a comprehensive overview of the pathophysiology and clinical expression of myocardial reperfusion injury and discuss the current status and possible future of hypothermia for cardioprotection in patients with acute myocardial infarction.

Myocardial reperfusion injury management: erythropoietin compared with postconditioning

2009 ◽  
Vol 297 (6) ◽  
pp. H2035-H2043 ◽  
Author(s):  
Sophie Tamareille ◽  
Nehmat Ghaboura ◽  
Frederic Treguer ◽  
Dalia Khachman ◽  
Anne Croué ◽  
...  
Keyword(s):  
Infarct Size ◽  
Reperfusion Injury ◽  
Isolated Heart ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Myocardial Reperfusion ◽  
Myocardial Reperfusion Injury ◽  
Gsk 3Β ◽  
Developed Pressure

Ischemic postconditioning (IPost) and erythropoietin (EPO) have been shown to attenuate myocardial reperfusion injury using similar signaling pathways. The aim of this study was to examine whether EPO is as effective as IPost in decreasing postischemic myocardial injury in both Langendorff-isolated-heart and in vivo ischemia-reperfusion rat models. Rat hearts were subjected to 25 min ischemia, followed by 30 min or 2 h of reperfusion in the isolated-heart study. Rats underwent 45 min ischemia, followed by 24 h of reperfusion in the in vivo study. In both studies, the control group ( n = 12; ischemia-reperfusion only) was compared with IPost ( n = 16; 3 cycles of 10 s reperfusion/10 s ischemia) and EPO ( n = 12; 1,000 IU/kg) at the onset of reperfusion. The following resulted. First, in the isolated hearts, IPost or EPO significantly improved postischemic recovery of left ventricular developed pressure. EPO induced better left ventricular developed pressure than IPost at 30 min of reperfusion (73.18 ± 10.23 vs. 48.11 ± 7.92 mmHg, P < 0.05). After 2 h of reperfusion, the infarct size was significantly lower in EPO-treated hearts compared with IPost and control hearts (14.36 ± 0.60%, 19.11 ± 0.84%, and 36.21 ± 4.20% of the left ventricle, respectively; P < 0.05). GSK-3β phosphorylation, at 30 min of reperfusion, was significantly higher with EPO compared with IPost hearts. Phosphatidylinositol 3-kinase and ERK1/2 inhibitors abolished both EPO- and IPost-mediated cardioprotection. Second, in vivo, IPost and EPO induced an infarct size reduction compared with control (40.5 ± 3.6% and 28.9 ± 3.1%, respectively, vs. 53.7 ± 4.3% of the area at risk; P < 0.05). Again, EPO decreased significantly more infarct size and transmurality than IPost ( P < 0.05). In conclusion, with the use of our protocols, EPO showed better protective effects than IPost against reperfusion injury through higher phosphorylation of GSK-3β.

Abstract 2667: Aspiration Coronary Thrombectomy for Acute Myocardial Infarction Improves Myocardial Salvage Index. Single Center Randomized Study

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Michal Ciszewski ◽  
Jerzy Pregowski ◽  
Anna Teresinska ◽  
Maciej Karcz ◽  
Witold Ruzyllo
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Infarct Size ◽  
Perfusion Imaging ◽  
Randomized Study ◽  
Myocardial Salvage ◽  
Aspiration Thrombectomy ◽  
Acute Stemi ◽  
Final Infarct Size ◽  
Myocardium At Risk

Primary percutaneus intervention (pPCI) is a recommended treatment strategy for acute myocardial infarction with ST segment elevation (STEMI). Adjunctive thrombectomy may add clinical benefits. The aim of our study was to compare the efficacy of aspiration thrombectomy versus standard pPCI for STEMI. The primary endpoint was salvage index assessed by sestamibi SPECT perfusion imaging. Single centre randomized study on aspiration thrombectomy in acute STEMI. 135 patients (88 males, mean age 64,3±12,4 yrs) with first acute STEMI were enrolled between Nov 2004 and Dec 2007. Inclusion criteria were: first anterior or inferior STEMI within 12 hours from pain onset with culprit lesion in left anterior descending (LAD) or right coronary artery (RCA) and TIMI flow ≤ 2. Patients were randomly assigned to thrombectomy with Rescue or Diver device followed by stent implantation (65) vs. standard pPCI with stenting (70 pts). 5 patients initially randomised to thrombectomy were finally treated with standard pPCI. Two SPECT examinations were performed: before and 5– 8 days after reperfusion therapy. Five patients died 3–7 days after the procedure, and in 3 pts second SPECT could not be performed because of patients’ severe condition. Thus two SPECT examinations were performed in 127 patients (63 treated with thrombectomy and 64 in control group). These 127 subject were the basis of the intention to treat analyses. There were 41 pts with anterior STEMI and 86 pts with inferior STEMI. Both treatment groups were similar regarding baseline demographic and clinical variables. Based on the SPECT perfusion imaging results, the final infarct size was assessed and myocardial salvage index (proportion of the myocardium at risk salvaged by reperfusion) was calculated. Baseline myocardium at risk area was 35,0%±2,8% in thrombectomy group vs 35,8%±10,9% in control patients. (p=NS). Myocardial salvage index was larger in patients treated with aspiration thrombectomy (0,33±0,27 vs. 0,20 ± 0,21 p = 0,004). Moreover, final infarct size was significantly smaller in patients treated with thrombectomy: 23,9% ± 13,1 % vs.28,3 % ±9,6% p = 0,005. Our results show that coronary thrombectomy is beneficial as an adjunctive therapy to pPCI in STEMI.

P3391Cholesterol crystals in culprit coronary artery with acute myocardial infarction and their relation to myocardial salvage

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
T Nunohiro ◽  
S Kuwasaki ◽  
T Fukushima ◽  
S Furudono ◽  
H Suenaga ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
At Risk ◽  
Coronary Artery ◽  
Infarct Size ◽  
Myocardial Salvage ◽  
Area At Risk ◽  
Risk Area ◽  
Contrast Enhanced ◽  
Delayed Enhancement Imaging

Abstract The involvement of cholesterol crystals (CCs) in plaque progression and destabilization of atherosclerotic plaques has been recently recognized. However, little is known about CCs and myocardial salvage in the Acute myocardial infarction (AMI) patients. This study aimed to evaluate the association between the existence of CCs at the site of culprit coronary artery and myocardial salvage index (MSI).To investigate, we applied the diagnostic resources of Optical Coherence Tomography (OCT). Methods This study included 53 AMI patients (90% with STEMI) who underwent primary PCI within 24h of onset. 53 STEMI patients underwent magnetic resonance imaging (CMR) of 5th days and 3 months after PCI. Infarct size was measured on delayed-enhancement imaging, and area at risk was quantified on T2-weighted imaging. MSI was calculated as [area at risk − infarct size] × 100/area at risk. 3 months CMR with contrast-enhanced imaging of late gadolinium enhancement-LGE. Patients were divided 2 groups according to the existence of CCs at the site of culprit coronary artery. Results CCs occurs in 26 of 53 (49%). Acute 5th days risk area (13.5±4.1 vs 12.6±4.9, P=0.48) and 3months infarct size (5.3±3.5 vs 7.0±3.2, P=0.066) were not significant between CCs and no CCs group. But salvage index were significantly lower in patients with CCs group (47.7±17.5% vs 60.1±20.2%, P=0.021) Conclusion Salvage index in patients that CCs were found by the OCT analysis, remain low after AMI. This study demonstrates the potential correlation between the myocardial salvage and vulnerable morphological features of culprit lesion to the presence of CCs with AMI patients.

Factors modifying protective effect of anti-CD18 antibodies on myocardial reperfusion injury in dogs

1996 ◽  
Vol 270 (1) ◽  
pp. H53-H64 ◽  
Author(s):  
R. G. Perez ◽  
M. Arai ◽  
C. Richardson ◽  
A. DiPaula ◽  
C. Siu ◽  
...  
Keyword(s):  
Infarct Size ◽  
Reperfusion Injury ◽  
Myocardial Reperfusion ◽  
Myocardial Reperfusion Injury ◽  
H2o2 Production ◽  
Myeloperoxidase Activity ◽  
Collateral Flow ◽  
Severe Ischemia

Anti-CD18 monoclonal antibodies (MAb) have demonstrated variable protection against neutrophil (PMN)-mediated myocardial reperfusion injury. To identify factors contributing to this variability, open-chest dogs underwent coronary artery occlusion for 90 min followed by reperfusion for 3.5 h. Ten minutes before reperfusion the dogs received saline (n = 18) or one of three anti-CD18 MAb: MHM.23, R15.7, or PLM-2 (2, 1, and 1 mg/kg and n = 19, 8, and 4, respectively). Collateral flow was measured with radioactive microspheres, area at risk was assessed with monastral blue dye, and infarct size was measured postmortem by triphenyltetrazolium chloride. In vitro, all three MAb bound to canine PMNs, but only MHM.23 and R15.7 inhibited their adherence to keyhole limpet hemocyanin-coated plastic. In vivo, only MHM.23 and R15.7 significantly reduced infarct size after adjusting for the effect of collateral flow. MHM.23 afforded protection in dogs with moderate ischemia (epicardial collateral flow > 0.1 ml.min-1.g-1, infarct size reduced 46%) but not in dogs with more severe ischemia. Only R15.7 was effective in dogs with severe ischemia. Although MHM.23 and R15.7 produced similar inhibition of tissue PMN accumulation, as reflected by myeloperoxidase activity. R15.7 markedly inhibited H2O2 production by PMNs after exposure to platelet-activating factor, whereas MHM.23 had only a minimal effect. The effectiveness of different anti-CD18 MAb in preventing reperfusion injury appears to be 1) highly dependent on the specific anti-CD18 MAb employed, 2) predicted only partially by in vitro binding to PMNs, static in vitro tests of PMN adherence, or the extent of inhibition of PMN accumulation in vivo, 3) related more to their ability to inhibit oxidant release from activated PMNs, and 4) strongly influenced by the severity of myocardial ischemia before reperfusion.

A sialyl Lewis(x)-containing carbohydrate reduces infarct size: role of selectins in myocardial reperfusion injury

1996 ◽  
Vol 271 (5) ◽  
pp. H2086-H2096 ◽  
Author(s):  
D. M. Flynn ◽  
A. J. Buda ◽  
P. R. Jeffords ◽  
D. J. Lefer
Keyword(s):  
Blood Flow ◽  
Infarct Size ◽  
Reperfusion Injury ◽  
Left Ventricular ◽  
Myocardial Reperfusion ◽  
Myocardial Reperfusion Injury ◽  
Sialyl Lewis X ◽  
Control Group ◽  
Leukocyte Accumulation ◽  
Sialyl Lewis

Previous studies have implicated the selectins (P- and L-selectin) in the acute phase of myocardial reperfusion injury. However, it is unclear whether these adhesion molecules are involved in the pathogenesis of myocardial reperfusion associated with longer periods of reperfusion. Dogs (n = 8/group) were subjected to 90 min of coronary ischemia and 48 h of reperfusion. Animals were initially treated with a 35 mg/kg intravenous bolus of a sialyl Lewis(x) oligosaccharide (SLe(x)-OS) 10 min before reperfusion, followed by a 1.75 mg.kg-1.h-1 infusion for the first 24 h of reperfusion. A control group of dogs received a normal saline bolus followed by saline infusion for the first 24 h of reperfusion. In a subsequent group of dogs treatment consisted of only the 35 mg/kg bolus of SLe(x)-OS to help elucidate the time course of selectin involvement. The saline control group exhibited marked decreases in blood flow in the ischemic-reperfused myocardium, sustained depression of left ventricular function, an average infarct size of 29 +/- 5% of the myocardial area at risk, and excessive polymorphonuclear leukocyte accumulation in the infarcted myocardium after 48 h of reperfusion. Dogs that received a bolus followed by an infusion of SLe(x)-OS exhibited significant preservation of myocardial blood flow and left ventricular function at 4.5 and 48 h of reperfusion, dramatic attenuation (56%) of infarct size (P < 0.05), and a 55% reduction (P < 0.05) in polymorphonuclear leukocyte accumulation compared with the saline group. Interestingly, SLe(x)-OS bolus treatment alone exerted early (i.e., at 4.5 h) cardioprotective effects that waned by 48 h of reperfusion. These results demonstrate that the selectin family of adhesion molecules plays an extended role in myocardial reperfusion injury and is not only involved in the acute phase of this disease process.

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