Tricuspid Valve Anulus

Whereas the base of the anterior and posterior leaflets is attached to the free wall of the right ventricle, the septal leaflet is inserted into the base of the interventricular septum. This line of leaflet attachment, known as the tricuspid valve anulus, is more a landmark than an actual fibrous ring. This absence of an encircling fibrotic structure explains the large changes in the tricuspid valve’s orifice during the cardiac cycle and its easy dilation in disease. The mobility and size of the tricuspid valve orifice are dependent on the transversely oriented myocardial fibers that surround the atrioventricular valves.¹ Tsakiris and associates² found in a canine model that the size of the tricuspid valve orifice changed continuously during the cardiac cycle. The orifice area contracted (from its maximal diastolic size) by 20% to 30%. Tei and associates³ confirmed these findings in humans by use of echocardiography. In our laboratory, we analyzed an ovine model for the changes in the normal tricuspid valve orifice during the cardiac cycle as detected by the changes in distance between ultrasound crystals placed around the line of insertion of the leaflets (Fig. 79-1).^4,5 The tricuspid valve orifice area expands and contracts twice during the cardiac cycle. Orifice contraction begins during the isovolumic relaxation phase of the cardiac cycle and continues through the first half of diastole. Starting with the beginning of isovolumic contraction, a second contraction occurs during ejection, which reduces the tricuspid valve orifice to its minimum area. This contraction corresponds to closure of the valve completed at the end of isovolumic contraction. The reduction in orifice perimeter is not uniform. The segment of the anulus corresponding to the septal leaflet shortens by 12%, the anterior segment by 15%, and the posterior segment by 17%.⁴ The notion that the length of the septal portion of the anulus can be used to determine the size of an anuloplasty device should be revised.

Figure 79–1 Changes in the normal tricuspid valve during the cardiac cycle. Top, Pressure curves of blood flow in the pulmonary artery (Pulm flow), the right ventricle (RVP), and the pulmonary artery (Pulm P). Bottom, Changes in the areas delineated by the ultrasound transducers placed around the tricuspid anulus (Anulus), the tips of the three papillary muscles (PM), and the free edges of the three leaflets (Leaflets) during two cardiac cycles. These recordings allowed the cardiac cycle to be split into diastole, systole, isovolumic contraction (IVC), and isovolumic relaxation (IVR).

(Reproduced with permission from Jouan J, Pagel MR, Hiro ME, et al. Further information from a sonometric study of the normal tricuspid valve annulus in sheep: geometric changes during the cardiac cycle.⁵)

This narrowing of the tricuspid valve orifice is due not only to contraction of its perimeter but, more important, to changes in the shape of the anulus. During contraction, the orifice becomes more elliptical because of displacement of the anteroposterior commissure toward the septum and the bulging of the septum. As in the mitral valve, the “anulus” is not in a single plane. In fact, the tricuspid valve anulus is saddle shaped, with its horn or pommel corresponding to the area of the anteroseptal commissure and its cantle to the midpoint of the base of the posterior leaflet (Fig. 79-2). This saddle shape or hyperbolic paraboloid, well known to architects as an ideal design to reduce building tension, has been shown in the mitral valve to significantly reduce peak leaflet stress.⁶ Furthermore, the increase in the saddle shape during contraction has a folding, reducing effect on the normal tricuspid valve orifice. In cases of tricuspid regurgitation, besides an increase of tricuspid valve anulus area, there is an increase in planarity or flattening of the normal anulus, which induces leaflet tethering.⁷ Rigid structures, such as stented prostheses and rigid anuloplasty rings, destroy this configuration and (most likely) have a negative impact on the function of the right ventricle.

Figure 79–2 Geometric changes of the normal tricuspid valve anulus during the cardiac cycle. Orthogonal representations of the tricuspid valve anulus at maximum (dotted line) and minimum (continuous line) area during the cardiac cycle. Circles and squares represent the location of transducers at the midpoint of the bases of the anterior (A), posterior (P), and septal (S) leaflets and at the anteroposterior (A-P), anteroseptal (A-S), and posteroseptal (P-S) commissures. Two relative maxima can be noted in the x-z (B) and y-z (C) planes. P and A-S represent the pommel and the cantle of the tricuspid valve’s saddle shape. The representation of the x-y plane is shown in A.

(Reproduced with permission from Jouan J, Pagel MR, Hiro ME, et al. Further information from a sonometric study of the normal tricuspid valve annulus in sheep: geometric changes during the cardiac cycle.⁵)

Leaflets

Although the number of tricuspid valve leaflets varies according to author,⁸ it is generally accepted that the tricuspid valve consists of three leaflets. These three leaflets are known as septal, anterior, and posterior, and they are separated by three clefts or commissures named anteroseptal, anteromedial, and posteroseptal (Fig.79-3A). These clefts do not reach the anulus but delineate small “commissural leaflets.” This is an important surgical point because in cases of fused commissures, their incision should not extend all the way to the anulus; doing so destroys the commissural leaflets. The largest leaflet is the anterior, followed by the posterior, with the septal being the smallest. The excursion of each leaflet (defined as the angle between leaflet free edge and the plane of the anulus) is different.⁵ The excursion of the septal leaflet is significantly smaller than that of the other leaflets. This normal, smaller septal excursion might explain the finding at surgery of a septal leaflet plastered against the septum. This finding, often seen in cases of functional regurgitation, is a sign of severity and a predictor of a poor result after repair.

Figure 79–3 Atrial view of the normal (A), stenotic (B), and insufficient (C) tricuspid valve.

(Reproduced with permission from Duran CMG. Duran ring annuloplasty of the tricuspid valve.⁷⁹)

Chordae Tendineae and Papillary Muscles

The leaflets are held down by marginal and basal chords that arise from three papillary muscle groups. The marginal chords are inserted into the leaflet’s free margin, and the basal chords are inserted into the ventricular surface of the leaflets. Elongation or rupture of the marginal chords results in leaflet prolapse. The tricuspid valve’s basal chords, although far less prominent than the mitral valve’s basal chords, probably play a similar role in maintaining valvular and ventricular geometry. In most tricuspid valve cases, three papillary muscle groups are found and can be identified as anterior, posterior, and septal. Whereas the anterior and posterior muscles are virtually always present, the septal muscle might be absent in 20% of patients. The anterior papillary muscle is the longest; it most often has a single head and sustains the largest number of chordae.^9,10

Terminology

New surgical techniques always demand deeper knowledge of the anatomy of the region and, consequently, more precise terminology. A common set of anatomic definitions is needed to report precise preoperative and postoperative echocardiographic information important to both echocardiologist and surgeon. In an attempt to standardize all anatomic findings, we developed a detailed tricuspid valve terminology that parallels previously described mitral valve nomenclature.¹¹ Although it is based on a surgical, atrial view of the valve, it encompasses all three elements of the tricuspid valve apparatus (i.e., leaflets, chords, and papillary muscles).¹⁰

This alphanumeric system is based on the three papillary muscle groups as defined by the numerals 1 for the anteroseptal, 2 for the posteroseptal, and 3 for the anteroposterior groups of muscles. Each leaflet is identified with the initial letter of its traditional name: S, septal; A, anterior; and P, posterior.

Because the lesion does not often affect the whole leaflet or is limited to the chordae, each leaflet is divided into two areas identified by the papillary origin of the corresponding chords. For instance, the septal leaflet (S) is divided into two halves (S1 and S2), identified by the chords that originate from the anteroseptal papillary muscle¹ or the chords that originate from the posteroseptal papillary muscle.² The commissures (C) are identified by their papillary origin (1, 2, or 3) as C1, C2, and C3. All chords are identified by their papillary origin and leaflet insertion.

Although it is initially confusing, this nomenclature makes it possible to pinpoint the exact location of a lesion and to describe the surgical maneuvers applied. Its use is particularly significant for reporting of chordal disease and chordal replacement.

Anatomic Relationships

The area corresponding to the anteroseptal commissure is very close to the aortic valve’s noncoronary sinus of Valsalva (Fig.79-4). This fact has important surgical implications because placement of anchoring sutures for a tricuspid valve prosthetic device can be difficult at this level if a stented aortic prosthesis is already present. When a concomitant aortic valve replacement is planned, it is preferable to place the tricuspid valve sutures before undertaking the aortic valve replacement because tears at this level can be difficult to repair.

Figure 79–4 Base of the heart showing the anatomic relationships of the tricuspid valve. LC, left coronary; NC, noncoronary; RC, right coronary.

(Reproduced with permission from Duran CMG. Duran ring annuloplasty of the tricuspid valve.⁷⁹)

The right coronary artery and sinus run parallel to the segment of the anulus corresponding to the right ventricular free wall. Despite this proximity, injury to these vascular structures in performing a valve replacement or anuloplasty is extremely rare. The ostium of the coronary sinus is situated above the posteroseptal commissure. Because of its distance from the conducting system (close to the right trigone), it is safe to place a pursestring suture around the ostium of the coronary sinus to hold a retrograde cardioplegia cannula.

Organic Tricuspid Valve Disease

A variety of etiologic factors can induce organic regurgitation, but today, the most frequent cause of organic tricuspid valve disease in urban populations is infective endocarditis (Table 79-1). Tricuspid valve endocarditis used to be relatively rare, with an incidence of only 5% to 10% of patients with infective endocarditis. However, its frequency has dramatically increased with the spread of intravenous drug abuse.¹³ In this population, the tricuspid valve usually has no preexisting pathologic change. The lesions vary from isolated vegetations to total destruction of the valve, including the anulus. Staphylococcus aureus remains the most common organism found in drug addicts, followed by gram-negative organisms and Candida. Fungal infections are also increasing because of longer periods of invasive monitoring of patients with multiorgan failure in intensive care units.

Table 79–1 Causes of Organic Tricuspid Valve Disease

In the developing world, rheumatic fever is the primary cause of organic valvular heart disease. Typical lesions show varying degrees of leaflet thickening and (most often) commissural fusion. In severe cases, the thickened leaflets become diaphragm-like, with a central circular orifice (see Fig. 79-3B). The subvalvular apparatus is seldom affected, and calcifications are rare. Although tricuspid valve stenosis is the classic lesion, predominant insufficiency is just as common. In a series of 253 patients with rheumatic heart disease who underwent tricuspid valve surgery, we found that organic involvement was present in 45% of the cases and that 45% of them also had anulus dilation.¹⁴ In a classic study of 100 postmortem hearts with rheumatic disease, Gross and Friedberg¹⁵ found microscopic evidence of inflammation in the anulus of all four valves (in the acute rheumatic attack). Rheumatic tricuspid valve disease is always associated with rheumatic mitral valve or mitral-aortic valve lesions. The incidence of chronic rheumatic tricuspid valve disease associated with rheumatic mitral valve disease varies widely, from 6% in an echocardiographic study¹⁶ to 33% in an anatomic series¹⁷ and 11% in our series of 1052 patients undergoing rheumatic valvular surgery.¹⁴ In a Mayo Clinic surgical pathology study of excised tricuspid valves at the time of valve replacement,¹⁸ postinflammatory etiology was responsible for 53% of the 363 valves studied. However, this frequency had diminished from 79% during the period from 1963 to 1967 to 24% during 1983 through 1987, reflecting the reduction in the incidence of rheumatic fever in the United States.

Leaflet tears and total or partial avulsion of a papillary muscle head occur after closed chest trauma. They are occasionally diagnosed at surgery and only classified postoperatively as traumatic by the patient, who recalls an old accident when prompted by the surgeon.^19–21

An occasional cause of traumatic tricuspid regurgitation is that induced by the bioptome during a right myocardial biopsy in transplanted patients. Leaflet tears or chordal avulsion results in severe regurgitation that requires urgent surgery.²²

Degenerative tricuspid regurgitation associated with mitral valve prolapse is being increasingly observed. This double valve lesion is particularly frequent in Marfan syndrome as a manifestation of a fibrillopathy that also involves the aortic valve and ascending aorta. The reported frequency of tricuspid valve involvement among patients with mitral valve myxomatous disease oscillates between 21% and 52%.^7,23,24

Less common causes include organic tricuspid valve lesions secondary to carcinoid syndrome and appetite-suppressant drugs.²⁵ In both cases, the leaflets are encased by a fibrous sheath that reduces their mobility, resulting in stenotic and regurgitant lesions. Other rare causes are listed in Table 79-1.^26–28

Functional Tricuspid Regurgitation

Functional tricuspid insufficiency is understood to be exclusively due to anulus dilation and dysfunction (see Fig. 79-3C). The leaflets, chords, and papillary muscles are otherwise normal. Because of the lack of an anatomic fibrous anulus, the tricuspid valve’s anulus follows the dilation of the right ventricle. The total perimeter of the normal anulus is approximately 100 to 120 mm. In cases of functional tricuspid regurgitation, the circumference of the anulus can reach 150 to 170 mm.^29,30 This anulus dilation is nonhomogeneous. In a postmortem study that included normal controls and hearts with rheumatic or myxomatous tricuspid valve disease, Carpentier and colleagues³¹ showed that the anterior and posterior segments of the anulus dilated far more than the septal portion of the anulus (Fig. 79-5). This report formed the basis for all anuloplasties that selectively reduce the whole anulus except at the level of the septum.

Figure 79–5 Diagram of the tricuspid valve anulus showing the normal (inner ellipse) and myxomatous (outer ellipse) valve in centimeters. A, anterior leaflet; P, posterior leaflet; S, septal leaflet.

(From Carpentier A, Deloche A, Hanania G, et al. Surgical management of acquired tricuspid valve disease. J Thorac Cardiovasc Surg 1974;67:55, with permission from Excerpta Medica, Inc.)

In congestive heart failure, functional tricuspid regurgitation is a predictor of poor survival³² and may be an independent risk factor for the development of cardiac cachexia and protein-losing enteropathy.³³ Koelling³⁴ studied a total of 1436 patients with left ventricular systolic dysfunction (ejection fraction <35%). Mitral regurgitation was moderate in 30% and severe in 19%. Moderate tricuspid regurgitation was present in 23% and severe in 12%. Patients with severe mitral regurgitation were more likely also to have tricuspid regurgitation.

Advances in echocardiography have revealed another subvalvular mechanism that applies to both mitral and tricuspid functional regurgitations. Originally observed in functional ischemic mitral regurgitations, it also applies to the ischemic tricuspid valve and most probably to all functional insufficiencies. Right (or left) ventricular remodeling induces a lateral displacement of one or more papillary muscles that apically pulls (through the basal chords) the body of the corresponding leaflet. The leaflet becomes tethered down, losing its coaptation.^7,35

Functional tricuspid regurgitation is an expression of right ventricular failure with a generalized distortion of ventricular geometry. Although anuloplasty can reduce or abolish functional tricuspid regurgitation (by reducing the dilated anulus), it does not address the altered subvalvular geometry. Awareness of this important mechanism is giving rise to new and exciting surgical approaches directed toward redressing the geometric distortion.³⁶