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 ◽  
...  

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.

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.


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.


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

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Kobara ◽  
N Naseratun ◽  
Y Watanabe ◽  
H Toba ◽  
T Nakata

Abstract Background Myocardial infarction (MI) is a major cause of death in western countries and Japan, and hypertension is a major risk factor of MI. In hypertensive heart, acute myocardial infarction often leads to lethal ventricular arrhythmia. Nicorandil, an ATP sensitive potassium channel (KATP) opener, is usually used in the treatment of acute myocardial infarction. The effects of nicorandil on ischemic myocyte are fully defined. On the other hand, KATP in neuroterminals is known to regulate norepinephrine release, but the effect of nicorandil on ischemic norepinephrine release in cardiac tissue has remained unexplored. Purpose We examined whether nicorandil suppressed norepinephrine release via neuronal KATP and ventricular arrhythmia during acute ischemia in pressure overload-induced hypertrophic hearts. Methods SD Rats were divided into two groups; abdominal aortic constriction (AAC) group and sham-operated (Sham) group. Four weeks after constriction, cardiac geometry and function were examined using echocardiography. Then, myocardial ischemia was induced by the left anterior descending artery occlusion for 100 minutes in the presence or absence of intravenous infusion of nicorandil. Cardiac interstitial norepinephrine concentration in ischemic region was measured using the microdialysis method and concentration of cyclic AMP, a second messenger of norepinephrine, in cardiac tissue was measured by ELISA. Ventricular arrhythmias were monitered by ECG during whole ischemic period. Results Four weeks after constriction, remarkable left ventricular wall thickening was observed in AAC group. Before ischemia, ventricular arrhythmia was not found in both groups. Number of ventricular arrhythmia, including ventricular tachycardia and ventricular fibrillation, was increased in early ischemic period (- 40 min) in both groups, and was grater in AAC group. Before ischemia, interstitial norepinephrine concentration in cardiac tissue was higher level in AAC group than in Sham group. Ischemia obviously increased norepinephrine concentration in both groups time dependently and AAC further increased norepinephrine than Sham group. Concentration of cyclic AMP in cardiac tissue was raised in early ischemic period (- 40 min) and then gradually decreased. Nicorandil significantly suppressed the number of ventricular arrhythmias, and abolished the ventricular tachycardia and fibrillation without hemodynamic alterations. Nicorandil also attenuated norepinephrine and cAMP enhancement in acute ischemic period in both groups. Conclusion Ischemia-induced ventricular arrhythmia was more frequent and severe in hypertrophic hearts and interstitial norepinephrine enhancement may play a role in this ischemic arrhythmia. Nicorandil suppressed ischemia-induced interstitial norepinephrine release by neuronal KATP opening, which attenuated ventricular arrhythmias in normal and hypertrophic hearts.


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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