Abstract
The process of left ventricular remodeling after acute myocardial infarction involves alterations in the topography of both infarcted and noninfarcted ventricular regions (1). In the infarcted area, infarct expansion with regional dilation and thinning of the infarct zone occur within 1 day after myocardial infarction (2). The myocardium remote from the area of infarction is subjected to increased diastolic wall stress (2, 3), resulting in myocyte slippage (3) as well as myocyte hypertrophy (4). The myocardial hypertrophy exhibits characteristics of combined pressure and volume overload (4, 5).
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Matsubara, H. et al. (1996). Regulation of Gene Transcription of Angiotensin II Receptor Subtypes in the Heart. In: Raizada, M.K., Phillips, M.I., Sumners, C. (eds) Recent Advances in Cellular and Molecular Aspects of Angiotensin Receptors. Advances in Experimental Medicine and Biology, vol 396. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-1376-0_3
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