Abstract

Unidirectional blood flow is essential and the primary function of heart valves. Malformation and dysfunction of these complex structures result in potentially fatal pathologies. In this chapter, the formation, anatomy, and histology of the four cardiac valves will be described. These four cardiac valves can be further classified as two atrioventricular (AV) valves and two semilunar valves; however, each valve is unique. The two classes of valves differ in how the valve leaflets are supported when they are undergoing mechanical loading. To prevent regurgitation, the AV valves use a tension apparatus, which is composed of fibrocartilage-containing chordae tendineae (heart strings) and extensions of ventricular myocardium known as papillary muscles. On the other hand, the semilunar or ventriculoarterial valve leaflets are self-supporting, each having three leaflets that collapse onto thickened edges as they snap shut. Despite the differences in the adult cardiac valves, they appear to develop in similar ways. Both the AV and semilunar valve primordia appear early in heart development as acellular swellings between the primitive myocardium and the endocardium. These swellings or cushions are filled with proteoglycans and glycosaminoglycans making them jelly-like in consistency. During development, genetic and mechanical factors shape and remodel the soft cardiac cushions into tough, complex, fibrous tissues that are capable of withstanding the increasing demand as adult physiology is achieved. Increasing evidence supports a fundamental role for mechanical forces in the formation and homeostasis of valve tissues. However, much remains unknown about the specific molecular mechanisms that transduce the various forces which the valves are subjected to during the cardiac cycle. Defining these mechanisms will be a key in the development of new replacement valve technologies and novel therapeutic approaches to treating malformations and dysfunctions of cardiac valves.

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