Cang-Song XIAO, Chang-Qing GAO, Li-Bing LI, Yao WANG, Tao ZhAO, Wei-Hua YE, Chong-Lei REN, Zhi-Yong LIU, Yang WU. Establishment of a chronic left ventricular aneurysm model in rabbit[J]. Journal of Geriatric Cardiology, 2014, 11(2): 158-162. DOI: 10.3969/j.issn.1671-5411.2014.02.009
Citation: Cang-Song XIAO, Chang-Qing GAO, Li-Bing LI, Yao WANG, Tao ZhAO, Wei-Hua YE, Chong-Lei REN, Zhi-Yong LIU, Yang WU. Establishment of a chronic left ventricular aneurysm model in rabbit[J]. Journal of Geriatric Cardiology, 2014, 11(2): 158-162. DOI: 10.3969/j.issn.1671-5411.2014.02.009

Establishment of a chronic left ventricular aneurysm model in rabbit

  • Objectives To establish a cost-effective and reproducible procedure for induction of chronic left ventricular aneurysm (LVA) in rabbits. Methods Acute myocardial infarction (AMI) was induced in 35 rabbits via concomitant ligation of the left anterior descending (LAD) coronary artery and the circumflex (Cx) branch at the middle portion. Development of AMI was confirmed by ST segment elevation and akinesis of the occluded area. Echocardiography, pathological evaluation, and agar intra-chamber casting were utilized to validate the formation of LVA four weeks after the surgery. Left ventricular end systolic pressure (LVESP) and diastolic pressure (LVEDP) were measured before, immediately after and four weeks after ligation. Dimensions of the ventricular chamber, thickness of the interventricular septum (IVS) and the left ventricular posterior wall (LVPW) left ventricular end diastolic volume (LVEDV), systolic volume (LVESV), and ejection fraction (EF) were recorded by echocardiogram. Results Thirty one (88.6%) rabbits survived myocardial infarction and 26 of them developed aneurysm (83.9%). The mean area of aneurysm was 33.4% ± 2.4% of the left ventricle. LVEF markedly decreased after LVA formation, whereas LVEDV, LVESV and the thickness of IVS as well as the dimension of ventricular chamber from apex to mitral valve annulus significantly increased. LVESP immediately dropped after ligation and recovered to a small extent after LVA formation. LVEDP progressively increased after ligation till LVA formation. Areas in the LV that underwent fibrosis included the apex, anterior wall and lateral wall but not IVS. Agar intra-chamber cast showed that the bulging of LV wall was prominent in the area of aneurysm. Conclusions Ligation of LAD and Cx at the middle portion could induce development of LVA at a mean area ratio of 33.4% ± 2.4% which involves the apex, anterior wall and lateral wall of the left ventricle.
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