Tricuspid Valve Anatomy
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The right atrioventricular valve complex (the tricuspid valve) is made up of the 3 valve leaflets, the annulus, the supporting chordae tendineae, and the papillary muscles. The atrial and ventricular masses, conduction system tissue, and support structure of the fibroelastic cardiac skeleton allow coordinated actions of the tricuspid valve. [1] See the following images.
The tricuspid valve is often called the “forgotten valve” or “lost valve,” because it is understudied relative to the other cardiac valves; variations in anatomic structures have been reported in the literature. The tricuspid valve has been described as having as few as 2 and as many as 6 leaflets, [2] whereas the papillary muscles have been reported to number from 2 to 9. [3]
The tricuspid valve is located between the right atrium and right ventricle and has a valve area of 4-6 cm 2 (see the following image and video). [4] The valve is nearly vertical and is approximately 45° to the sagittal plane. The valve itself is slightly inclined to the vertical so that the margins of the valve are anterosuperior, inferior, and septal, and the cusps take their name from these attachment sites. [1]
The anterosuperior (anterior or infundibular) cusp is the largest cusp of the 3 and is located between the conus arteriosus and atrioventricular orifice. The posterior (marginal) cusp is the next largest cusp and is named for its relative posterior position and is connected to the posterior aspect of the right ventricle. The third and smallest cusp, the septal (medial) cusp, is attached to the right and left fibrous trigones and the atrial and ventricular septa. These fibrous attachments make the septal cusp relatively immobile; therefore, most of the tricuspid annular descent takes place along the margins of the anterior and posterior cusps. [1, 4] During diastole, the major cusps (anterior and posterior) move like sails and meet to join the smaller septal leaflet. Thus, functionally, the tricuspid valve acts more like a bicuspid valve. [1]
The tricuspid subvalvular apparatus consists of anterior, posterior, and septal papillary muscles and their true chordae tendineae. False chordae can connect 2 papillary muscles, connect a papillary muscle to the ventricular wall, or connect points on the ventricular walls. The true chordae typically originate from the apical third of the papillary muscle but can originate from the ventricular walls, as is the case for the septal leaflet.
The anterior papillary muscle is the largest, the posterior is often bifid or trifid, and the septal is the smallest. These papillary muscles supply the chordae for the adjacent components of the cusps they support. The anterior papillary muscle provides chordae to the anterior only or the anterior and septal leaflet; the posterior papillary muscle provides chordae to the posterior and septal leaflets; and the septal papillary provides chordae to the septal and anterior leaflets. [5] Characteristically, the septal leaflet is also supported by chordae that arise from the ventricular septum. [1, 4, 6] .
Functionally, the papillary muscles contract just prior to the onset of right ventricular systole so as to increase tension in the chordae tendinae and maximize coaptation of the 3 cusps, thereby reducing regurgitation across the tricuspid valve. [7]
The tricuspid valve is formed in weeks 5-6 of embryonic development. After the atrioventricular (AV) endocardial cushions fuse, each atrioventricular orifice is surrounded by local proliferations of mesenchymal tissue, from which the AV valves form and are attached to the ventricular wall by muscular cords. Finally, muscular tissue in the cords degenerates and is replaced by dense connective tissue with the valve itself covered by endocardium. [8]
The following image shows the AV valve leaflet and its attachment to the fibrous skeleton of the heart. The AV valve leaflet is formed by a fold or duplication of the endocardium; a dense connective tissue core forms the central part of the valve leaflet. The upper or atrial surface of the valve is thick and resembles atrial endocardium, and the lower or ventricular surface of the valve is thin and resembles ventricular endocardium.
Ebstein anomaly occurs in approximately 1 in 200,000 live births, accounts for less than 1% of all congenital heart diseases, and is associated with maternal lithium use during the first trimester of pregnancy. Ebstein anomaly is characterized by the following [9] : (1) adherence of the septal and posterior leaflets to the underlying myocardium; (2) apical displacement of the functional annulus; (3) dilatation of the “atrialized” portion of the right ventricle with thinning of the wall; (4) redundancy, fenestration, and tethering of the anterior leaflet; and (5) dilatation of the true tricuspid annulus. (See Ebstein Anomaly.)
Tricuspid atresia may be defined as a congenital absence or agenesis of the tricuspid valve; this is the third most common cause of cyanotic congenital heart defects. There are 6 forms of tricuspid atresia with differing underlying anatomic pathology; see Tricuspid Atresia for more information.
Congenital tricuspid stenosis has several manifestations. The tricuspid valve may have incompletely developed leaflets, shortened or malformed chordae, small annuli, abnormal size and number of the papillary muscles, or any combination of these defects. [10] Congenital tricuspid stenosis is rare and is usually associated with other anomalies, such as severe pulmonary stenosis or atresia and secondary hypoplasia of the right ventricle. [11, 10]
Congenital cleft of the anterior leaflet of the tricuspid valve is rare and usually associated with perimembranous ventricular septal defects, pulmonary stenosis, or atrial septal defects. [12]
Gray H. Standring S, ed. Gray’s Anatomy: The Anatomical Basis of Clinical Practice. 39th ed. Edinburgh, UK: Churchill Livingstone Elsevier; 2005. 1003-4.
Wafae N, Hayashi H, Gerola LR, Vieira MC. Anatomical study of the human tricuspid valve. Surg Radiol Anat. 1990. 12(1):37-41. [Medline].
Aktas EO, Govsa F, Kocak A, Boydak B, Yavuz IC. Variations in the papillary muscles of normal tricuspid valve and their clinical relevance in medicolegal autopsies. Saudi Med J. 2004 Sep. 25(9):1176-85. [Medline].
Rogers JH, Bolling SF. The tricuspid valve: current perspective and evolving management of tricuspid regurgitation. Circulation. 2009 May 26. 119(20):2718-25. [Medline].
Martinez RM, O’Leary PW, Anderson RH. Anatomy and echocardiography of the normal and abnormal tricuspid valve. Cardiol Young. 2006 Sep. 16 Suppl 3:4-11. [Medline].
Shah PM. Tricuspid valve, pulmonary valve, and multivalvular disease. Fuster V, O’Rourke RA, Walsh RA, Poole-Wilson P, eds. Hurst’s The Heart. 12th ed. New York, NY: McGraw-Hill; 2008. Chapter 78.
Xanthos T, Dalivigkas I, Ekmektzoglou KA. Anatomic variations of the cardiac valves and papillary muscles of the right heart. Ital J Anat Embryol. 2011. 116 (2):111-26. [Medline].
Sadler TW. Langman’s Medical Embryology. 11th ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2009.
Attenhofer Jost CH, Connolly HM, Dearani JA, Edwards WD, Danielson GK. Ebstein’s anomaly. Circulation. 2007 Jan 16. 115(2):277-85. [Medline].
Mancini MC. Tricuspid stenosis. Medscape Reference. July 29, 2008. [Full Text].
Mancini MC. Tricuspid atresia. Medscape Reference. May 26, 2011. [Full Text].
Lokhandwala YY, Rajani RM, Dalvi BV, Kale PA. Successful balloon valvotomy in isolated congenital tricuspid stenosis. Cardiovasc Intervent Radiol. 1990 Dec. 13(6):354-6. [Medline].
Okutan H, Yavuz T, Bilgin S, Düver H, Kutsal A. Congenital cleft of anterior tricuspid leaflet in adolescent. Asian Cardiovasc Thorac Ann. 2002 Sep. 10(3):262-3. [Medline].
Nyal E Borges, MD Hugh Jackson Morgan Chief Resident, Instructor of Medicine, Department of Medicine, Vanderbilt University Medical Center
Nyal E Borges, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, Phi Kappa Phi
Disclosure: Nothing to disclose.
John A McPherson, MD, FACC, FACP Professor of Medicine, Sol and Marvin Rosenblum Chair in Medical Education, Vice-Chair for Education, Department of Medicine, Vanderbilt University Medical Center
John A McPherson, MD, FACC, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, Association of Program Directors in Internal Medicine
Disclosure: Nothing to disclose.
Richard A Lange, MD, MBA President, Texas Tech University Health Sciences Center, Dean, Paul L Foster School of Medicine
Richard A Lange, MD, MBA is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, Association of Subspecialty Professors
Disclosure: Nothing to disclose.
Michael A Barnett, MD Fellow, Division of Cardiovascular Medicine, Vanderbilt University Medical Center
Disclosure: Nothing to disclose.
The author would like to acknowledge Arthur Dalley II, PhD, Professor and Director of the Medical Gross Anatomy Program and Facilities, Vanderbilt University School of Medicine, for his contributions to this article.
The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author John A McPherson, MD, FACC, FSCAI, to the development and writing of this article.
Tricuspid Valve Anatomy
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