Abstract
When a pressure overload is placed on the myocardium, systolic wall stress is initially increased. The increased load, through an unknown mechanism, is a stimulus to the laying down of sarcomeres in parallel, producing concentric hypertrophy. The resulting increased wall thickness “absorbs” the increase in pressure and helps reestablish wall stress at a normal level [1, 2]. Since afterload is a key determinant of ejection performance of the ventricle, this compensation is adaptive, because by normalizing stress, ventricular ejection performance is maintained. However, when the pressure overload is severe and prolonged, muscle dysfunction may occur. Thus, pressure-overload concentric hypertrophy may be either compensatory or pathologic, depending on the clinical situation. The following is a synopsis of current knowledge regarding the effects of pressure overload and hypertrophy on the human left and right ventricles.
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© 1985 Martinus Nijhoff Publishing, Boston
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Carabello, B.A., Grossman, W. (1985). Pressure Overload: Human Studies. In: Levine, H.J., Gaasch, W.H. (eds) The Ventricle. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2599-4_11
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DOI: https://doi.org/10.1007/978-1-4613-2599-4_11
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