Effect of Anemia and Red Blood Cell Transfusion in Acute Myocardial Infarction.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 454-454
Author(s):  
Anargyros Xenocostas ◽  
Houxiang Hu ◽  
Xiangru Lu ◽  
Ian Chin-Yee ◽  
Qingping Feng

Abstract Background: The optimal hemoglobin (Hb) in the setting of acute myocardial infarction (MI) is unknown. Anemia reduces the oxygen carrying capacity of blood and may theoretically exacerbate ischemia increasing myocardial injury. The benefit of transfusion to correct anemia in acute coronary syndromes is also controversial. The goal of this study was to determine the optimal Hb in the setting of acute MI and whether transfusion reduces myocardial injury and improves outcome. Experimental design: Ninety-two male Sprague-Dawley rats (170–190g) were divided into 8 groups: 1: Normal Hb, sham operation; 2: Normal Hb, MI; 3: Hb 80–90g/L, sham; 4: Hb 80–90g/L, MI; 5: Hb 70–80g/L, sham; 6: Hb 70–80g/L, MI; 7: Hb 80–90g/L, MI with transfusion to 100g/L; 8: Hb 80–90g/L, MI with transfusion to 120g/L. To determine the effect of blood transfusion, fresh blood was immediately transfused following MI. Induction of myocardial infarction was preformed by left coronary artery ligation. Sham-operated rats underwent the same surgical procedure without ligation. At 24 hours post-MI, rats were re-anaesthetized and hemodynamic measurements preformed. Area at risk and infarct size was measured by Evans blue and triphenyltetrazolium chloride, respectively. Results: In the normal Hb group (140–150g/L), survival following sham or MI surgery was 100%. Reduction of Hb to 80–90 and 70–80g/L significantly decreased survival post-MI to 42% and 47%, respectively. Survival was significantly improved after transfusion of fresh blood to raise the hemoglobin from 80–90g/L to 100g/L (P<0.05). However, there was no improvement in survival when Hb was raised by transfusion to 120g/L (P=NS). Twenty-four hours post-MI, the ischemic to non-ischemic left ventricle (LV) weight ratios were not significantly different between any groups indicating similar areas of myocardial ischemia among all groups (P=NS). However, the infarct size to area at risk ratios were significantly increased in both 70–80g/L and 80–90g/L groups compared to the normal Hb group (P<0.05). Transfusion from Hb 80–90g/L to 100g/L significantly decreased infarct size compared to the Hb 80–90g/L group (P<0.05). However, transfusion to Hb 120g/L resulted in a significantly larger infarct size compared to the Hb 100g/L transfused group (P<0.05). Cardiac function was determined at 24 hours post-MI. Heart rate, MAP, LVSP and LVEDP were not significantly different among all groups but anemic groups 80–90 and 70–80g/L showed a significant decrease in LV +dP/dtmax and −dP/dtmin in both sham and MI rats (P<0.01) with the most significant decrease noted in MI rats compared to sham operated rats (P<0.05). Blood transfusion post-MI from a Hb 80–90 to 100g/L significantly improved LV +dP/dtmax (P<0.05). Transfusion to Hb 120g/L did not result in any further improvement in cardiac function. Conclusions: In the setting of acute MI, anemia increased mortality and infarct size compared to non-anemic controls. At 24 hours post-MI, anemia also impaired cardiac function. Transfusion of anemic animals up to a Hb of 100g/L with fresh RBCs reduced mortality and infarct size and improved cardiac function. However, transfusion to a Hb of 120g/L did not demonstrate any additional benefit and was associated with larger infarcts.

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 661-661
Author(s):  
Anargyros Xenocostas ◽  
Houxiang Hu ◽  
Nicolas J Chin-Yee ◽  
Ian Chin-Yee ◽  
Qingping Feng

Abstract Abstract 661 Background: Anemia is a predictor of poor outcomes in acute myocardial infarction (MI) and may increase the degree of ischemia, resulting in greater tissue injury. The only existing therapeutic intervention used to acutely correct anemia is red blood cell (RBC) transfusion, although its effectiveness at improving outcomes in anemic subjects following MI remains controversial. We have previously shown that transfusion of fresh blood in anemic rats following MI decreased infarct size, and improved cardiac function and survival (Hu et al. Transfusion 2010; 50:243-251). However, it was not known if the transfusion of stored blood, which develops a series of chemical and corpuscular changes collectively known as the “storage lesion”, would be equally effective in this model. Experimental Design: Acute MI was induced by coronary artery ligation in 49 male Sprague-Dawley rats, 38 of which were made anemic (Hb = 80–90 g/L) using a combination of dietary iron deprivation and phlebotomy, and 11 with normal Hb levels. Rat blood was stored for 7 days in CPDA-1 to induce a storage lesion similar to the one seen in human blood stored under identical conditions for 28 days (d'Almeida et al. Transfusion Medicine 2000; 10:291-303). Anemic animals were randomly assigned to one of three groups: i) fresh blood transfusion (stored for <4 hours) to increase the Hb to 100 g/L, ii) transfused with stored blood to increase the Hb to 100 g/L, or iii) no transfusion. At 24 hours post-MI, infarct size, cardiac function and survival rates were determined. Results: A similar degree of left ventricular (LV) myocardial ischemia (area at risk) was induced in all groups (P=NS). In agreement with previous results, the infarct size to area at risk ratios were significantly increased in the anemic (Hb 80–90 g/L) animals compared to non-anemic MI controls, and transfusion of fresh blood to a target Hb level of 100 g/L after MI decreased infarct size (P<0.05) and improved both systolic (+dP/dtmax) and diastolic (−dP/dtmin) LV function compared to anemic animals (P<0.05). However, the transfusion of stored blood into anemic animals post-MI did not have these effects when compared to the group receiving fresh blood (P<0.05). Furthermore, survival was increased in anemic animals receiving fresh blood (9/11; P<0.05) but not stored blood (7/14; P=NS) compared to the non-transfused group (5/13). Conclusions: The prolonged storage of blood negates the beneficial effects of fresh blood transfusion, which include reductions in infarct size, and improvements in cardiac function and short-term survival following acute MI in this animal model. (This study was supported by the Canadian Institutes of Health Research, Canadian Blood Services and the Bayer Partnership Fund). Disclosures: No relevant conflicts of interest to declare.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
T Nunohiro ◽  
S Kuwasaki ◽  
T Fukushima ◽  
S Furudono ◽  
H Suenaga ◽  
...  

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.


Animals ◽  
2020 ◽  
Vol 10 (9) ◽  
pp. 1576
Author(s):  
Patricia Genovés ◽  
Óscar J. Arias-Mutis ◽  
Germán Parra ◽  
Luis Such-Miquel ◽  
Manuel Zarzoso ◽  
...  

A chronic model of acute myocardial infarction was developed to study the mechanisms involved in adverse postinfarction ventricular remodeling. In an acute myocardial infarction (AMI), the left circumflex coronary artery of New Zealand White rabbits (n = 9) was occluded by ligature for 1 h, followed by reperfusion. A specific care protocol was applied before, during, and after the intervention, and the results were compared with those of a sham operated group (n = 7). After 5 weeks, programmed stimulation and high-resolution mapping were performed on isolated and perfused hearts using the Langendorff technique. The infarct size determined by 2,3,5-triphenyltetrazolium chloride inside of the area at risk (thioflavin-S) was then determined. The area at risk was similar in both groups (54.33% (experimental infarct group) vs. 58.59% (sham group), ns). The infarct size was 73.16% as a percentage of the risk area. The experimental infarct group had a higher inducibility of ventricular arrhythmias (100% vs. 43% in the sham group, p = 0.009). A reproducible chronic experimental model of myocardial infarction is presented in which the extent and characteristics of the lesions enable the study of the vulnerability to develop ventricular arrhythmias because of the remodeling process that occurs during cardiac tissue repair.


2009 ◽  
Vol 11 (S1) ◽  
Author(s):  
Jamieson M Bourque ◽  
David K Glover ◽  
Craig C Goodman ◽  
Mirta R Herrera ◽  
Fred Epstein ◽  
...  

2019 ◽  
Author(s):  
Lan Wu ◽  
Rajeev Dalal ◽  
Connie Cao ◽  
J. Luke Postoak ◽  
Qinkun Zhang ◽  
...  

AbstractAcute myocardial infarction (MI) provokes an inflammatory response in the heart that removes damaged tissues to facilitate repair. However, exaggerated and/or persistent inflammation compromises healing, which may be counteracted by regulatory immune mechanisms. A key regulatory factor in an inflammatory response is the anti-inflammatory cytokine IL-10, which can be produced by a number of immune cells including subsets of B lymphocytes. Here, we investigated IL-10-producing B cells in pericardial adipose tissues (PATs) and their role in the healing process following acute MI in mice. We found abundant IL-10-producing B cells in PATs under homeostatic conditions, with the majority of them bearing cell surface CD5 (CD5+ B cells). These cells were detected early in life, maintained a steady presence during adulthood, and resided in fat-associated lymphoid clusters (FALCs). The cytokine IL-33 was preferentially expressed in PATs under homeostatic conditions and contributed to enrichment of IL-10-producing CD5+ B cells in PATs. CD5+ B cells expanded in PATs following MI, and accumulated in the infarcted heart during the resolution of MI-induced inflammation. B cell-specific deletion of IL-10 worsened cardiac function after MI, exacerbated myocardial injury, and delayed resolution of inflammation. These findings reveal a significant contribution of IL-10-producing B cells to the anti-inflammatory mechanism that terminates MI-induced inflammation, and identify these cells as novel therapeutic targets to improve the outcome of MI.Significance StatementMyocardial infarction (MI) remains a leading cause of mortality and morbidity worldwide. Although it is now recognized that a balanced and timely terminated pro-inflammatory response following acute MI is essential in promoting tissue repair, the underlying regulatory mechanisms are poorly defined. In this report, we show that IL-10-producing B cells in mice 1) are enriched in pericardial adipose tissues (PATs) and influenced by cytokine IL-33 under homeostatic conditions; 2) expand in PATs following MI and accumulate in the infarcted heart during the resolution of MI-induced inflammation; and 3) facilitate resolution of inflammation and reduce myocardial injury to preserve cardiac function after MI. These findings identify IL-10-producing B cells as novel therapeutic targets to improve the outcome of MI.


2013 ◽  
Vol 6 (3) ◽  
pp. 358-369 ◽  
Author(s):  
Martin Hadamitzky ◽  
Birgit Langhans ◽  
Jörg Hausleiter ◽  
Carolin Sonne ◽  
Adnan Kastrati ◽  
...  

2020 ◽  
Vol 15 (1) ◽  
Author(s):  
Andreas Boening ◽  
Maximilian Hinke ◽  
Martina Heep ◽  
Kerstin Boengler ◽  
Bernd Niemann ◽  
...  

Abstract Background Because hearts in acute myocardial infarction are often prone to ischemia-reperfusion damage during cardiac surgery, we investigated the influence of intracellular crystalloid cardioplegia solution (CCP) and extracellular blood cardioplegia solution (BCP) on cardiac function, metabolism, and infarct size in a rat heart model of myocardial infarction. Methods Following euthanasia, the hearts of 50 rats were quickly excised, cannulated, and inserted into a blood-perfused isolated heart apparatus. A regional myocardial infarction was created in the infarction group (18 hearts) for 120 min; the control group (32 hearts) was not subjected to infarction. In each group, either Buckberg BCP or Bretschneider CCP was administered for an aortic clamping time of 90 min. Functional parameters were recorded during reperfusion: coronary blood flow, left ventricular developed pressure (LVDP) and contractility (dp/dt max). Infarct size was determined by planimetry. The results were compared between the groups using analysis of variance or parametric tests, as appropriate. Results Cardiac function after acute myocardial infarction, 90 min of cardioplegic arrest, and 90 min of reperfusion was better preserved with Buckberg BCP than with Bretschneider CCP relative to baseline (BL) values (LVDP 54 ± 11% vs. 9 ± 2.9% [p = 0.0062]; dp/dt max. 73 ± 11% vs. 23 ± 2.7% [p = 0.0001]), whereas coronary flow was similarly impaired (BCP 55 ± 15%, CCP 63 ± 17% [p = 0.99]). The infarct in BCP-treated hearts was smaller (25% of myocardium) and limited to the area of coronary artery ligation, whereas in CCP hearts the infarct was larger (48% of myocardium; p = 0.029) and myocardial necrosis was distributed unevenly to the left ventricular wall. Conclusions In a rat model of acute myocardial infarction followed by cardioplegic arrest, application of BCP leads to better myocardial recovery than CCP.


Radiology ◽  
2009 ◽  
Vol 250 (3) ◽  
pp. 916-922 ◽  
Author(s):  
Declan P. O'Regan ◽  
Rizwan Ahmed ◽  
Narayan Karunanithy ◽  
Clare Neuwirth ◽  
Yvonne Tan ◽  
...  

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