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.

scholarly journals The Assessment of Area at Risk and Myocardial Salvage After Coronary Revascularization in Acute Myocardial Infarction

2013 ◽  
Vol 6 (3) ◽  
pp. 358-369 ◽  
Author(s):  
Martin Hadamitzky ◽  
Birgit Langhans ◽  
Jörg Hausleiter ◽  
Carolin Sonne ◽  
Adnan Kastrati ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
At Risk ◽  
Coronary Revascularization ◽  
Myocardial Salvage ◽  
Area At Risk

scholarly journals Development and Long-Term Follow-Up of an Experimental Model of Myocardial Infarction in Rabbits

Animals ◽  
2020 ◽  
Vol 10 (9) ◽  
pp. 1576
Author(s):  
Patricia Genovés ◽  
Óscar J. Arias-Mutis ◽  
Germán Parra ◽  
Luis Such-Miquel ◽  
Manuel Zarzoso ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
At Risk ◽  
Infarct Size ◽  
Experimental Model ◽  
Ventricular Arrhythmias ◽  
Sham Group ◽  
Ventricular Remodeling ◽  
Area At Risk ◽  
Care Protocol

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.

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
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
At Risk ◽  
Blood Transfusion ◽  
Cardiac Function ◽  
Infarct Size ◽  
Myocardial Injury ◽  
Fresh Blood ◽  
Area At Risk ◽  
Acute Mi

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.

Abstract 12: EMMPRIN-Targeted Magnetic Nanoparticles for in vivo Visualization and Regression of Acute Myocardial Infarction in a Model of Acute Coronary Artery Occlusion

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Irene Cuadrado ◽  
Maria Jose Garcia Miguel ◽  
Irene Herruzo ◽  
Mari Carmen Turpin ◽  
Ana Martin ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Extracellular Matrix ◽  
Coronary Artery ◽  
Left Ventricle ◽  
Infarct Size ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Gadolinium Enhancement

Extracellular matrix metalloproteinase inducer EMMPRIN, is highly expressed in patients with acute myocardial infarction (AMI), and induces activation of several matrix metalloproteinases (MMPs), including MMP-9 and MMP-13. To prevent Extracellular matrix degradation and cardiac cell death we targeted EMMPRIN with paramagnetic/fluorescent micellar nanoparticles with an EMMPRIN binding peptide AP9 conjugated (NAP9), or an AP9 scramble peptide as a negative control (NAPSC). NAP9 binds to endogenous EMMPRIN as detected by confocal microscopy of cardiac myocytes and macrophages incubated with NAP and NAPSC in vitro, and in vivo in mouse hearts subjected to left anterior descending coronary artery occlusion (IV injection 50mγ/Kg NAP9 or NAP9SC). Administration of NAP9 at the same time or 1 hour after AMI reduced infarct size over a 20% respect to untreated and NAPSC injected mice, recovered left ventricle ejection fraction (LVEF) similar to healthy controls, and reduced EMMPRIN downstream MMP9 expression. In magnetic resonance scans of mouse hearts 2 days after AMI and injected with NAP9, we detected a significant gadolinium enhancement in the left ventricle respect to non-injected mice and to mice injected with NAPSC. Late gadolinium enhancement assays exhibited NAP9-mediated left ventricle signal enhancement as early as 30 minutes after nanoprobe injection, in which a close correlation between the MRI signal enhancement and left ventricle infarct size was detected. Taken together, these results point EMMPRIN targeted nanoprobes as a new tool for the treatment of AMI.

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.

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