title: Chronic right ventricular pressure overload results in a hyperplastic rather than a hypertrophic myocardial response.
abstract: Myocardial hyperplasia is generally considered to occur only during fetal development. However, recent evidence suggests that this type of response may also be triggered by cardiac overload after birth. In congenital heart disease, loading conditions are frequently abnormal, thereby affecting ventricular function. We hypothesized that chronic right ventricular pressure overload imposed on neonatal hearts initiates a hyperplastic response in the right ventricular myocardium. To test this, young lambs (aged 2-3 weeks) underwent adjustable pulmonary artery banding to obtain peak right ventricular pressures equal to left ventricular pressures for 8 weeks. Transmural cardiac tissue samples from the right and left ventricles of five banded and five age-matched control animals were studied. We found that chronic right ventricular pressure overload resulted in a twofold increase in right-to-left ventricle wall thickness ratio. Morphometric right ventricular myocardial tissue analysis revealed no changes in tissue composition between the two groups; nor were right ventricular myocyte dimensions, relative number of binucleated myocytes, or myocardial DNA concentration significantly different from control values. In chronic pressure overloaded right ventricular myocardium, significantly (P < 0.01) more myocyte nuclei were positive for the proliferation marker proliferating cellular nuclear antigen than in control right ventricular myocardium. Chronic right ventricular pressure overload applied in neonatal sheep hearts results in a significant increase in right ventricular free wall thickness which is primarily the result of a hyperplastic myocardial response.
authors.affiliation: Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands.
authors.forename: Boudewijn P J
authors.initials: BP
authors.lastname: Leeuwenburgh
authors.forename: Willem A
authors.initials: WA
authors.lastname: Helbing
authors.forename: Arnold C G
authors.initials: AC
authors.lastname: Wenink
authors.forename: Paul
authors.initials: P
authors.lastname: Steendijk
authors.forename: Roos
authors.initials: R
authors.lastname: de Jong
authors.forename: Enno J
authors.initials: EJ
authors.lastname: Dreef
authors.forename: Adriana C
authors.initials: AC
authors.lastname: Gittenberger-de Groot
authors.forename: Jan
authors.initials: J
authors.lastname: Baan
authors.forename: Arnoud
authors.initials: A
authors.lastname: van der Laarse
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D009202:Cardiomyopathies / Q000209:etiology* / Q000503:physiopathology; D006352:Heart Ventricles; D006965:Hyperplasia; D007150:Immunohistochemistry; D008026:Ligation; D023421:Models, Animal; D032383:Myocytes, Cardiac / Q000473:pathology*; D011651:Pulmonary Artery; D012756:Sheep; D017725:Ventricular Pressure