It is still unclear what initiates the degenerative cellular changes in the mitral valve and myocardium that lead to disease. The dominate theories for mechanisms underlying IMR include: (i) imbalance of leaflet tethering and closing force, (ii) left ventricular remodeling, (iii) left ventricular dysfunction, (iv) dyssynchrony of the left ventricular electromechanical activity and (v) changes in spatial structure of the annulus. According to previous reports, the incidence of IMR can increase to (i) 40% after myocardial infarction, (ii) 20% during coronary artery disease and (iii) 50% during congestive heart failure. IMR is an important clinical cardiovascular problem as it is one of the most common complications associated with myocardial infarction resulting from changes in left ventricular structure and function. Ischemic mitral regurgitation (IMR) is characterized by the backflow of blood from the left ventricle into the left atrium of the heart. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Ĭompeting interests: The authors have declared that no competing interests exist. All relevant data are included within the paper and its Supporting Information files.įunding: This work is sponsored by the Beijing Science and Technology Committee (Project No: Z101107052210004) and Natural Science Foundation of China (Project No: 81370190). This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.ĭata Availability: The authors confirm that, for approved reasons, some access restrictions apply to the data underlying the findings. Received: MaAccepted: OctoPublished: December 5, 2014Ĭopyright: © 2014 Cui et al. PLoS ONE 9(12):Įditor: Kathrin Eller, Medical University of Graz, Austria (2014) A Pig Model of Ischemic Mitral Regurgitation Induced by Mitral Chordae Tendinae Rupture and Implantation of an Ameroid Constrictor. ![]() The pathological features of this pig IMR model were found to mimic the natural history and progression of IMR in patients.Ĭitation: Cui Y-C, Li K, Tian Y, Yuan W-M, Peng P, Yang J-Z, et al. We have developed a pig model of IMR using the posterior mitral chordae tendineae rupture technique and implantation of an ameroid constrictor. Transmission electron microscopy highlighted the presence of contraction bands and edema surrounding the ischemia area, including inflammatory cell infiltration within the ischemic area. ![]() Pathological changes were observed in the heart, which included scar tissue in the ischemic central area of the LV. LV end diastolic and systolic volumes as well as LA end diastolic and systolic volume were also significantly higher in pig hearts post-operation when compared to baseline. ![]() Echocardiography and MRI further detected a gradual increase in LA and LV volumes from two weeks post-operation. ECG analysis highlighted an increase in the diameter of the left atria (LA) at two weeks post-operation as well as ischemic changes in the left ventricle (LV) and LA wall at four weeks post-operation. Angiographic analyses revealed that the LCX closure was 10–20% at one week, 30–40% at two weeks and 90–100% at four weeks subsequent ameroid constrictor implantation. Blood velocity of the mitral regurgitation was found to be between medium and high levels. X-ray coronary angiography, ECG analysis, echocardiography, and magnetic resonance imaging (MRI) were used to evaluate heart structure and function in pigs at baseline and one, two, four and eight weeks after the operation. A 2.5-mm ameroid constrictor was placed around the left circumflex coronary artery (LCX) of male Tibetan miniature pigs to induce ischemia, while the posterior mitral chordae tendinae was also ruptured. ![]() A miniature pig model of ischemic mitral regurgitation (IMR) was developed by posterior mitral chordae tendinae rupture and implantation of an ameroid constrictor.
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