Abstract
… grossly the infarct of the heart wall is primarily a large area of congestion which undergoes the change described as coagulation necrosis. The area gradually undergoes decolorization, becomes smaller, more sharply defined, removed from the site of arterial occlusion and is accompanied by thinning of the heart wall in the late stages. There is only a rare zone of reactionary hyperemia; fibrosis appears first in the margins and finally extends throughout the infarct [1].
The term remodeling is frequently used in broad context in describing the infarcted heart and therefore can create confusion. It would appear timely to suggest a refinement in terminology. The following is proposed with a view toward specifying the nature of remodeling under consideration. Geometric remodeling, for example, refers to the heart’s solid geometry — the three-dimensional configuration of its ventricles. This includes the size and shape of a ventricular chamber or the thickness of its wall. Following myocardial infarction (MI) the left ventricle may dilate, its normally elliptical shape may become more spherical, the infarcted segment initially thinned and the scar ultimately contracted [2, 3]. Structural remodeling connotes an alteration in microscopic structure of the myocardium. Following MI, this might include the hypertrophy of viable cardiac myocytes, an atrophy of myocytes encased in fibrillar collagen at the interface between viable and scarred tissues, and various morphologic expressions of fibrous tissue formation that appear at and remote to the MI [4]. Studies of structural remodeling have largely focused on results and consequences of cardiac myocyte injury [5]. Biochemical remodeling addresses alterations in the chemical composition of constituent myocytes (eg., contractile proteins isoforms, high energy phospate stores). as reviewed elsewhere in this text.
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© 1996 Birkhäuser Verlag Basel/Switzerland
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Weber, K.T., Sun, Y., Cleutjens, J.P.M. (1996). Structural remodeling of the infarcted rat heart. In: Karmazyn, M. (eds) Myocardial Ischemia: Mechanisms, Reperfusion, Protection. EXS, vol 76. Birkhäuser Basel. https://doi.org/10.1007/978-3-0348-8988-9_30
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