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Left ventricular function declined with the onset of failure. Left ventricular myocyte volume increased 27% exclusively because of myocyte lengthening (29% increase). The onset of left ventricular failure resulted in a 72% increase in right ventricular myocyte volume. Right ventricular myocyte growth, however, was proportional, with a 23% increase in myocyte length and 18% increase in myocyte width. Changes in left ventricular myocyte shape were virtually identical to data collected previously from patients with similar disease, suggesting that this is a relevant animal model. Evidence suggests that left ventricular myocyte transverse growth is defective because dilation and failure were associated with cell lengthening, without a change in myocyte diameter. Although severe hypertrophy was present in the right ventricle as a result of left ventricular failure, myocyte growth was proportional, suggesting that cell shape was properly regulated in this chamber.<\/jats:p>","DOI":"10.1161\/01.hyp.28.4.609","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:53:46Z","timestamp":1339462426000},"page":"609-614","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":51,"title":["Myocyte Remodeling During the Progression to Failure in Rats With Hypertension"],"prefix":"10.1161","volume":"28","author":[{"given":"A. Martin","family":"Gerdes","sequence":"first","affiliation":[{"name":"the Department of Anatomy and Structural Biology, University of South Dakota, College of Medicine, Vermillion, and the Department of Food Science and Technology, Ohio State University, Columbus (S.A.M.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tatsuyuki","family":"Onodera","sequence":"additional","affiliation":[{"name":"the Department of Anatomy and Structural Biology, University of South Dakota, College of Medicine, Vermillion, and the Department of Food Science and Technology, Ohio State University, Columbus (S.A.M.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xuejun","family":"Wang","sequence":"additional","affiliation":[{"name":"the Department of Anatomy and Structural Biology, University of South Dakota, College of Medicine, Vermillion, and the Department of Food Science and Technology, Ohio State University, Columbus (S.A.M.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sylvia A.","family":"McCune","sequence":"additional","affiliation":[{"name":"the Department of Anatomy and Structural Biology, University of South Dakota, College of Medicine, Vermillion, and the Department of Food Science and Technology, Ohio State University, Columbus (S.A.M.)."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0046-8177(75)90003-9"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1536\/ihj.25.955"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.49.6.1153"},{"key":"e_1_3_2_4_2","unstructured":"Dodge HT Stewart DK Frimer M. 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