scholarly journals Prophylactic amiodarone and lidocaine improve survival in an ovine model of large size myocardial infarction

2013 ◽  
Vol 185 (1) ◽  
pp. 152-158 ◽  
Author(s):  
Tieluo Li ◽  
Xufeng Wei ◽  
A. Claire Watkins ◽  
Pablo G. Sanchez ◽  
Zhongjun J. Wu ◽  
...  
1997 ◽  
Vol 152 (3) ◽  
pp. 489-493 ◽  
Author(s):  
C J Charles ◽  
S J Rogers ◽  
R A Donald ◽  
H Ikram ◽  
T Prickett ◽  
...  

Although previous studies have described the hypothalamo–pituitary–adrenal (HPA) response to the stress of acute myocardial infarction, it is not possible to study the hormone changes immediately after infarction in humans. Accordingly, we have examined the HPA response to microembolization of coronary arteries in 13 sheep compared with 5 sham control sheep. Plasma vasopressin (AVP; P<0·001), ACTH (P=0·005) and cortisol (P=0·005) were all increased 2 h (first sample time) after embolization. Plasma ACTH and cortisol levels returned to baseline levels by 6 h but plasma AVP levels did not return to baseline levels until more than 12 h after embolization. Plasma corticotrophin-releasing hormone (CRH) showed no significant change in response to embolization. In a subset of six animals which were sampled more frequently, the peak responses for plasma AVP, ACTH and cortisol occurred at 40 min after embolization. The maximum responses in any individual sheep observed at this time point were 744 pmol/l for AVP, 144 pmol/l for ACTH and 492 nmol/l for cortisol. CRH levels tended to increase across the first hour but these changes were not statistically significant. In conclusion, the stress hormone responses to microembolization of the coronary arteries have been defined in an ovine model of myocardial infarction. This model is suitable for studying the effects of novel treatments to reduce the stress of myocardial infarction. Journal of Endocrinology (1997) 152, 489–493


1992 ◽  
Vol 73 (3) ◽  
pp. 841-846 ◽  
Author(s):  
G. Kreiner ◽  
C. D. Gottlieb ◽  
S. Furukawa ◽  
M. B. Simson ◽  
G. S. Tyson ◽  
...  

The development of slow conduction during the first hours of acute transmural myocardial infarction (ATMI) was studied by signal-averaged electrocardiograms (SAE) in 19 adult anesthetized sheep. SAEs were recorded before and after intravenous infusions of lidocaine and bretylium were begun and 10, 30, and 60 min after ATMI produced by ligation of the left anterior descending and second diagonal coronary arteries. Four sheep died promptly of ventricular tachyarrhythmias; two others developed sustained ventricular arrhythmias, which precluded additional data. Biphasic changes in QRS duration, root mean square voltage of the terminal 40 ms of the QRS complex, and duration of terminal low-amplitude (less than 30 microV) signal were observed. Peak changes in conduction occurred 30 min after infarction and regressed toward baseline thereafter. At 30 min, all animals developed late potentials, which were defined as signals that exceeded both after-drug QRS duration and duration of terminal low-amplitude signal less than 30 microV by more than two standard deviations. At 60 min, only 3 of 13 (23%) animals had late potentials. Conduction is slowest 30 min after ATMI in sheep but may not be related to development of ventricular arrhythmias. In five of six sheep (83%), ventricular arrhythmias occurred within 15 min of infarction before peak slowing was observed by SAE.


2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Tyler Spata ◽  
Daniel Bobek ◽  
Bryan A. Whitson ◽  
Sampath Parthasarathy ◽  
Peter J. Mohler ◽  
...  

Objective. There is a paucity of a biological large animal model of myocardial infarction (MI). We hypothesized that, using autologous-aggregated platelets, we could create an ovine model that was reproducible and more closely mimicked the pathophysiology of MI.Methods. Mepacrine stained autologous platelets from male sheep (n=7) were used to create a myocardial infarction via catheter injection into the mid-left anterior descending (LAD) coronary artery. Serial daily serum troponin measurements were taken and tissue harvested on post-embolization day three. Immunofluorescence microscopy was used to detect the mepacrine-stained platelet-induced thrombus, and histology performed to identify three distinct myocardial (infarct, peri-ischemic “border zone,” and remote) zones.Results. Serial serum troponin levels (μg/mL) measured0.0±0.0at baseline and peaked at297.4±58.0on post-embolization day 1, followed by153.0±38.8on day 2 and76.7±19.8on day 3. Staining confirmed distinct myocardial regions of inflammation and fibrosis as well as mepacrine-stained platelets as the cause of intravascular thrombosis.Conclusion. We report a reproducible, unique model of a biological myocardial infarction in a large animal model. This technique can be used to study acute, regional myocardial changes following a thrombotic injury.


1999 ◽  
Vol 22 (4) ◽  
pp. 605-614 ◽  
Author(s):  
SVEN REEK ◽  
JEANETTE L. BICKNELL ◽  
GREGORY P. WALCOTT ◽  
SANFORD P. BISHOP ◽  
WILLIAM M. SMITH ◽  
...  

2006 ◽  
Vol 41 (4) ◽  
pp. 739-739
Author(s):  
L.A. Ladd ◽  
K.D. Tinworth ◽  
D.L. Bailey ◽  
G.J. Bautovich ◽  
E.A. Bailey ◽  
...  

Author(s):  
Pei Zhang ◽  
Tieluo Li ◽  
Katrina Williams ◽  
Shuyin Li ◽  
Xufeng Wei ◽  
...  

In the United States, over one million patients sustain left ventricular (LV) injury after myocardial infarction (MI). LV remodeling is an adaptive process of hypertrophy that includes infarct expansion, reduced contractility and LV dilation. Progressive enlargement of non-ischemic, hypocontractile myocardium in the adjacent zone (AZ) following the transmural MI has been identified clinically, which contributes to the development post-MI cardiomyopathy in patients. Till now, how the early regional biomechanical and cellular changes, particularly in the AZ, relate to LV remodeling process remains incompletely understood. This study aims to investigate the temporal and/or spatial variations of strain/stress and myocyte size in an ovine model with various MI sizes.


2020 ◽  
Author(s):  
Sander A J Damen ◽  
Gilbert E Cramer ◽  
Hendrik-Jan Dieker ◽  
Helmut Gehlmann ◽  
Ton J M Oude Ophuis ◽  
...  

Abstract Background Troponin composition characterization has been implicated as a next step to differentiate among non-ST elevation myocardial infarction (NSTEMI) patients and improve distinction from other conditions with troponin release. We therefore studied coronary and peripheral troponin compositions in relation to clinical variables of NSTEMI patients. Methods Samples were obtained from the great cardiac vein (GCV), coronary sinus (CS), and peripheral circulation of 45 patients with NSTEMI. We measured total cTnI concentrations, and assessed both complex cTnI (binary cTnIC + all ternary cTnTIC forms), and large-size cTnTIC (full-size and partially truncated cTnTIC). Troponin compositions were studied in relation to culprit vessel localization (left anterior descending artery [LAD] or non-LAD), ischemic time window, and peak CK-MB value. Results Sampling occurred at a median of 25 hours after symptom onset. Of total peripheral cTnI, a median of 87[78-100]% consisted of complex cTnI; and 9[6-15]% was large-size cTnTIC. All concentrations (total, complex cTnI, and large-size cTnTIC) were significantly higher in the CS than in peripheral samples (P &lt; 0.001). For LAD culprit patients, GCV concentrations were all significantly higher; in non-LAD culprit patients, CS concentrations were higher. Proportionally, more large-size cTnTIC was present in the earliest sampled patients and in those with the highest CK-MB peaks. Conclusions In coronary veins draining the infarct area, concentrations of both full-size and degraded troponin were higher than in the peripheral circulation. This finding, and the observed associations of troponin composition with the ischemic time window and the extent of sustained injury may contribute to future characterization of different disease states among NSTEMI patients.


2009 ◽  
Vol 32 (7) ◽  
pp. 851-861 ◽  
Author(s):  
JIM POULIOPOULOS ◽  
ARAVINDA THIAGALINGAM ◽  
VICKI E. EIPPER ◽  
CRAIG CAMPBELL ◽  
DAVID L. ROSS ◽  
...  

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