Anatomy and Function of the Heart Valves What are heart valves? The four heart valves include the following: tricuspid valve: located between the right atrium and the right ventricle pulmonary valve: located between the right ventricle and the pulmonary artery mitral valve: located between the left atrium and the left ventricle aortic valve: located between the left ventricle and the aorta How do the heart valves function?
The following is a step-by-step illustration of how the valves function normally in the left ventricle: After the left ventricle contracts, the aortic valve closes and the mitral valve opens, to allow blood to flow from the left atrium into the left ventricle.
As the left atrium contracts, more blood flows into the left ventricle. When the left ventricle contracts again, the mitral valve closes and the aortic valve opens, so blood flows into the aorta.
What is heart valve disease? Heart valves can have one of two malfunctions: Regurgitation- the valve s does not close completely, causing the blood to flow backward instead of forward through the valve.
The reason why we need we need valves in our heart is because the valves in our heart will open and close. When the valves in our heart open, they allow blood to go into places in our body where blood is needed. When the blood passes through, the valve closes. They regulate the blood flow. Ventricle pressure withing the heart causes the AV valves to open and when the blood pressure exerted on their atrial side is greater then on the ventricle side cause AV valves to close.
Due to pressure changes in different chambers of the heart. For example, when the atria contract, the bicuspid and tricuspid valves open. They get closed, when the ventricles contract. When the ventricles contract the aortic and pulmonary valves open. Aortic and pulmonary valves close, when the ventricles relax.
No, they both close. The valves leading away from the heart aortic and pulmonary valves open. Blood is pumped through the chambers, aided by four heart valves.
The valves open and close to let the blood flow in only one direction. Valves prevent blood from going backward. Valves in general open to allow or close to prevent liquid flow. Heart valves opens to let blood into the heart then close to keep it there so that when the heart muscle contracts and squeezes the blood it is then forced out into the arteries of the body.
Higher pressure on the convex side from the heart contracting than the concave side causes them to open and when the pressure reverses the heart relaxes they close. Higher pressure on the convex side from the heart contracting than the concave side causes them to open. When the pressure reverses the heart relaxes they close. When the heart is relaxed, the AV valves are open and the SL valves are closed. When the heart contracts, the AV valves are closed and the SL valves are open.
It's when the electrical charge is not going through the heart correctly causing the valves to not open and close in sync. The four heart valves are the tricuspid, pulmonary, mitral, and aortic. To keep blood flowing they close between beats so it doesn't drain outThe purpose of the heart valves is to avoid back flow of blood. It is caused by the veins in the heart open and close.
The valves open and close to allow the blood to flow only in only one direction. They wouldn't be able to open and close correctly, resulting in backflow of blood. The blood rushing through the valves as the open and close - thump-thump-thump. Current medical therapy for valve disease treats the symptoms of cardiovascular disease.
For example, some medicines are directed at the important symptoms that result from congestive heart failure, but do not impact the underlying cause or the primary problem, valve disease.
As the genetic and developmental basis of valve malformation and disease is elucidated, opportunities for novel medical therapies will emerge and potentially preclude or delay the need for surgery. Defining regulation of valve tissue maintenance and homeostasis will provide exciting opportunities for cell-based or molecular therapies for valve disease.
Together, the stratified ECM and VIC homeostatic mechanisms underlie valve structure and function and coordinate maintenance of valve tissue throughout a lifetime.
Heart valve disease is characterized by dysregulation of ECM organization and VIC activation with induction of regulatory pathways active in valve development. Valve disease pathogenesis is being elucidated through study of animal models, and a better understanding of these mechanisms will allow the development of novel therapeutics.
Valve structure is dynamic and composed of interacting cells and stratified extracellular matrix. Valve disease has a genetic basis characterized by aberrant developmental programs and maladaptive ECM remodeling. Translational efforts combining basic and clinical research may identify ways to manipulate faulty valve tissue maintenance.
Identify novel pharmacologic therapeutics using developmental pathways to elucidate valve disease pathogenesis. Develop durable valve bioprostheses using a combination of clinical, molecular and engineering approaches. Valve annulus: the support structure of valve tissue, AV valves have rings, SL valves have crowns. Sinus of Valsalva: the arterial pouches within the aortic root that function in coordination with the aortic valve annulus.
We thank Elaine Wirrig for critical reading of the manuscript and advice on figure preparation. Research in K. The authors are not aware of any affiliations, memberships, funding or financial holdings that might be perceived as affecting the objectivity of this review. National Center for Biotechnology Information , U. Annu Rev Physiol.
Author manuscript; available in PMC Oct Robert B. Hinton 1 and Katherine E. Katherine E. Author information Copyright and License information Disclaimer.
Copyright notice. The publisher's final edited version of this article is available at Annu Rev Physiol. See other articles in PMC that cite the published article. Abstract The mature heart valves are made up of highly organized extracellular matrix ECM and valve interstitial cells VIC surrounded by an endothelial cell layer. Keywords: heart, cardiac development, animal models, valve disease.
Open in a separate window. Figure 1. Embryonic origins of valve precursor cells Heart valve cells come from multiple sources in the developing embryo. Molecular regulation of valvulogenesis Several developmentally important signaling pathways have critical functions in endocardial cushion induction and EMT.
Figure 2. Table 1 Mouse mutations in ECM genes associated with heart valve abnormalities. Biomechanics and hemodynamics Valve structure-function relationships provide important insight in understanding mechanisms of valve homeostasis as well as developmental and disease processes.
Table 2 Human mutations in ECM genes associated with heart valve abnormalities. Gene Syndrome Valve phenotype Ref. Valve malformation underlies valve disease Although valve disease has been recognized as a significant cause of morbidity and mortality for a long time, it was not until the s that isolated aortic valve disease in the context of valve malformation was appreciated. Valve histopathology identifies two basic disease processes Valve histopathology tends to conform to one of two patterns, myxomatous change or fibrotic change.
Figure 3. Genetic syndromes and animal models of valve disease Normal heart valve function is dependent on the biomechanical properties of the stratified ECM, and mutations in a variety of ECM genes are associated with human heart valve disease Table 2. Valve disease treatment The treatment of valve disease remains primarily surgical.
Future issues. List of definitions. Acknowledgements We thank Elaine Wirrig for critical reading of the manuscript and advice on figure preparation. Footnotes Disclosure Statement The authors are not aware of any affiliations, memberships, funding or financial holdings that might be perceived as affecting the objectivity of this review.
Literature Cited 1. Schoen FJ. Evolving concepts of cardiac valve dynamics. Armstrong EJ, Bischoff J. Heart valve development: Endothelial cell signaling and differentiation. Circ Res. Bruneau BG. The developmental genetics of congenital heart disease. On the biomechanics of heart valve function. J Biomech. The incidence of congenital heart disease. J Am Coll Cardiol. The epidemiology of valvular heart disease: a growing public health problem.
Heart Fail Clin. Frequency by decades of unicuspid, bicuspid and tricuspid aortic valves in adults having isolated aortic valve replacement for aortic stenosis, with or without associated aortic regurgitation. Anatomy of the human atrioventricular junctions revisited.
Anat Rec. Anderson RH. Clinical anatomy of the aortic root. Misfeld M, Sievers HH. Heart valve macro- and microstructure. Hearts and bones: Shared regulatory mechanisms in heart valve, cartilage, tendon, and bone development. Dev Biol. Zimmerman J, MBailey C. The surgical significance of the fibrous skeleton of the heart.
J Thorac Cardiovasc Surg. The aortic outflow and root: a tale of dynamism and crosstalk. Ann Thorac Surg. Aortic root geometry: pattern of differences between leaflets and sinuses of Valsalva. J Heart Valve Dis. Histological and immunohistochemical studies.
Activated interstitial myofibroblasts express catabolic enzymes and mediate matrix remodeling in myxomatous heart valves. Heart valve development: Regulatory networks in development and disease.
Cell biology of cardiac cushion development. Int Rev Cytol. Lineage and morphogenetic analysis of the cardiac valves. Development of heart valve leaflets and supporting apparatus in chicken and mouse embryos. Dev Dyn. Form and function of developing heart valves: coordination by extracellular matrix growth and signaling.
J Mol Med. Transitions in early embryonic atrioventricular valvular functions correspond with changes in cushion biomechanics that are predictable with tissue composition. Extracellular matrix remodeling and organization in developing and diseased aortic valves. Human semilunar cardiac valve remodeling by activated cells from fetus to adult. Origin and fate of cardiac mesenchyme.
Genetic fate mapping demonstrates contribution of epicardium-derived cells to the annulus fibrosis of the mammalian heart. Epicardium-derived cells contribute a novel population to the myocardial wall and the atrioventricular cushions.
Neural crest cells retain multipotential characteristics in the developing valves and label the cardiac conduction system. Bmp2 is essential for cardiac cushion epithelial-mesenchymal transition and myocardial patterning.
Beta-catenin is required for endothelial-mesenchymal transformation during heart cushion development in the mouse. J Cell Biol. Notch promotes epithelial-mesenchymal transition during cardiac development and oncogenic transformation. Genes Dev. Epithelial-Mesenchymal transition: At the crossroads of development and tumor metastasis. Dev Cell. Twist1 function in endocardial cell proliferation, migration, and differentiation during heart valve development.
Shared gene expression profiles in developing heart valves and osteoblasts. Physiol Genomics. Role of NF-ATc transcription factor in morphogenesis of cardiac valves and septum.
The transcription factor NF-ATc is essential for cardiac valve formation. Wnt signaling in heart valve development and osteogenic gene induction. Atrioventricular valve development during late embryonic and postnatal stages involves condensation and extracellular matrix remodeling. Gross L, Kugel MA. Topographic anatomy and histology of the valves in the human heart. Am J Path. Broom ND. The observation of collagen and elastin structures in wet whole mounts of pulmonary and aortic leaflets.
Ultrastructure of the human aortic valve. Acta Anat Basel ; 98 — Specific regional and directional contractile responses of aortic cusp tissue. Heart valve function: a biomechanical perspective. Aortic valve structure-function correlations: Role of elastic fibers no longer a stretch of the imagination.
Vesely I. The role of elastin in aortic valve mechanics. Disruption of hyaluronan synthase-2 abrogates normal cardiac morphogenesis and hyaluronan-mediated transformation of epithelium to mesenchyme. J Clin Invest. The cspg2 gene, disrupted in the hdf mutant, is required for right cardiac chamber and endocardial cushion formation. Hyperplastic conotruncal endocardial cushions and transposition of great arteries in perlecan-null mice.
Cartilage link protein 1 Crtl1 , an extracellular matrix component playing an important role in heart development. Elastin is an essential determinant of arterial morphogenesis.
Novel arterial pathology in mice and humans hemizygous for elastin. Elastin Haploinsufficiency results in progressive aortic valve malformation and latent valve disease in a mouse model. Periostin is required for maturation and extracellular matrix stabilization of noncardiomyocyte lineages of the heart.
Periostin regulates atrioventricular valve maturation. ColVa1 and ColXIa1 are required for ventricular chamber morphogenesis and heart valve development. Otto CM. Valvular aortic stenosis: disease severity and timing of intervention. Vesely I, Noseworthy R. Micromechanics of the fibrosa and the ventricularis in aortic valve leaflets. Stress variations in the human aortic root and valve: the role of anatomic asymmetry.
0コメント