Abstract
Pressure and/or volume overload has been regarded in the past as the leading mechanism through which an increase in blood pressure may trigger the development of left ventricular hypertrophy1. However, studies performed in recent years both in experimental animals and in man have suggested that not only mechanical but also sympathetic, genetic and hormonal factors (e.g. angiotensin II, insulin, thyroid hormones, etc) may significantly contribute to the development of the cardiac structural alterations frequently detected in the clinical course of the hypertensive state2,3.
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Grassi, G., Seravalle, G., Mancia, G. (1997). Left Ventricular Hypertrophy and Sympathetic Activity. In: Zanchetti, A., Devereux, R.B., Hansson, L., Gorini, S. (eds) Hypertension and the Heart. Advances in Experimental Medicine and Biology, vol 432. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5385-4_18
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DOI: https://doi.org/10.1007/978-1-4615-5385-4_18
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