The study details the collagenous skeleton of human mitral papillary muscles, highlighting how fibrosis in hypertensive hearts may impair contractile capabilities and electrical conductance, contributing to heart failure.
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May contribute to contractile and conduction deficits in hypertension; animal data leaves open human anti-fibrotic targets.
The papillary muscles (PM) of the heart have been the subject of numerous structural and functional studies. However, despite the importance of the collagenous compartment of the heart in the mechanical and electrical properties of the myocardium, little information is available on the structural organization of collagen within the PM. We study here the structural organization of collagen within the mitral papillary muscles (PM) of the human heart. Fragments of human mitral PM from normal and hypertensive subjects were macerated in NaOH to eliminate the cellular components. Macerated and nonmacerated samples were then studied with the scanning electron microscope (SEM). SEM shows that cardiac myocytes and endomysial capillaries are ensheathed in a layer of collagenous tissue. The myocyte sheath wall is formed by thin collagen fibers oriented at right angles to the main cell axis. These sheaths are open structures, collagen fibers continuing into adjacent sheaths at the points of lateral communications. Thick perimysial septa do not divide the PM tissue into separate compartments. Hypertensive hearts show perivascular and interstitial fibrosis. In addition, the lumen of the coronary vessels is reduced or obliterated, and large areas of the myocardium are substituted by densely packed collagen. Endomysial sheaths constitute a continuous collagenous layer that replicates the myocyte network. The endomysium should play a complex role in myocardial mechanics, assuring the equal distribution of force during the cardiac cycle. The absence of insulating boundaries should facilitate lateral propagation of excitation. Fibrosis in hypertensive hearts appears to be both reactive and reparative. The increase in the amount of collagen should greatly impair contractile capabilities and electrical conductance, severely compromise heart function, and contribute to development of heart failure.
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Icardo et al. (1998) studied this question.
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