Growth and remodeling of the left ventricle: A case study of myocardial infarction and surgical ventricular restoration |
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| Affiliation: | 1. Department of Surgery, Division of Adult Cardiothoracic Surgery, UC San Francisco, San Francisco, CA 94121, USA;2. Departments of Mechanical Engineering, UC Berkeley, Berkeley, CA 94720, USA;3. Departments of Thoracic and Cardiovascular Surgery, Biomedical Engineering, Transplantation Center, Cleveland Clinic, Cleveland, OH 44195, USA;4. Departments of Biomedical Engineering, Surgery, Cellular and Integrative Physiology, Indiana University – Purdue, Indianapolis, IN 46202, USA;5. Departments of Mechanical Engineering, Bioengineering, and Cardiothoracic Surgery, Stanford University, Stanford, CA 94305, USA;6. Departments of Mechanical Engineering and Surgery, University of Kentucky, Lexington, KY 40506, USA;1. Department of Electronic and Electrical Engineering, University of Strathclyde, Glasgow, G1 1XW, United Kingdom;2. School of Engineering, University of Glasgow, James Watt South Building, Glasgow G12 8QQ, United Kingdom;1. School of Mechanical Engineering, Faculty of Engineering, Tel Aviv University, Tel Aviv 6997801, Israel;1. School of Mechanical Engineering, Faculty of Engineering, Tel Aviv University, Tel Aviv 6997801, Israel;2. Department of Biomedical Engineering, Stony Brook University, Stony Brook, NY, USA;1. Department of Surgery, University of California, San Francisco, California;2. Department of Bioengineering, University of California, San Francisco, California;3. University of California, San Francisco, California;4. Veterans Affairs Medical Center, San Francisco, California;1. Division of Vascular Surgery, Stanford University, Stanford, Calif;2. Cardiovascular Institute, Stanford University, Stanford, Calif;3. Department of Pediatrics (Cardiology), Stanford University, Stanford, Calif;4. Department of Bioengineering, Stanford University, Stanford, Calif |
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| Abstract: | Cardiac growth and remodeling in the form of chamber dilation and wall thinning are typical hallmarks of infarct-induced heart failure. Over time, the infarct region stiffens, the remaining muscle takes over function, and the chamber weakens and dilates. Current therapies seek to attenuate these effects by removing the infarct region or by providing structural support to the ventricular wall. However, the underlying mechanisms of these therapies are unclear, and the results remain suboptimal. Here we show that myocardial infarction induces pronounced regional and transmural variations in cardiac form. We introduce a mechanistic growth model capable of predicting structural alterations in response to mechanical overload. Under a uniform loading, this model predicts non-uniform growth. Using this model, we simulate growth in a patient-specific left ventricle. We compare two cases, growth in an infarcted heart, pre-operative, and growth in the same heart, after the infarct was surgically excluded, post-operative. Our results suggest that removing the infarct and creating a left ventricle with homogeneous mechanical properties does not necessarily reduce the driving forces for growth and remodeling. These preliminary findings agree conceptually with clinical observations. |
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