Download Imaging Evaluation of Tricuspid Valve: Analysis of Morphology and

C a r d i o p u l m o n a r y I m a g i n g • R ev i ew
Saremi et al.
Imaging Evaluation of Tricuspid Valve
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Cardiopulmonary Imaging
Review
Imaging Evaluation of Tricuspid
Valve: Analysis of Morphology and
Function With CT and MRI
Farhood Saremi1
Cameron Hassani1
Victoria Millan-Nunez 2
Damián Sánchez-Quintana3
Saremi F, Hassani C, Millan-Nunez V,
Sánchez-Quintana D
OBJECTIVE. In this article we show the morphologic detail of the tricuspid valve (TV)
apparatus and discuss the spectrum of diagnostic information that CT and MRI can provide
regarding pathologic processes. We also compare the strengths and limitations of these modalities with currently established echocardiographic diagnostic parameters.
CONCLUSION. The TV plays an important role in a number of pathologic states, and
its abnormality can directly or indirectly influence morbidity and mortality in different cardiac disorders. However, the importance of the role of the TV has been overlooked primarily
because TV malfunction may remain less symptomatic for a long time. Along with rapid development in imaging technology, improvement in postoperative management, and better understanding of the pathophysiologic mechanisms of TV dysfunction, more attention is being
given to careful imaging analysis of this “forgotten valve.”
T
Keywords: CT, MRI, tricuspid dysfunction, tricuspid valve
DOI:10.2214/AJR.14.13551
Received July 22, 2014; accepted after revision
September 14, 2014.
Presented at the 2014 annual meeting of the Radiological
Society of North America, Chicago, IL.
1
Department of Radiology, University of Southern
California, USC Keck Hospital, 1500 San Pablo St,
Los Angeles, CA 90033. Address correspondence to
F. Saremi ([email protected]).
2
Department of Cardiovascular Medicine, Hospital
Infanta Cristina, University of Extremadura,
Extremadura, Badajoz, Spain.
3
Department of Anatomy, Faculty of Medicine, University
of Extremadura, Extremadura, Badajoz, Spain.
WEB
This is a web exclusive article.
AJR 2015; 204:W531–W542
0361–803X/15/2045–W531
© American Roentgen Ray Society
he tricuspid valve (TV) plays an
important role in a number of
pathologic states, and its abnormality may directly or indirectly
influence morbidity and mortality in many
clinical scenarios involving right or left heart
diseases [1, 2]. In this regard, the unique morphology of the TV apparatus plays a crucial
role, and understanding anatomic changes of
the TV has helped to explain the pathophysiologic mechanisms of different clinical presentations [1]. The primary imaging of choice for
the TV is echocardiography. Because tricuspid dysfunction is often associated with other
cardiac abnormalities, especially left heart
diseases that are a common indication for cardiac MRI or CT, understanding the spectrum
of imaging findings in TV abnormalities can
improve CT and MRI interpretation and may
be crucial for clinical management of patients.
In this article, we review the roles of CT and
MRI in the assessment of anatomy and morphologic changes of the tricuspid apparatus
and describe the important functional parameters of the TV under normal circumstances
and in patients with functional and structural
TV abnormalities.
Morphology
Normal Tricuspid Apparatus
The septal leaflet of the TV, aortic leaflet of the mitral valve, and atrioventricular
fibrous continuity between these valves develop from the mesenchyme of the inferior and superior atrioventricular endocardial
cushions [3]. Later, the tricuspid septal leaflet delaminates from the muscular ventricular septum. The mural leaflets, including the
anterior and posterior (inferior) leaflets of
the TV and the posterior leaflet of the mitral
valve, are mainly derived from mesenchymal cushions that arise laterally in the atrioventricular canal after cushion fusion [3–5].
A complete failure of development of the
atrioventricular cushions results in atrioventricular canal defect with variable degrees of
insufficiency, whereas incomplete resorption
of the myocardial tissue on the TV septal
leaflet can result in Ebstein anomaly or accessory conduction pathways [5].
The TV apparatus consists of the leaflets, fibrous annulus, and supporting tension
apparatus, the latter consisting of the chordae tendineae (tendinous chords) and papillary muscles (PMs) (Fig. 1). The leaflets
include anterior (superior), septal, and posterior (inferior) [6, 7]. The PMs include anterior, posterior, and sometimes medial (septal) leaflets. The posterior leaflet appears to
be of lesser functional significance because
it can be removed without impairment of
valve function. The septal leaflet is smaller
than the anterior leaflet and arises medially directly from the tricuspid annulus above
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Saremi et al.
the interventricular septum. The commissure between the septal and anterior leaflets
is located over the membranous septum and
divides it into the atrioventricular and interventricular components [7, 8] (Fig. 2). The
anterior PM provides chordae to the anterior
and posterior leaflets, and the posterior PM
provides chordae to the posterior and septal
leaflets. The septal PM of the conus or right
ventricular (RV) septal wall provides chordae to the anterior and septal leaflets. It represents an important surgical landmark for
location of the right bundle branch to avoid
injury during surgical correction of certain
types of ventricular septal defects (VSDs).
Tricuspid Annulus
The normal tricuspid annulus has an elliptical shape and appears nonplanar, with the
posteroseptal portion “lowest” (toward the
apex) [1] (Fig. 3). As a result of this inferior
migration of the septal leaflet, the distance
between the mitral and tricuspid leaflets is
maximum where posterior cardiac crux is located [7] (Fig. 2). In this region, also known
as the muscular interventricular septum, the
cavity of the right atrium is separated from
that of the left ventricle by invagination of the
atrioventricular junction myocardial walls,
which are filled with epicardial fibrofatty tissue where the atrioventricular nodal artery
passes. Therefore, this is not a true muscular atrioventricular septum [8]. An important
consideration regarding the structure of the
TV annulus that makes it different from the
mitral annulus is the lack of extensive fibrous
elements in the peripheral (mural) part of the
valve to support its leaflets [8].
Imaging of the Tricuspid Valve
Apparatus Morphology
Compared with the mitral valve, which
can be optimally evaluated in most routine
coronary CT angiography (CTA) studies, visualization of the right atrioventricular junction in detail can be challenging. Clear depiction of this region requires homogeneous
enhancement of the structures around the TV
annulus. Most ECG gated or triggered cardiac CTA techniques modified for the right
heart examination (i.e., 50% contrast agent
and saline chase in routine coronary CTA)
can provide good-quality motion-free images of the RV outlet and trabeculated portions.
However, the quality may not be high enough
to show the details of the RV inlet [9]. This
is mainly because of inhomogeneous enhancement of the right atrium and steak ar-
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tifacts arising from high-attenuation superior vena cava contrast enhancement when
mixed with unenhanced blood of the inferior vena cava. The right atrial artifacts may
be decreased when injections are performed
through the femoral vein. The best results,
however, may be obtained with simultaneous injection of contrast agent in both femoral and antecubital veins [10]. Although
semiinvasive, the latter technique provides
the quality required to assess the anatomy of
the TV valve and associated structures, including the triangle of Koch and the cavotricuspid isthmus. Nevertheless, all these techniques for evaluation of small abnormalities,
such as vegetation and leaflet deformities,
can be difficult and unreliable.
One advantage of CT is that it can show
the extent of calcifications in this region. Degenerative calcium deposition in the TV annulus is relatively rare compared with the mitral annulus, likely because of an incomplete
fibrous ring on the right side. Reported calcifications are usually secondary to diffuse
cardiac calcinosis in chronic dialysis patients
and in patients with inflammatory processes,
such as rheumatic heart disease [11]. Some
additional potential advantages of CT are
that it enables evaluation of TV annuloplasty ring dislodgement and helps identify inappropriate position of the RV pacemaker lead
at the TV level and related complications.
MRI can be useful for assessing TV annulus size and shape changes with the cardiac
cycle [12, 13]. Compared with real-time 3D
echocardiography, MRI is accurate in measurements of tricuspid annular area and fractional shortening or area change [13].
Because of the nonplanar morphology of
the TV, it may be difficult to show all three
leaflets in one short-axis plane. Three-dimensional echocardiography can show all
leaflets through an endoscopic view [14].
However, deriving accurate and reliable
quantitative data from these images is difficult. Although endoscopic views of the RV
including the TV annulus with CT are possible, CT would still be technically limited in
showing all TV leaflet positions at a specific
time frame of the cardiac cycle [9]. The septal leaflet can be best assessed in four-chamber views (Fig. 2). In some cases, small defects of the membranous septum can only be
seen in this projection. In this regard, MRI
also provides not only data about the anatomy of this region but also the existence of
any shunt can be shown using cine or phase
contrast MRI. Measurements of the septal
isthmus width and visualization of its relation with the coronary sinus orifice and the
atrioventricular node artery are generally
simple on good-quality four-chamber cardiac CT images. Evaluation of TV prolapse
also would be easier on long-axis views.
Two-chamber CT of the right heart can show
the relationship of the anterior and posterior leaflets. It is the optimum view to measure the cavotricuspid isthmus superior to
the hinge of posterior TV leaflet. Visualization of the posterior TV leaflet is technically challenging in transthoracic echocardiography, but this leaflet is easy to visualize on
CT or MRI. Congenital defects in valve leaflets also are difficult to show, but with goodquality CT, clefts in the tricuspid leaflet may
be detectable. The degree of tricuspid leaflet
migration in Ebstein anomaly will be shown
by CT and MRI. In most congenital heart
diseases (CHDs), both MRI and CT provide
comprehensive data and show recurrent or
neglected abnormalities.
Tricuspid Valve Annulus Measurements
In healthy subjects, the annulus is oval
shaped and appears approximately 30% longer in the medial to inferolateral direction.
The average diameter (± SD) of the TV annulus is 4.0 ± 0.7 cm. The mean maximum
tricuspid annular circumference and area in
healthy subjects are 12 ± 1 cm and 11 ± 1. 8
cm2, respectively [15, 16]. The tricuspid annulus area changes approximately 30% (~
20% diameter) during the cardiac cycle [16,
17]. With moderate or greater tricuspid regurgitation (TR), the TV annulus becomes dilated, more planar with decreased high-low distance (< 4 mm), and more circular (Fig. 4).
Patients with mild functional TR may have
normal TV 3D geometry. In these cases, as
shown by a recent cardiac MRI study, the longitudinal displacement of the TV annulus, especially on the lateral margin of the annulus,
is smaller than in healthy individuals (12.3 ±
3.7 vs 21.4 ± 3.7, respectively) [12].
Tricuspid Valve Morphology in Congenital
Heart Disease
Primary malformations of the TV are rare
anomalies, with the Ebstein anomaly the
most common. In contrast, secondary tricuspid dysfunction is a common associated finding in adult CHD, typically related to chronic RV volume overloading. Functional TR is
also common in the systemic RV because of
pressure and volume overload (i.e., corrected
transposition of the great arteries) [18]. Eb-
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Imaging Evaluation of Tricuspid Valve
stein anomaly is due to failure of delamination of the valve tissue from the underlying
myocardium, resulting in a more apical attachment of the posterior and septal leaflets.
In Ebstein anomaly, precise delineation of
the degree of apical displacement of the posterior and septal leaflets and volumetric and
functional assessment of the ventricles are
feasible with MRI. CT is an alternative imaging modality, particularly in patients unable to undergo cardiac MRI (Fig. 5).
The displacement of the TV septal leaflet in
Ebstein anomaly results in an “atrialized RV”
and a “functional RV” [19, 20] (Fig. 5). In
contrast, the anterior leaflet of the TV is rarely
displaced but is often redundant or “saillike.”
Double-orifice TV presents with TR in
62% of cases and combined stenosis and regurgitation in 25% [21]. Cleft on the anterior TV leaflet usually presents with TR [22].
Dysplastic or cleft TV may be seen in association with perimembranous VSD.
The imaging characteristics of tricuspid
atresia include the classic fatty wedge seen
in the right atrioventricular groove on axial
or long-axis four-chamber views along with
a dilated systemic venous system and right
atrial and severe RV hypoplasia [23].
In the congenital form of atrioventricular membranous defect (Gerbode defect),
an elongated saillike anterior TV leaflet in
a perimembranous VSD may partially close
the defect or in some cases direct the shunt
from the left ventricle into the right atrium.
The acquired form of the disease (e.g., bacterial endocarditis) may not show this phenomenon [24, 25]. In aneurysm of the interventricular membranous septum, it is believed
that the aneurysm results from adhesion of
the septal or anterior leaflets to the rim of a
perimembranous VSD, causing complete or
incomplete closure of the defect [25]. The
characteristic windsock appearance on CT
or MRI results from aneurysmal distention
during ventricular systole.
Tricuspid Valve Masses
Tumors arising from the valve are usually papillary fibroelastoma, commonly involving the aortic valve and rarely the TV
[26–28]. The differential diagnoses of TV
masses include valve myxoma, thrombus,
vegetation, metastasis, and other rare primary benign or malignant tumors [26–30]. On
MRI, papillary fibroelastoma usually presents as a hyperintense mobile pedunculated mass on T2-weighted imaging with some
enhancement that can be indistinguishable
from myxoma or hemangioma. In contrast,
thrombus is usually hypointense on T2-imaging and remains low in signal intensity
with no enhancement on delayed contrastenhanced imaging, although the signal intensity may vary depending on the stage of
evolution. Hemangioma and angiosarcoma
are among the vascular masses with variable
enhancing patterns.
Function
Tricuspid Dysfunction
Appendix 1 shows the causes of TV malfunction classified into two major groups of
primary (intrinsic, organic, or structural)
and secondary (functional or anatomically normal) diseases. In the secondary group
(more common), tricuspid dysfunction usually presents as mild to moderate TR in a
patient with left heart disease or pulmonary
hypertension and may resolve after treatment
of the primary disease. Isolated primary disease of the TV is less common and usually secondary to rheumatic heart disease and
CHD. The valve morphology can help differentiate the two groups. Rheumatic disease
has been the leading cause for TV dysfunction [31]. This trend has changed over past
decades, and the relative frequency of CHD
has increased [32]. In all groups, the most
common clinical presentation is TR. TV stenosis, especially in its isolated form, is a rare
phenomenon and appears to be congenital
(bicuspid, dysplastic) in most cases or, less
likely, due to endocarditis, rheumatic disease, or carcinoid [21, 31, 33, 34].
Tricuspid Regurgitation
The causes of TR are listed in Appendix
2. Trivial to mild TR is common (60–70%)
and appears to be more common in patients
more than 50 years old [35]. Although little
is known about the significance of mild TR,
moderate to severe TR has been associated
with increased mortality [35, 36].
Functional tricuspid regurgitation—The
most common cause of TR is dilatation of the
TV annulus caused by pulmonary hypertension primary or secondary to left heart failure
[36]. As mentioned earlier, functional TR is
associated with flattening of the tricuspid annulus, dilatation, and decreased annular longitudinal excursion during the cardiac cycle
(especially in severe TR) [37, 38]. RV dilatation leads to a distortion of the normal geometric relationships of the tricuspid leaflets,
chords, and PMs. With annulus flattening, the
lowest point of the annulus is displaced away
from the PMs, resulting in tethering of the
leaflets and regurgitation due to incomplete
coaptation of the leaflets. The critical diameter for annular dilatation to cause functional TR is approximately 27 mm/m2 of body
surface area [37]. In an in vivo study of porcine TVs by Spinner et al. [39], all valves lost
competence at 40% dilatation.
Tethering of the leaflets as a result of annular remodeling and flattening has been
reemphasized by Fukuda et al. [38], who
showed that after ring annuloplasty, in spite
of reduction of the annulus diameters to normal limits, TR can persist and its persistence
is primarily related to leaflet tethering. The
distance and area of tethering (tenting) can
be measured by echocardiography, MRI, or
CT (Figs. 6 A and B). In addition to tricuspid dilatation, three important factors determine whether TR occurs: preload, afterload,
and right ventricular function. These factors
should be taken into consideration in the imaging and clinical study of TR [40].
Pulmonary hypertension and tricuspid
regurgitation—Pulmonary hypertension increases RV systolic pressure and may lead to
RV dilatation and dysfunction, TR annulus
dilation, PM displacement, tethering of the
leaflets, and finally TR. Chronic TR, in turn,
contributes to progression of the RV volume
overload and right atrial enlargement, which
exacerbates RV and tricuspid annular dilatation and can reduce RV systolic function and
cardiac output [41] (Figs. 6 D–E).
Among the different causes of pulmonary hypertension and secondary TR, mitral valve disease is of special significance.
Moderate TR may be present in up to 30% of
patients with mitral valve disease [42]. Over
time, significant TR recurs after mitral valve
surgery in many patients; this entity has been
termed “late TR.” Late TR is associated with
a very poor prognosis [43]. Once the tricuspid annulus is dilated, its size does not return to normal and may even dilate further,
requiring a second operation years after the
initial mitral valve repair [40]. That is why
almost half of patients who undergo mitral
valve repair also undergo tricuspid annuloplasty and a maze procedure if atrial fibrillation exists [40, 44].
Structural causes of tricuspid regurgitation—Rheumatic heart disease remains a major origin of heart valve disease in the developing world [45]. The mitral valve is most often
involved [46]. TV involvement is seen in 6.0–
8.5% of cases, and TR develops in two thirds
of those patients. In one third of patients, TR
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Saremi et al.
TABLE 1: Noninvasive Imaging Parameters for Assessment of Tricuspid Regurgitation
Mode
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Qualitative
Parameters
Mild
Moderate
Severe
Imaging
Tricuspid morphology
Normal nonplanar
Nonplanar, tethered Planar with large coaptation defect
CT, MRI, 3D echocardiography
TR jet
Small central
Intermediate
Large central or eccentric jet
MRI, echocardiography
Hepatic vein inflow
Systolic dominance
Systolic blunting
Systolic reversal
MRI, echocardiography, CT
Tricuspid inflow
Normal pattern
Normal pattern
Early systole wave dominant > 1 m/s Echocardiography, MRI
Quantitative Regurgitant area (cm2)
<5
6–10
> 10
MRI, echocardiography
TR length (cm)
2
3–5
>5
MRI, echocardiography
TR (%)a
20
20–34
> 35
MRI, echo
Vena contracta width (mm)
Not defined
< 6.5
>7
MRI, echocardiography
PISA radius (mm)
<5
6–9
>9
Echocardiography
Regurgitant orifice area (mm2) Not defined
Not defined
> 40
CT, MRI, 3D echocardiography
Regurgitant volume (mL)
Not defined
Not defined
> 45
Echocardiography, MRI
RA, RV, IVC dimensions
Nonspecific
Nonspecific
IVC > 2 cm
CT, MRI
Note—PISA = proximal isovelocity surface area, RA = right atrium, RV = right ventricle, IVC = inferior vena cava [1, 2, 59,70].
aRatio of maximal regurgitant area to RA area.
is functional [47, 48]. Imaging criteria include
thickened leaflets with restriction in motion,
diastolic doming (hemispheric shape of the
leaflets due to adhesion), and encroachment
of the leaflet tips on the ventricular inlet [48].
In carcinoid syndrome, the TV is the most
frequently involved valve (97%), followed
by the pulmonary valve (49%). Endocardial
plaques of fibrous tissue on both sides of the
TV leaflets and subvalvular apparatus result
in moderate to severe regurgitation in 90%
and TV stenosis in 10% of cases [49, 50].
Endocardial fibrous plaques in the RV and its
valves can be visualized with cardiac MRI on
delayed contrast-enhanced imaging [50, 51].
Prolapse is diagnosed if one or more leaflets extend beyond the tricuspid annulus plane
in systole (Fig. 7). Myxomatous degeneration
and Marfan syndrome affecting the mitral
and tricuspid valves can lead to chordal elongation and prolapsing leaflets [52]. TV prolapse is seen in 20% of cases of myxomatous
mitral valve disease and primarily involves
the anterior and septal leaflets. Determination
of tricuspid prolapse is difficult because the
tricuspid ring is not easy to define.
Infective endocarditis of TV is seen in
5–10% of infective endocarditis and can involve a native TV or valve prosthesis [53].
TV endocarditis is mainly a disease of IV
drug abusers. CT has limited value for detection of small vegetations (< 4 mm) and small
valve perforations [54, 55]. Associated findings include thickening, shortening, perforations, or complete destruction of the leaflets
and intramural or perivalvular abscesses. TR
can rarely develop after inferior wall myocardial infarction and appear to be primarily
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related to the dysfunction of the PM complex
[56]. Patients with a permanent pacemaker
or automatic implantable cardioverter-defib­
rillator leads have an increased prevalence
of significant TR [57]. After lead implantation, 18% of patients with baseline mild TR
develop moderate to severe TR. TR can be
caused by direct lead interference with valve
closure, laceration or perforation, infection,
and fibrous adhesions.
Imaging of Tricuspid Function
Table 1 shows the imaging parameters for
assessment of TR using different modalities.
MRI evaluation of TV function is performed
in a manner analogous to that in the ventriculoarterial valves, but in some cases it can be
difficult because of more extensive excursion
of the valve annulus during the cardiac cycle
unless it is corrected for motion [58]. In general, gradient-recalled echo (GRE) pulse sequences are more sensitive to dephasing effects than balanced steady-state free precession
(SSFP). Therefore, the jet of regurgitation, especially when it is mild, can be better shown
by GRE imaging. Velocity mapping and flow
quantification by phase contrast MRI enable
direct measurement of the regurgitant flow
[59]. On in-plane balanced SSFP or phase contrast cine imaging, the regurgitant flow is typically shown as a triangular jet into the right
atrium. Obtaining a short-axis image orthogonal to the jet flow can optimally provide information about the velocity and direction of flow
(Fig. 8). Short-axis slices will be obtained at
three levels: above, at, and below the valve. In
most cases, a velocity encoding (VENC) value of < 200 cm/s is enough to prevent aliasing.
In severe stenosis, higher VENC values are required. Quantification of regurgitation is possible by measuring peak systolic velocity (PSV)
across the valve. Quantification of regurgitation is performed by measuring retrograde
flow across the valve and dividing this measure by the anterograde flow, thus obtaining
the regurgitant fraction. PSV is used to quantify the pressure gradient and thus to estimate
RV systolic pressure. The pressure difference
(gradient) between the right atrium and the RV
is calculated by the Bernoulli equation: Δ p =
4. (PSV)mm2. The addition of right atrial pressure (7–10 mm Hg) to the Δ p gives an estimate
of the RV systolic pressure that is equal to the
systolic pulmonary artery pressure (if there is
no pulmonary valve stenosis) in mm Hg [60].
The regurgitant orifice area can be directly
evaluated on short-axis through-plane views.
The short plane of the TV is different from the
mitral valve and can be best scanned using two
orthogonal long-axis RV views. This method
is difficult in Ebstein anomaly cases because
of the difficulty of identifying the valve level
on short-axis images [61]. The 3D three-directional acquisition method with retrospective
valve tracking is currently the best technique to
overcome the limitations of the 2D technique
and to correct for valve motion in the apicalbasal direction. Using this technique, velocity encoding in three orthogonal directions is
applied and a free-breathing 3D acquisition is
performed in approximately 5 minutes with an
additional 5 minutes for data processing [62].
An alternative method for calculating
tricuspid regurgitant volume is to subtract
RV stroke volume calculated by balanced
SSFP cine images from forward stroke vol-
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Imaging Evaluation of Tricuspid Valve
ume in the pulmonary artery measured on a
phase contrast sequence. The difference between the two volumes yields the regurgitant
volume. The regurgitant fraction will be:
TV / RV stroke volumes × 100%. This method is commonly used for the mitral valve
with high accuracy rates [59]. The accuracy
of this method for TR measurement is lower
in the presence of irregular rhythms or pulmonary valve regurgitation. TR quantification can also be obtained by the difference in
right-left ventricular stroke volumes if only a
single valve (TV or mitral) is involved [63].
Grading of regurgitation—Note that the degree of TR is variable and heavily dependent
on intravascular volume status, RV loading,
and RV function. The visual assessment of jet
area (maximal of planimetric jet area in cm2)
is a common method to evaluate valvular regurgitation and correlates well with regurgitant
fraction [64]. Eccentric regurgitant jets that
impinge on the atrial wall are less predictable
and usually have much smaller areas than central jets with same degree of severity. Visual
grading of the TR jet can best be obtained in
four-chamber views (Fig. 9). Although thresholds for guiding the severity of TR on MRI are
not well described, the echocardiography definitions can still help to diagnose severe cases of
TR. In mild TR, the jet extends up to 2 cm into
the right atrium. In moderate regurgitation, it
extends 3–5 cm. The TV flow varies with inspiration, and obtaining the measurements
at end-expiration is suggested [59]. Respiratory variation of TR can be checked by realtime MRI on a single-shot cine-balanced SSFP
sequence. TR almost universally increases in
volume during inspiration. This variation is
primarily secondary to an increase in venous
return to the right heart. With inspiration, the
RV and the systolic TV annulus become larger,
and there will be increased valve-tenting height
during systole, causing an increase in regurgitant orifice and volume [65].
Evaluation of severe TR—The most appropriate imaging method to evaluate the severity of TR or mitral regurgitation is uncertain.
Noninvasive quantification of a severe TR jet
has limitations. Cine MRI provides several
measurements, including the area, volume,
and maximum length of the signal intensity
void; and the ratio of the signal intensity void
area to the area of the right atrium [66].
Hepatic vein systolic flow reversal has been
shown to have 80% sensitivity for moderate to
severe TR but is a nonspecific finding [67]. A
common and easy way to determine TR severity is the ratio between the regurgitant jet area
and the right atrial area (Fig. 9). However, this
method is semiquantitative and rather subjective. Direct measurement of the regurgitant
area on cine MRI has also been suggested as a
reliable method of regurgitation severity analysis on balanced SSFP images (severe > 0.92
cm2) [68]. Values are smaller using phase imaging compared with balanced SSFP.
A more quantitative assessment of TR can
be obtained by measuring the width of the
vena contracta, which is measured as the narrowest neck of regurgitant flow near the regurgitant orifice and before expansion of the turbulent jet [69]. The vena contracta is typically
measured in the four-chamber view, and plan­
imetry of the maximal area of the regurgitant
jet or the regurgitant orifice is performed on
short-axis images (Fig. 9). Width of the vena
contracta greater than 7.0 mm is an additional
indicator of severe regurgitation [69, 70]. Intermediate values are not accurate for distinguishing moderate from mild TR. The method
is not accurate in assessing eccentric jets.
Tricuspid Valve Surgery
Two common types of tricuspid valve repair include suture annuloplasty using a
“purse-string” suture and ring annuloplasty
of Carpentier (26- to 36-mm open) [71] (Fig.
10). Annuloplasty with a rigid or flexible ring
has better durability compared with pursestring suture and is considered the standard
of care. The ring is C-shaped, and its gap is
placed at the site of the septal leaflet of the
TV to prevent complications to the conduction
system (Fig. 10). Posterior annular bicuspidization is another form of annuloplasty that is
not commonly used. Any patient with moderate TR or a tricuspid annular diameter greater
than 40 mm in any imaging view is considered for TV annuloplasty during any left-sided valve surgery [72]. TV annulus is surgically reduced to 3.0 cm or by at least 20–30%
from the values. If the functional TR is purely due to annular enlargement without tenting and the RV function is normal, usually
annuloplasty is preferred [38]. Tenting is described as displacement of the TV leaflet tips
toward the RV in systole because of cord tethering (Fig. 6). Tenting distances greater than
0.76 cm and areas greater than 1.63 cm2 are
important predictors of persistence or recurrence of functional TR after annuloplasty, and
either valve replacement or elongation of anterior leaflet tissue by pericardial patches may
be necessary [38, 73]. Tenting is also seen in
pulmonary hypertension or increased afterload (i.e., systemic ventricle) (Fig. 6).
Conclusion
The TV plays an important role in a number of pathologic conditions and its abnormality can influence the morbidity and mortality
in a number of acquired and congenital cardiac abnormalities. In this article, we have
reviewed the morphologic details of the TV
apparatus and discussed the spectrum of diagnostic information that CT and MRI can
provide regarding its pathologic processes
and compared the strengths and limitations
of these modalities with currently established
echocardiographic diagnostic parameters.
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APPENDIX 1: Causes of Tricuspid Valve Dysfunction
A. Primary
• Rheumatic valve disease
• Endocarditis: infective, hypereosinophilic syndrome
• Carcinoid heart disease
• Toxic: fenfluramine, methysergide
• Tumors: myxoma, metastasis
• Iatrogenic: pacemaker lead trauma
• Trauma: blunt or penetrating injuries
• Degenerative (valve prolapse)
• Congenital: atresia, hypoplasia, Ebstein
B. Secondary
• Right ventricular dilatation
• Pulmonary hypertension
• Global right ventricular dysfunction: cardiomyopathy, myocarditis,
• Segmental right ventricular dysfunction: ischemia/infarction, endomyocardial fibrosis, arrhythmogenic right ventricular dysplasia
APPENDIX 2: Causes of Tricuspid Regurgitation (TR)
A. Functional (secondary) (75%)
1. Right ventricular dysfunction
• Left heart disease
• Right ventricular dysplasia
• Ischemic right ventricle
• Systemic right ventricle
2. Increased afterloada
• Primary pulmonary hypertension
• Secondary pulmonary hypertension
Left ventricular dysfunction
Mitral valve disease
Chronic obstructive pulmonary disease
Thromboembolism
Left to right shunt
• Systemic RV
3. Others
•Physiologic
• Atrial fibrillation
• Right atrial tumors
a Left
B. Structural (25%)
1. Acquired
• Rheumatic heart
•Prolapse
•Endocarditis
Infective, Löeffler syndrome
• Endomyocardial fibrosis
•Carcinoid
•Tumors
•Traumaticb
• Papillary muscle dysfunction
•Iatrogenic
Pacemaker
Right ventricular biopsy
Drugs, radiation
2. Congenital
• Ebstein anomaly
•Dysplasia
• Leaflet cleft
•Hypoplasia
• Double orifice
• Unguarded orifice
•Bicuspid
heart dysfunction is the most common cause of pulmonary hypertension, associated right heart failure, and TR.
implantation.
bLead
(Figures start on next page)
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Saremi et al.
A
Fig. 1—Tricuspid valve (TV) apparatus.
A and B, Photographs obtained from cadavers
show that TV has largest orifice among four cardiac
valves. Anterior (mural) leaflet is largest (A). Septal
leaflet base inserts obliquely across membranous
interventricular septum where anteroseptal
commissure is located (asterisks, A). Inferior
(posterior) leaflet has more scallops and is relatively
difficult to see with echocardiography compared
with CT and MRI. TV papillary muscles (B) are smaller
than mitral apparatus, often multiple, and widely
separated. AA = ascending aorta, MV = mitral valve,
RCA = right coronary artery, LCx = left circumflex
artery, PV = pulmonary valve, MPA = main pulmonary
artery, AVNa = atrioventricular node artery.
A
B
B
C
Fig. 2—Cadaveric images of 45-year-old man who had nonspecific chest pain.
A–C, Horizontal long axis (A) and CT angiography (B) images obtained through atrioventricular junction septum at three levels, with corresponding levels of slices shown
on right heart view of ventricular septum (C). Septal leaflet of tricuspid valve (STV) divides membranous septum (mbS) into two parts: interventricular and atrioventricular.
Inferior to membranous septum is anatomic location of “muscular” atrioventricular septum (AVS). Section below that, above coronary sinus (CS) ostium, is where
atrioventricular node (AVN) resides. Note offsetting of attachments of mitral and tricuspid valves (TVs) at level of muscular AVS. RBB = right bundle branch, LBB = left
bundle branch, MV = mitral valve, PM = papillary muscle, IVS = interventricular septum, IAS = interarterial septum, His = bundle of His, CFB = central fibrous body.
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Imaging Evaluation of Tricuspid Valve
Fig. 3—32-year-old woman with transposition of
great arteries after Mustard procedure for tricuspid
valve (TV) annulus.
A and B, Color-coded volume rendered four-chamber
(A) and superior (B) CT images show normal tricuspid
annulus in this patient with systemic right ventricle
(RV) demarcated by green ring. Normal nonplanar
shape due to oblique attachment of septal (sep)
leaflet to septum is well preserved. TV annulus is
generally weaker compared with mitral annulus and
therefore dilates more easily with pressure or volume
overload. 1 and 2 = septal attachment, 3 = lateral
(Lat) wall, Post= posterior/inferior attachment, Ant =
anterior/superior attachment.
A
B
Fig. 4—Shape of tricuspid annulus in healthy
34-year-old man and in 32-year-old woman with
functional tricuspid regurgitation (TR) who had right
heart enlargement.
In normal condition (left), annulus appears oval
shaped and is usually 30% longer in medial to
inferolateral (double-headed red arrows). In
functional TR (right), dilatation primarily involves right
ventricle free wall (green double-headed arrows) and
annulus becomes rounded. Septal portion of tricuspid
annulus (double-headed yellow arrows) remains
relatively fixed. Normal tricuspid valve annulus is
dynamic, and up to 30% reduction in annular area in
atrial systole can occur.
A
B
Fig. 5—Color-coded CT angiography in 45-year-old
woman with Ebstein anomaly.
A, Four-chamber volume rendered and corresponding
2D (inset) views show concept of atrialized right
ventricle (aRV) and functional RV (fRV). Mitral valve
(Mv) and tricuspid valve (Tv) are shown in blue.
Expected tricuspid annular plane is shown by dashed
white line. RA = right atrium.
B, On inferior surface rendered view, green bands
demarcate peripheral attachments of Mv and
displaced Tv. Septal and inferior leaflets of Tv are
displaced apically, resulting in aRV and fRV. Expected
tricuspid annular plane is shown by dashed white line.
Dysplastic leaflets and dilated atrioventricular ring
both contribute significantly to malfunctioning of Tv
and resultant right heart enlargement as was seen in
this patient. Of note, anatomically normal Tv typically
shows < 8 mm/m2 apical displacement relative to
hinge point of mitral valve. LV = left ventricle.
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Saremi et al.
A
B
C
D
Fig. 6—Tricuspid leaflet tenting.
A and B, Distance of tricuspid valve (TV) tethering is measured from annulus
plane to coaptation point (dashed red line) and tethering area by tracing leaflets
from annulus plane on four-chamber (dashed yellow line) (A) or two-chamber
(B) images. In this 40-year-old man with hypertrophied systemic right ventricle
(RV), tricuspid annulus diameter was normal (30 mm in systole) but with abnormal
tenting (10 mm). Tenting distance > 0.76 cm and area > 1.63 cm2 are important
parameters for predicting residual tricuspid regurgitation (TR) after tricuspid
annuloplasty. This phenomenon is also seen in pulmonary hypertension or
systemic right ventricle.
C–E, Ancillary findings in severe tricuspid regurgitation due to pulmonary
hypertension in 39-year-old woman with history of atrial septal defect. Fourchamber (C) and short-axis (D) CT images show specific signs of TR, lack
of coaptation of leaflets (green arrow, C), and annulus diameter of > 40 mm.
Nonspecific signs include straightening of septum (orange arrows, D), atrial septal
leftward bulging (C), and markedly dilated right atrium (RA). Enlarged pulmonary
artery (PA) and mild pulmonary regurgitation (PR) (red arrow, E) are also related to
pulmonary hypertension.
E
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A
Systole
400
Fig. 7—Myxomatous disease of tricuspid valve.
A and B, Four-chamber MR image (A) shows mild
disease in 32-year-old man, and right ventricle (RV)
two-chamber CT image (B) in 21-year-old woman
shows moderate disease. Prolapse is diagnosed if
one or more leaflets extend beyond tricuspid annulus
in systole and usually involves anterior (A) and septal
(S) leaflets. Visualization of tricuspid prolapse may be
difficult because tricuspid ring is not easy to define.
Confirmation in two perpendicular images improves
diagnosis. I = inferior leaflet.
B
Tv
Fig. 8—48-year-old man with moderate functional tricuspid regurgitation (TR) and
diastolic dysfunction. Pulmonary valve function was normal. Both atria are dilated.
Note enlargement of atrial contraction waveform, indicating impaired ventricular
relaxation and mild dyssynchrony between right and left ventricles reflected by
early onset and peak of tricuspid valve (Tv) diastolic forward flow compared with
mitral valve (Mv) possibly due to TR.
Mv
Diastole
300
Volume (mL/s)
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Imaging Evaluation of Tricuspid Valve
200
100
Mv
0
Tv
Mv
Tv
–100
–200
0
100
200
300
400
500
Time (ms)
600
700
800
900
A
B
Fig. 9—Vena contracta (VC) shown by cine MRI in 48-year-old man with moderate to severe tricuspid regurgitation (TR).
A and B, Thickened noncoapting leaflets are shown on short-axis image (A). VC is smallest regurgitant flow diameter (area) before
expansion of jet, best measured on four-chamber view (B). It is great quantitative assessment of functional TR and corresponds
hydrodynamically with regurgitant orifice area (blue dotted line). Severe TR is defined as TR jet area > 10 cm2 , ratio of jet-right atrium (RA)
area > 35%, regurgitant orifice area > 40 mm2 , and VC > 7 mm (arrows). RV = right ventricle.
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Saremi et al.
A
B
C
Fig. 10—Surgery in functional tricuspid regurgitation (TR).
A, Short-axis CT image obtained at level of atrioventricular node (arrow, AVN) (red) shows relationship of annuloplasty ring (blue) to AVN.
B, Drawings show annuloplasty types. Standard of care (due to durability compared with purse-string suture) is rigid or flexible ring, which reduces annular size and
constricts it to predetermined size. It is preferred if tricuspid regurgitation (TR) is due to pure annular enlargement (without tenting and normal right ventricle [RV]
function). Posterior annular bicuspidization is pledget-supported mattress suture from anteroposterior commissure to posteroseptal commissure along posterior
annulus. S = septal tricuspid leaflet.
C, Short-axis CT image shows tricuspid valve annuloplasty and mitral valve replacement. Open ring spares AVN, thus reducing risk of heart block. Note clear
membranous septum (arrow) region, approximate site of AVN.
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