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1540

DIAGNOSTIC TECHNIQUES
JACC Vol. 3, No.6
June 1984: 1540-50
Tricuspid Regurgitation: Noninvasive Techniques for Determining
Causes and Severity
NICHOLAS L. DEPACE, MD, JOHN ROSS, RCPT, ABDULMASSIH S. ISKANDRIAN, MD, FACC,
PASQUALE F. NESTICO, MD, MORRIS N. KOTLER, MD, FACC, GARY S. MINTZ, MD, FACC,
BERNARD L. SEGAL, MD, FACC, A-HAMID HAKKI, MD, FACC, JOEL MORGANROTH MD, FACC
Philadelphia. Pennsylvania
Tricuspid regurgitation is often not apparent on physical
examination and several methods are now available to
aid in this difficult assessment. Cardiac catheterization
using right ventriculography, previously considered the
diagnostic standard, has several limitations. Currently
available noninvasive tools such as Mmode and two-
Tricuspid regurgitation, first formally recognized in 1836
(1), was described in greater detail the following year by
King (2). Duroziez (3) is credited with the description of
the physical findings.
Normal closure of the tricuspid valve depends on com-
plex integrated functions of the leaflets, chordae tendineae,
papillary muscles and the adjacent right ventricular myo-
cardium. Malfunction of anyone of these components may
result in tricuspid regurgitation. Tricuspid regurgitation can
be classified as primary when it is due to intrinsic abnor-
mality in the valve apparatus or secondary (functional) when
it is due to right ventricular pressure or volume overload.
Several factors have made possible and necessary a more
careful clinical evaluation of tricuspid regurgitation: 1) ad-
vances in surgical management with anuloplasty or valve
replacement; 2) improved medical management with vaso-
dilators (4); and 3) recognition that residual unrecognized
tricuspid regurgitation contributes to surgical morbidity and
mortality.
Clinical recognition of mild to moderate tricuspid re-
gurgitation is often difficult (5,6). Several techniques can
aid in the diagnosis, but some may not be more valuable
than careful clinical evaluation. The purpose of this review
is to evaluate the value and limitations of current nonin-
From the Likoff Cardiovascular Institute of the Hahnemann University
Hospital, Philadelphia, Pennsylvania. Manuscript received July II, 1983;
revised manuscript received January 10, 1984, accepted January 19, 1984.
Address for reprints: Joel Morganroth, MD, Likoff Cardiovascular
Institute. Hahnemann University Hospital, 230 North Broad Street, Phil-
adelphia. Pennsylvania 19102.
1984 by the American College of Cardiology
dimensional echocardiography (with or without con-
trast), Doppler techniques and even radionuclide car-
diologic imaging have added significantly to the precise
assessment of the presence and severity of tricuspid re-
gurgitation. This review examines the comparative use
and limitations of these various techniques.
vasive techniques in determining the presence, causes and
severity of tricuspid regurgitation.
Tricuspid Valve Morphology
Details of the morphologic features of the tricuspid valve
may be found in the excellent review by Silver et al. (7).
Diagnosis and Quantitation of
Tricuspid Regurgitation
Phonocardiography. Phonocardiography is useful in
demonstrating the increase in the systolic murmur of tri-
cuspid regurgitation with inspiration, passive leg raising or
any maneuver that augments right heart filling. Intracardiac
phonocardiography reveals that the murmur originates in
the right ventricular inflow tract, and augmentation of the
murmur with inspiration can thereby be documented (8-11).
This method, however, is not frequently used. The steth-
oscope still remains an important clinical tool for detection
of the murmur.
Echocardiography (Table 1). M-mode echocardiog-
raphy. The normal tricuspid valve has a pattern of motion
similar to that of the mitral valve on M-mode echocardi-
ography (Fig. I) (12). The posterior cusp is difficult to
visualize. In normal subjects, it is usually difficult to record
the entire motion of the tricuspid valve. If the tricuspid valve
is recorded easily, this generally indicates right ventricular
enlargement. The diastolic (EF) slope of the tricuspid valve
is of little value in determining whether tricuspid regurgi-
0735-1097/84/$3.00
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JACC Vol. 3. NO.6
June 1984: 1540-50
DEPACE ET AL.
TRICUSPID REGURGITATION
1541
o = not significant; ::!:: = low; + = medium; + + = high.
Contrast echoes across tricuspid valvc + +
Contrast echoes in inferior vcna cava ::!:: ++
Diameter of hepatic vein ::!:: ::!::
Distortion of interatrial septum ::!:: ::!::
Right atrial expansion index
+
()
Reduction in ahnormal tricuspid valve ::!:: ::!::
circumference
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1
Figure I. M-mode echocardiogram of the normal tricuspid valve
(TV). ECG = electrocardiogram.
is considered specific for this condition (Fig. 3). 2) An A
wave synchronous pattern in which the contrast echo entered
the inferior vena cava during atrial contraction. This pattern
was seen in conditions associated with forceful right atrial
contraction, such as pulmonary and tricuspid stenosis and
pulmonary hypertension. 3) A random pattern in which con-
trast echoes were recorded in the inferior vena cava ran-
domly with no relation to the cardiac cycle. This pattern
could be due to inappropriate transducer position. at or
above the inferior vena cava-right atrial junction. and thus
may be seen in normal subjects.
Mintz et a!. (23) analyzed the severity of tricuspid re-
gurgitation by measuring the amplitude of V waves on the
inferior vena cava echocardiogram. A V wave 140% or
greater of the end-diastolic inferior vena cava dimension
was observed in 75% of patients with severe tricuspid re-
gurgitation. However. dilation of the inferior vena cava can
also he seen in patients with heart failure, constrictive per-
icarditis or cardiac tamponde. In another contrast echocar-
diographic pattern reported by Tei et a!. (24) using the M-
mode technique. linear contrast echoes were seen passing
posteriorly through the tricuspid valve in systole, a rather
characteristic pattern for tricuspid regurgitation.
Two-dimensional echocardiography. With contrast two-
dimensional echocardiography. a "back and forth" motion
+
o
+
o
++
Sensitivity
+
o
o
o
++
A. M-Mode Echoeardiography
B. Two-Dimensional Echocardiography
Specificity
Right ventricular enlargement
Paradoxical septal motion
Diastolic fluttering of the tricuspid valve
Contrast caval echogram showing V
wave synchronous pattern
Amplitude of V wave of inferior vena
caval echogram
tation is present. Right ventricular diastolic volume overload
is common but not specific for tricuspid regurgitation (13-17)
and is suggested by two indexes: I) increased right ven-
tricular index (right ventricular end-diastolic dimen-
sion/body surface area; normal, 0.3 to 1.1 mean
0.7), and 2) paradoxical septal motion, a nonspecific finding
that reflects right ventricular dilation of any origin (Fig. 2).
The inference can be made that the midpoint of the septum
moves during systole toward the center of the ventricular
mass, whether the stimulus to dilation is volume or pressure
overload (18).
Using contrast echocardiography, one can visualize echoes
moving back and forth through the tricuspid valve orifice
(17) or into the inferior vena cava during systole (19,20).
Because the inferior vena cava is imaged with the subcoastal
technique, the echoes emanating from the lungs and bones
will not interfere. The inferior vena cava can be recognized
in a nonnal subject as an echo-free space, slightly to the
right of the midline at a depth range of 6 to 15 cm from
the abdominal wall. The normal inferior vena cava echo-
gram reveals A and V pulsations: the A pulsation is slightly
more prominent than the V pulsation, and there is a char-
acteristic inspiratory collapse (21).
Contrast echocardiographv. Meltzer et a!. (22) used
contrast echocardiography in three groups of patients: pa-
tients with clinical tricuspid regurgitation, patients with con-
ditions that may be associated with tricuspid regurgitation
and normal subjects. Several patterns of contrast echoes in
the inferior vena cava were noted: I) AV wave synchronous
pattern, indicating the appearance of contrast echoes in the
inferior vena cava only during systole. This pattern was
seen only in patients with tricuspid regurgitation and, thus.
Table I. Echocardiographic Features in
Diagnosing Regurgitation
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1542
DEPACE ET AL.
TRICUSPID REGURGITATION
JACC Vol. 3. No.6
June 1984: 1540-50
1111\1111111111111111111111111111111
-
---- _.. ._-".--=- -
Figure 2. Paradoxical septal motion
(arrow) in a patient with right ven-
tricular volume overload and tricuspid
regurgitation. ECG = electrocardio-
gram; LY = left ventricle; PW = pos-
terior left ventricular wall; RY = right
ventricle.
of contrast echoes across the tricuspid valve can be visu-
alized in patients with tricuspid regurgitation (25). Systolic
microcavitation in the inferior vena cava appears to be a
sensitive marker for tricuspid regurgitation (Fig. 4), espe-
cially if the echocardiogram is performed during a Yalsalva
maneuver with the injectant being delivered immediately
Figure 3. Subcostal M-mode echocardiographic view during sa-
line ejection in a patient with tricuspid regurgitation. Contrast
bubbles appear just during systole (arrows) in the inferior vena
cava (IYC), a specific sign of tricuspid regurgitation. ECG =
electrocardiogram.
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JACC Vol. 3. No.6
June 1984: 1540-50
DEPACE ET AL.
TRICUSPID REGURGITATION
1543
A
-5
,
p
Figure 4. SlIbcostal two-dimensional view
of the inferior vena cava (lye) in a patient
with tricuspid regurgitation. The hepatic
vein (HY) is at a right angle. Top left,
before contrast injection; top right, after
contrast injection. (Note the microcavi-
tations in the inferior vena cava.) A =
anterior; I = inferior; LA = left atrium;
P = posterior; RA = right atrium; S =
superior.
after the release phase (26). Chen et al. (27) suggested that
for the diagnosis of tricuspid regurgitation, the microcavi-
tations should be visualized in both the inferior vena cava
and hepatic veins for at least three consecutive cardiac cycles.
There is no correlation between the persistence or intensity
of microcavitation and the severity of tricuspid regurgitation.
The diameter of the right superior hepatic vein, when
visualized by the subcostal technique, may provide an ap-
propriate assessment of central venous pressure and the se-
verity of tricuspid regurgitation. A maximal transverse di-
ameter of at least 1.8 cm was found to be highly sensitive
and specific for tricuspid regurgitation in a study of 55
patients with and 18 subjects without tricuspid regurgitation
(28). Similarly, a diameter of more than 1.5 cm predicted
an elevated central venous pressure (> 6 mm Hg) in 87%
of these patients. This technique is not useful if other causes
of hepatic vein enlargement, such as intrahepatic disease,
are present.
Distortion of the shape and motion of the interatrial sep-
tum has also been reported in tricuspid regurgitation (29).
In normal subjects, the interatrial septum is slightly convex
toward the left atrium at end-diastole. In patients with tri-
cuspid regurgitation, in the absence of mitral regurgitation,
systolic expansion of the right atrium may be noted with
the interatrial septum markedly convex toward the left atrium
(Fig. 5) (30).
DePace et al. (30) showed that the right atrial expansion
index (end-systolic volume - end-diastolic volume), mea-
sured with a computerized light pen system in a four cham-
ber apical view, was useful in differentiating patients with
severe tricuspid regurgitation from patients with mild or no
tricuspid regurgitation.
Tei et al. (31) observed that the tricuspid anular circum-
ference was significantly larger in patients with tricuspid
valve prolapse than in normal subjects. Also, the percent
of anular reduction from diastole to systole was significantly
lower in patients with tricuspid valve prolapse than in normal
subjects.
Doppler echocardiography. In the early 1970s, Ben-
chimol et al. (32,33) detected tricuspid regurgitation with
the use of a catheter-tipped Doppler ultrasonic flowmeter
positioned in the right atrium or the superior vena cava. By
means of an external Doppler flowmeter probe (which mea-
sures jugular-subclavian venous flow velocity transcutane-
ously), Benchimol et al. (34) found that peak systolic to
diastolic wave ratio was less than I in patients with and
more than I in patients without tricuspid regurgitation. How-
ever, peak systolic to diastolic ratio of less than I could
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1544
DEPACE ET AL.
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A
END DIASTOLE
lAce Vol. 3. No.6
lune 1984: 1540-50
B
END SYSTOLE
Figure 5. Four chamber two-di-
mensional echocardiographic view
in a patient with tricuspid regurgi-
tation and mitral stenosis. Note the
markedly enlarged right atrium (RA)
encroaching on the left atrium (LA).
The bottom panels show the right
atrium and right ventricle (RY) after
contrast injection, outlining the
cavities.
C
END DIASTOLE
D
END SYSTOLE
also be seen in conditions such as sinus bradycardia, atrio-
ventricular block, junctional rhythm (35,36), obstructive
cardiomyopathy of the right side and ventricular septal de-
fect (37). The use of a bidirectional Doppler flowmeter may
be more useful than a single directional probe, because the
depth of the negative systolic wave was found to correlate
with the severity of tricuspid regurgitation (38,39).
Waggoner et al. (40) studied six open chest mongrel dogs
with surgically created tricuspid regurgitation and were able
to detect tricuspid regurgitation by means of pulsed Doppler
echocardiography in all six. Turbulent flow in the right
atrium during systole was found in 61 of 101 patients ex-
amined by the pulsed Doppler technique, although only 18
patients had clinically evident tricuspid regurgitation. Un-
fortunately, right ventriculography was performed in only
21 patients.
Garcia-Dorado et al. (41) found the two-dimensional
echocardiographic pulsed wave Doppler ultrasound tech-
nique to be sensitive in detecting tricuspid regurgitation
when the sample volume was placed behind the tricuspid
valve in the parasternal short-axis or four chamber apical
view in systole. The diagnosis of tricuspid regurgitation in
these patients was confirmed by right ventriculography. Its
severity was assessed by: 1) the systolic turbulence in the
right atrium, and 2) the ratio of maximal systolic velocity
to maximal diastolic velocity in the superior vena cava.
Miyatake et al. (42), using pulsed Doppler gated with
two-dimensional echocardiography, reported pansystolic
abnormal Doppler signals in the right atrial cavity in 58 of
62 patients with suspected tricuspid regurgitation. The tri-
cuspid regurgitation was graded on a scale of I to 4 + on
the basis of the distance traveled by the abnormal signals
from the tricuspid orifice toward the posterior right atrial
wall. The right ventriculograms were also graded on a 4
point scale. Grades matched exactly in 36 patients but dif-
fered by I point in 23 and by 2 points in 3 patients. Thus,
it may be concluded that the pulsed Doppler technique is
the most reliable noninvasive method for assessing the se-
verity of tricuspid regurgitation (Fig. 6), and that it is useful
even in patients with atrial fibrillation, congestive heart fail-
ure or right ventricular pressure overload.
Nuclear imaging. Equilibrium radionuclide gated an-
giography provides a noninvasive method for evaluating
aortic or mitral insufficiency. There are only a few reports
of investigators using scintigraphic techniques in the diag-
nosis and quantitation of tricuspid regurgitation. In two such
studies (43,44), when the radionuclide was injected into a
peripheral vein, radioactivity was detected in the inferior
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JACC Vol. 3, No.6
June 1984: 1540--50
DEPACE ET AL.
TRICUSPID REGURGITATION
1545
Figure 6. Pulsed mode Doppler wave trac-
ings with sampled volume in the lower right
atrium in a patient with significant tricuspid
regurgitation secondary to multiple thrombi
in the right atrium and on pacemaker wire.
The tracing was obtained at the cardiac apex.
From top to bottom: electrocardiogram
(ECG) showing paced beats (P); amplitude
tracing of the Doppler signal showing tri-
cuspid valve closure (TVC); spectral Dop-
pler signal showing the direction and con-
centration of red blood cells from the baseline
([ +] = positive flow toward the Doppler
transducer, [-] == negative flow away from
the Doppler transducer). Aand E = Aand
Epoint, respectively, of the tricuspid valve;
TR = tricuspid regurgitation of negative
flow in the right atrium away from the trans-
ducer. Calibration of flow velocity = 2
mls .
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confirm the diagnosis. Therefore, it is difficult to be certain
if the reflux in these patients was indeed secondary to tri-
cuspid regurgitation.
Noninvasive Diagnosis of Etiology of
Tricuspid Regurgitation
The causes of organic tricuspid regurgitation are listed
in Table 2.
Rheumatic heart disease. Rheumatic heart disease may
cause tricuspid regurgitation by primary involvement of the
valve (organic) (Fig. 7) or by secondary involvement (func-
tional or nonorganic) as a result of pulmonary hypertension
that is generally secondary to mitral valve disease. Rheu-
matic tricuspid regurgitation is almost always associated
with mitral valve disease (47). Tricuspid stenosis is also
present in 4 to 33% of the patients, depending on the method
of diagnosis, the lower valve probalby being more reflective
Common
Table 2. Causes and Origins of Organic
Tricuspid Regurgitation
Rare
Ruptured chordae tetltlineae
Congenital tricuspid
dysplasia (dysgenesis)
Endocardial cushion defects
Amyloid heart disease
Eosinophilic endomyocardial
disease
Endocardial fibroelastosis
Trauma
Rheumatic valvular disease
Tricuspid valve prolapse
Ebstein's anomaly
Carcinoid heart disease
Bacterial endocarditis
vena cava in the presence of tricuspid regurgitation, after it
had entered the right ventricle. Handler et al. (45) computed
a regurgitant index (the ratio of left ventricular stroke counts
to right ventricular stroke counts) and found the ratio to be
less in patients with tricuspid regurgitation than in normal
subjects. They found the ratio to be 0.7 0.1 in 9 patients
with clinical significant tricuspid regurgitation and 1.4 ::t
0.1 in 39 patients without tricuspid regurgitation. Time-
activity variation over the liver was used to compute the
hepatic expansion fraction, which was significantly higher
in patients with tricuspid regurgitation than in control sub-
jects. Fourier analysis of time-activity variation in each pixel
was used in generating amplitude and phase images. All
patients with tricuspid regurgitation had more than 100 pix-
els over the liver automatically retained by the computer,
whereas only I of 39 patients without tricuspid regurgitation
had pixels retained by the computer. However, the results
of these techniques in patients with severe right heart failure
and hepatic congestion but without tricuspid regurgitation
were not compared. Also, because no standard was available
for assessing tricuspid regurgitation, data on sensitivity and
specificity of this method are lacking. Further work is needed
to determine whether this method will allow quantification
of the severity of the lesion.
Winzelberg et al. (46) examined the areas above and
below the right atrium for tracer reflux in the right brachi-
ocephalic vein, hepatic veins and inferior vena cava during
ventricular systole. Tracer reflux was observed in 25 of 37
patients, including all 10 patients who had clinically evident
tricuspid regurgitation. Many patients wtih reflux did not,
however, have clinically diagnosed tricuspid regurgitation.
Unfortunately, right ventriculography was not performed to
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1546
DEPACE ET AL.
TRICUSPID REGURGITATION
A
of the incidence (16,47-51). Doming of the tricuspid valve
on the two-dimensional echocardiogram is believed to be a
specific sign of concomitant tricuspid stenosis (48,49). The
typical two-dimensional and M-mode echocardiographic
findings of rheumatic mitral disease have been described
(52).
Previous classification of tricuspid regurgitation of rheu-
matic origin into functional and organic categories was based
on the presence and degree of pulmonary hypertension (53).
This categoriZation, however, is riot precise. We observed
patients with pulmonary hypertension who had echographic
features of organic tricuspid valve disease; thus, organic and
functional factors may coexist in some patients (54). In a
large series of patients with rheumatic mitral valve disease
(55), 60/0 had evidence of organic tricuspid valve disease
by two-dimensional echocardiography and cardiac cathe-
terization could not differentiate orgnic from nonorganic
causes.
Endocarditis. Infective endocarditis may produce veg-
tations on one or more of the leaflets (56,57), varying in
number, shape and size. Occasionally, the abnormal echoes
are seen anterior to the tricuspid valve in the right ventricular
inflow or outflow tract, or multiple-layered echoes may be
seen posterior to the tricuspid valve, resembling atrial myxoma
on M-mode echocardiography (58).
lerii
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JACC Vol. 3. NO.6
June 1984:1540-50
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Figure 7. Echocardiographic and hemodynamic findings in pa-
tients with rheumatic trisucpid valve disease. Panel A (top left).
M-mode findings of a decreased tricuspid valve EF slope, which
is consistent with but not specific for the presence of tricuspid
stenosis. TV = tricuspid valve, Panel B. Simultaneous right atrial
and right ventricular pressure tracings in a patient with mixed
tricuspid valve disease. The pressure curves show elevated right
ventricular and right atrial pressures. A large V wave in the right
atrial pressure tracing is the result of tricuspid regurgitation. In
addition, a small end-diastolic gradient is noted (scale 0 to 40 mm
Hg). RA = right atrium; RV = right ventricle. Panel C , Two-
dimensional echocardiographic parasternal view of a right ven-
tricular inflow tract, showing thickened anterior and posterior tri-
cuspid valve leaflets in a patient with organic tricuspid regurgitation
and stenosis. The right atrium is enlarged. Doming of the tricuspid
leaflets is noted in the right panel during diastole. A = anterior;
ATL = anterior tricuspid leaflet; Inf = inferior; P = posterior;
PTL = posterior tricuspid leaflet; RA = right atrium; RV = right
ventricle; Sup = superior. Panel D, Four chamber apical two-
dimensional echocardiographic view in same patient as in C, show-
ing thickening of the anterior (ATL) and septal (STL) tricuspid
leaflets with restricted motion and doming in diastole (right side).
The anterior mitral valve leaflet and posterior mitral leaflet are
also thickened and restricted in motion, reflecting rheumatic in-
volvement of both anterior valves. AML = anterior mitral leaflet;
L = \eft; LA = left atrium; LV = left ventricle; PML = posterior
mitral leaflet; RA = right atrium; RV = right ventricle.
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1547
Two-dimensional echocardiography permits assessment
of the size and extent of vegetations and can identify com-
plications of endocarditis, such as valve ring abcesses (59),
and is more valuable than M-mode echocardiography for
this pUrPOse (60,61). Vegetations may decrease in size or
disappear in most of these ptients in the follow-up period
(62-64).
Tricuspid valve prolapse. Tricuspid valve prolapse seen
in association with mitral valve prolapse (65) is caused by
myxomatous degeneration, resulting in redundancy of the
leaflets. The diagnosis can be made by M-mode echocardi-
ography, which demonstrates findings similar to those of
mitral valve prolapse (Fig. 8) (66-75).
The two-dimensional echocardiographic features of pro-
lapse of the tricuspid valve include visualization of one or
more leaflets prolapsing beyond the atrioventricular ring into
the right atrium (Fig. 8). The parastemallong-axis approach
may be preferred over the apical four chamber view for
visualization of the prolapse (72,73). In some patients, the
subxiphoid approach may show the prolapse when the other
approaches fail (74). Between 3 and 52% of patients with
mitral valve prolapse may have associated tricuspid valve
prolapse (65,68,72,73,75,76). An association between tri-
cuspid prolapse and atrial septal defect has been noted (69).
Occasionally, aortic valve prolapse may be seen in asso-
ciation with mitral and tricuspid valve prolapse, that is, the
"floppy valve syndrome" (72,73,76).
The incidence of tricuspid regurgitation in patients with
tricuspid valve prolapse has not been clearly defined, but
has been reported to be as high as 48% (29,75). Occasion-
ally, tricuspid valve prolapse has been reported without
associated mitral valve prolapse (69,76).
Papillary muscle rupture or dysfunction and rupture
of chordae tendineae. Ruptured chordae tendineae may
cause tricuspid regurgitation (77-79). Rupture of the pap-
illary muscle as a result of direct chest trauma (for example,
during cardiopulmonary resuscitation or as a complication
of acute infarction) or as a consequence of endocarditis may
also cause tricuspid regurgitation (80). Papillary muscle dis-
continuity is a potential complication of endomyocardial
biopsy.
The two-dimensional echocardiographic features of flail
tricuspid valve were first reported by Mintz et al. (81). The
diagnostic criteria include systolic motion of the flail leaflet
beyond the closure line into the right atrium, with loss of
the usual coaptation point (43,78).
Congenital heart disease. The most common cause of
congenital tricuspid regurgitation is Ebstein' s anomaly, which
can be readily diagnosed by two-dimensional echocardi-
ography (52). If one measures the length (in em) from the
apex of the left ventricle to the mitral valve ring in the apical
four chamber view, and compares it with the ratio from the
apex of the right'ventricle to the septal tricuspid valve ring,
a ratio of these lengths greater than 2: 1 is diagnostic of
Ebstein's disease (82). The clinical severity of this disease
depends on the degree of tricuspid valve displacement, the
size of the atrialized right ventricle, the size and functional
capacity of the true right ventricle, the severity of tricuspid
regurgitation and the presence of associated abnormalities
such as atrial septal defect. Several other congenital anom-
alies can produce tricuspid regurgitation, for example, con-
genital tricuspid dysplasia (dysgenesis) (83).
Carcinoid heart disease. The carcinoid syndrome is most
common in patients with metastatic ileocecal carcinoid tuc
mors (84). Cardiac involvement occurs as a late compli-
cation in approximately 50% of these patients; such com-
plications include pulmonary regurgitation, tricuspid
regurgitation and pulmonary stenosis. The echocardio-
graphic features include right ventricular overload; thick-
ening and restriction of the tricuspid valve valve motion,
which stays in a half-open position (Fig. 9) and thickening
and restriction of the pulmonary valve (85-87). Doming of
the tricuspid valve, which may be seen in rheumatic heart
disease, is not a feature of carcinoid heart disease (84).
Other causes. Myxomas of the right atrium may produce
tricuspid regurgitation and can be detected by two-dimen-
sional echocardiography (88). Other rare causes include
amyloid heart disease, which can affect the tricuspid valve
and produce thickening (89) and can be readily detected on
the two-dimensional echocardiogram. Eosinophilic endo-
myocardial disease and endocardial fibroelastosis have rarely
been reported to involve the tricuspid valve (90).
Figure 8. Echocardiographic features in patients
with tricuspid valve prolapse. The left panel is an
M-mode echocardiogramof the tricuspid valve with
systolic prolapse (black arrow). The right panel
is an apical four chamber two-dimensional view in
a patient with combined mitral valve (open arrow)
and tricuspid valve (closed arrow) prolapse. LA
= left arium; LV = left ventricle; TV = tricuspid
valve.
I' ,.
-.. '"f ..
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1548
DEPACE ET AL.
TRICUSPID REGURGITATION
DIASTOLE
JACC Vol. 3. No.6
June 1984:1540-50
SYSTOLE
Figure 9. Echocardiographic find-
ings in a patient with carcinoid heart
disease. The top panel is a two-di-
mensional echocardiographic para-
sternal view of the right ventricular
inflow tract in a patient with carci-
noid heart disease. Note the thick-
ened tricuspid valve with reduced
motion from systole to diastole. In
addition. systolic coaptation is not
maintained. The bottom panel is an
apical four chamber view in the same
patient, detailing a thickened tricus-
pid valve and an enlarged right atrium.
TV = tricuspid valve.
Summary
Tricuspid regurgitation is often not apparent on physical
examination, but several methods are available for its di-
agnosis. Cardiac catheterization with right ventriculography
has been the historical diagnostic standard for all cardio-
vascular diagnoses. However, the need to place a catheter
across the right-sided valves has limited its usefulness in
the diagnosis of tricuspid and pulmonary valve regurgitation
because valvular insufficiency may be produced by the cath-
eter distorting the valve it traverses. Currently available
noninvasive tools, such as M-mode and two-dimensional
echocardiography (with or without contrast), Doppler tech-
niques and radionuclide cardiologic imaging, have made
possible the evaluation of tricuspid regurgitation without the
need to invade the patient. Contrast M-mode echocardi-
ography is now the diagnostic standard to detect the presence
of tricuspid regurgitation. However, this technique is not
totally noninvasive as it is necessary to perform a veni-
in one cannot ascertain the severity of
tncuspld regurgitatIOn. Two-dimensional echocardiog-
raphy, when employed with the M-mode technique in a
patient with suspected tricuspid regurgitation, can be used
to evaluate the severity of tricuspid regurgitation by noting
the size and expansion of the right atrium, inferior vena
cava and hepatic veins. In addition, the cause of tricuspid
regurgitation can be best discerned using two-dimensional
echocardiography. Radionuclide cardiac imaging tech-
.require a venipuncture and are not available in many
mstltutlOns. Further work is needed to determine this tool's
value in the assessment of tricuspid regurgitation. The Dop-
pler technique may be the most sensitive tool to detect the
presence of tricuspid regurgitation and define its severity.
The combination of Doppler study with two-dimensional
echocardiography (for guiding where to sample blood flow)
will probably become the method of choice for the diagnosis
and assessment of tricuspid regurgitation once the combined
method becomes standardized and more readily available.
References
I. Benson C. A case of pulsation in the veins of the upper extrernilies.
Dublm J Med Chern Sci 1836;8:324-32.
2. King TW. An essay on thc safety valve function of the right ventricle
ot the human heart and on the gradation of function in warm blooded
animals. Guys Hosp Rep 1837;2:104-78.
3. Duroziez M. Du Retrecissement de la Tricuspide. Gaz Hop Paris
1868;41 :310.
4. Chatterjee K. Parmley WW. The role of vasodilator therapy in heart
failure. Prog Cardiovasc Dis 1977; 19:301-25.
Downloaded From: http://content.onlinejacc.org/pdfAccess.ashx?url=/data/Journals/JAC/22684/ on 12/03/2013
JACC Vol. 3. No.6
June 1984: 1540-50
DEPACE ET AL.
TRICUSPID REGURGITATION
1549
5. Ahn AJ, Segal BL Isolated tricuspid insufficiency: clinical features,
diagnosis and management. Prog Cardiovasc Dis 1967;9:166-93.
6. Sepulveda G, Lukas DS. The diagnosis of tricuspid insufficiency:
clinical features in 60 cases with associated mitral valve disease.
Circulation 1955:11:552-63.
7. Silver MD, Lam JH, Ranganathan N, Wigle ED. Morphology of the
human tricuspid valve. Circulation 1971 ;43:333-48.
8. Delzant JF, Forman J, Machado C, Calisti G. Insuffisance tricuspi-
dienne fonctionnelle et organique (a propos de 60 case etudies par
catheterisme et phonocardiographic intracavitaire). Arch Mal Coeur
1968;61 :305-32.
9. Forman J, Varin G. Fouchard 1. Le retrecissement tricuspidienne. In
Soulie P, ed. Le Catheterisme des Cavites Droites et Gauches du
Couer au Micromanometre. Paris: Bailliere, 1971:291-305.
10. Cha SD, Gooch AS, Maranhao V. Intracardiac phonocardiography in
tricuspid regurgitation: relation to clinical and angiographic findings.
Am J Cardiol 1981;48:578-83.
II. Wooley CF. Intracardiac phonocardiography-intracardiac sound and
pressure in man. Circulation 1978;57:1039-54.
12. Edler I, Gustafson A, Karlefors T, Christensson B. Ultrasound car-
diography. Acta Med Scand 1961;170(suppl 370):67-82.
13. Assad-Morell JL. Tajik AJ, Giuliani ER. Echocardiographic analysis
of the ventricular septum. Prog Cardiovasc Dis 1974;17:219-37.
14. Kessler KM, Foianini JE. Davia JE, et al. Tricuspid insufficiency due
to nonpenetrating trauma. Am J Cardiol 1976;37:442-4.
15. Seides SF, Dejoseph RL, Brown AE, Damato AN. Echocardiographic
findings in isolated, surgically created tricuspid insufficiency. Am J
Cardiol 1974;35:679-82.
16. Eslami B, Roitman D, Sheffield LT. Ambiguous heart murmurs clar-
ified by echocardiogram. JAMA 1974;230:873-6.
17. McCann WD, Harbold NB, Giuliani ER. The echocardiogram in right
ventricular overload. JAMA 1972;221:1124-45.
18. Pearlman AS. Clark CE, Henry WL. Morganroth J, Itscoitz SB. Ep-
stein SE. Determinants of ventricular septal motion. Influence of rel-
ative right or left ventricular size. Circulation 1976;54:83-91.
19. Nanda NC, Shah PM, Gramiak R. Echocardiographic evaluation in
tricuspid valve incompetence by contrast injections (abstr). Clin Res
1976;24:233A.
20. Wise NK, Myers S, Stewart JA, Waugh R, Fraker T, Kisslo J. Echo
inferior venacavography: a technique for the study of right sided heart
disease (abstr). Circulation 1979;60(suppl 11):11-202.
21. Meltzer RS. McGhie J. Roelandt J. Inferior vena cava echocardiog-
raphy. JCU 1982;10:47-51.
22. Meltzer RS. Hoogenhuyze DV, Serruys PW, Haalebos MMP, Hu-
genholtz PG, Roelandt J. Diagnosis of tricuspid regurgitation by con-
trast echocardiography. Circulation 1981 ;63: 1093-9.
23. Mintz GS, Kotler MN, Parry WR, Iskandrian AS, Kane SA. Real-
time inferior vena caval ultrasonography: normal and abnormal find-
ings and its use in assessing right-heart function. Circulation
1981 ;64: 1018-25.
24. Tei C, Shah PM, Ormiston JA. Assessment of tricuspid regurgitation
by directional analysis of right atrial systolic linear reflux echoes with
contrast M-mode echocardiography. Am Heart J 1982;103:1025-30.
25. Grison D, Lassabe G, Chemama F, Sacrez A. L'ech6 cardiographie
bidimensionnelle avec contraste dans l'insuffisance tricuspidienne.
Cardiology 1981;68:(suppl 1):75-80.
26. Lieppe W, Behar VS, Scallion R, Kisslo JA. Detection of tricuspid
regurgitation with two-dimensional echocardiography and peripheral
vein injections. Circulation 1978;57:128-32.
27. Chen CC, Morganroth J, Mardelli TJ, Naito M. Tricuspid regurgitation
in tricuspid valve prolapse demonstrated with cross-sectional echo-
cardiography. Am J Cardiol 1980;46:983-7.
28. Reeves WC. Leaman DM. Buonocore E. et al. Detection of tricuspid
regurgitation and estimation of central venous pressure by two-di-
mensional contrast echocardiography of the right superior hepatic vein.
Am Heart J 1981;102:374-7.
29. Tei C, Tawaka H. Kashima T, Yoshimura H, Minagoe S. Kanehisa
T. Real-time cross-sectional echocardiographic evaluation of the in-
teratrial septum by right atrium-interatrial septum-left atrium direction
of ultrasound beam. Circulation 1979;60:539-46.
30. DePace NL, Kotler MN, Ren JF, Kalman P, Mintz GS. Two-dimen-
sional estimation of the severity of tricuspid regurgitation (abstr).
Circulation 1982;66(suppl 11):11-362.
31. Tei C, Shah PM, Chenan G. Wang M, Ormistron JA. Tricuspid valve
prolapse: a two-dimensional echocardiographic study of annular and
leaflet abnormalities (abstr). Am J Cardiol 1982;49: 1009.
32. Benchimol A, Stegall HF, Gartlan JL Barreto EC, Goldstein MR,
Sandoval J. Right atrium and superior vena cava flow velocity in man
measured with the Doppler-catheter flowmeter-telemetry system. Am
J Med 1970;48:303-8.
33. Benchimol A, Desser KB. Clinical application of the Doppler ultra-
sonic flowmeter. Am J Cardiol 1972;29:540-5.
34. Benchimol A, Harris CL, Desser KB. Noninvasive diagnosis of tri-
cuspid insufficiency utilizing the external Doppler flowmeter probe.
Am J Cardiol 1973;32:868-73.
35. Kalmanson D, Veyrat C, Chiche P. Venous return disturbances in-
duced by arrhythmias: a transcutaneous, instantaneous, flowmetric
study at the site of the jugular vein. Cardiovasc Res 1970;4:279-90.
36. Kalmanson D, Veyrat C. Chiche P. Atrial versus ventricular contri-
bution in determining systolic venous return. Cardiovasc Res
1971 ;5:293-302.
37. Kalmanson D, Veyrat C, Chiche P. Diagnostic par voie externe des
cardiopathies droites et des shunts intra-cardiaques gauche-droite 11
I' aide du fluxmetre directionnel 11 effet Doppler. Presse Medicaie
1970;78: 1053-6.
38. Kalmanson D, Veyrat C. Tricuspid incompetence. atrial fibrillation
and diagnostic value of Doppler ultrasound. Am J Cardiol
1974;34:619-20.
39. Sivaciyan V, Ranganathan N. Transcutaneous Doppler jugular venous
flow velocity recording: clinical and hemodynamic correlates. Cir-
culation 1978:57:930-9.
40. Waggoner AD, Quinones MA, Young JB, et al. Pulsed Doppler echo-
cardiographic detection of right-sided valve regurgitation. Am J Car-
dioI1981;47:279-86.
41. Garcia-Dorado D, Falzgraf S. Almazan A, Delean JL, Lopez-Bescos
L, Menarquez L Diagnosis of functional tricuspid insufficiency by
pulsed-wave Doppler ultrasound. Circulation 1982:6: 1315-21.
42. Miyatake K, Okamoto M, Kinoshita N, et al. Evaluation of tricuspid
regurgitation by pulsed Doppler and two-dimensional echocardiog-
raphy. Circulation 1982;66:777-84.
43. Bardy GH. Talano JV, Meyers S. Lesch M. Acquired cyanotic heart
disease secondary to traumatic tricuspid regurgitation: case report with
a review of the literature. Am J Cardiol 1979;44:1401-6.
44. Mishkin FS, Mishkin ME. Documentation of tricuspid regurgitation
by radionuclide angiography. Br Heart J 1974;36: 1019-22.
45. Handler B, Pavel D, Pietras R, et al. Radionuclide angiography in
patients with tricuspid insufficiency (abstr). Am J Cardiol 1982;49:922.
46. Winzelberg GG, Boucher CA, Pohost GM, et al. Right ventricular
function in aortic and mitral valve disease. Chest 1981;79:520-8.
47. Salazar E, Levine HD. Rheumatic tricuspid regurgitation. Am J Med
1962;33:111-29.
48. Nanna M, Chandraratna PAN, Reid C, Nimalasuriya A, Rahimtoola
SH. Value of two-dimensional and M-mode echocardiography in de-
tection of tricuspid stenosis (abstr). Circulation 1982;66(suppl 11):11-
189.
49. Daniels SJ, Mintz GS, Kotler MN, Rheumatic tricuspid valve disease:
echocardiographic and catheterization features (abstr). Circulation
1982;66(suppl 11):11-356.
Downloaded From: http://content.onlinejacc.org/pdfAccess.ashx?url=/data/Journals/JAC/22684/ on 12/03/2013
1550
DEPACE ET AL.
TRICUSPID REGURGITATION
JACC Vol. 3, No.6
June 1984: 1540--50
50. EI-Sherif N. Rheumatic tricuspid stenosis: a hemodynamic correlation.
Br Heart 11971;33:16-31.
51. Kitchin A, Turner R. Diagnosis and treatment of tricuspid stenosis.
Br Heart 1 1964;26:354-79.
52. Kotler MN, Mintz GS, Segal BL, Parry WR. Clinical use of two-
dimensional echocardiography. Am 1 CardioI1980;45:1061-82.
53. Grossman W, Dexter L. Profiles in valvular heart disease. In: Gross-
man W, ed. Cardiac Catheterization and Angiography. Philadelphia:
Lea & Febiger, 1980:322.
54. DePace NL, Kotler MN, Ren IF, Kimbiris D, Kalman P, Mintz GS.
Two-dimensional echocardiographic determination of right atrial emp-
tying volume: a non-invasive index in quantifying the degree of tri-
cuspid regurgitation. Am 1 Cardiol 1983;52:525-9.
55. Daniels Sl, Mintz GS, Kotler MN. Rheumatic tricuspid valve disease:
two-dimensional echocardiographic, hemodynamic, and angiographic
correlations. Am 1 Cardiol 1983;51 :492-6.
56. Come PC, Kurland GS, Vine HS. Two-dimensional echocardiography
in differentiating right atrial and tricuspid valve mass lesions. Am 1
CardioI1979;44:1207-12.
57. Kisslo 1, VonRamm OT, Haney R, 10nes R, luk SS, Behar VS.
Echocardiographic evalution of tricuspid valve endocarditis. Am 1
Cardiol 1976;38:502-7.
58. Chandraratna PAN, Aronow WS. Spectrum of echocardiographic find-
ings in tricuspid valve endocarditis. Br Heart 1 1979;42:528-32.
59. Scanlan JG, Seward JB, Tajik AI. Valve ring abscess in infective
endocarditis: visualization with wide angle two-dimensional echo-
cardiography. Am 1 Cardiol 1982;49:1794-800.
60. Crawford FA, Wechsler AS, Kisslo lA. Tricuspid endocarditis in a
drug addict. Detection of tricuspid vegetation by two-dimensional
echocardiography. Chest 1978;74:473-5.
61. Sheikh U, Ali N, Covarrubias E, Fox LM, Morjaria M, Dejeo 1.
Right-sided infective endocarditis: an echocardiographic study. Am J
Med 1979;66:283-7.
62. Ginzton LE, Siegel Rl, Criley 1M. Natural history of tricuspid valve
endocarditis: a two-dimensional echocardigraphic study. Am 1 Cardiol
1982;49: 1853-9.
63. Stafford A, Wann LS, Dillon lC, Weyman AE, Feigenbaum H. Serial
echocardiographic appearance of healing bacterial vegetations. Am 1
Cardiol 1979;44:754-60.
64. Berger M, Delfin LA, lelvch M, Goldberg E. Two-dimensional echo-
cardiographic findings in right-sided infective endocarditis. Circulation
1980;61 :855-61.
65. Gooch AS, Maranhao V, Scampardonis G, Cha SD, Yang SS. Pro-
lapse of both mitral and tricuspid leaflets in systolic murmur-click
syndrome. N Engl 1 Med 1972;287:1218-22.
66. Chandraratna PAN, Lopez 1M, Fernandez 11, Cohen LS. Echocar-
diographic detection of tricuspid valve prolapse. Circulation
1975;51 :823-6.
67. Horgan IH, Beachley MC, Robinson FD. Tricuspid valve prolapse
diagnosed by echocardiography. Chest 1975;68:822-4.
68. Werner lA, Schiller NB, Prasquier R. Occurrence and significance of
echocadiographically demonstrated tricuspid valve prolapse. Am Heart
1 1978;96:180-6.
69. Chandraratna PAN, Lillmann BB, Wilson D. The association between
atrial septal defect and prolapse of the tricuspid valve. An echocar-
diographic study. Chest 1978;73:839-42.
70. Sasse L, Froelich CR. Echocardiographic tricuspid prolapse and non-
ejection systolic click. Chest 1978;73:869-70.
71. Mardelli TJ, Morganroth 1, Meixell LL, Vergel 1. Enhanced diagnosis
of tricuspid valve prolapse by cross sectional echocardiography (abstr).
Am 1 Cardiol 1979;43:385.
72. Morganroth 1, Jones RH, Chen CC, Naito M. Two-dimensional echo-
cardiography in mitral, aortic and tricuspid valve prolapse: the clinical
problem, cardiac imaging considerations and a proposed standard for
diagnosis. Am 1 Cardiol 1980;46:1164-77.
73. Ogawa S, Hayashi 1, Sasaki H, et al. Evaluation of combined valvular
prolapse syndrome by two-dimensional echocardiography. Circulation
1982;65: 174-80.
74. Inoue D, Furukawa K, Matsukubo H, Watanabe T, Katsume H. Subxi-
phoid two-dimensional echocardiographic detection of tricuspid valve
prolapse. Chest 1979;76:693-4.
75. Ainsworth RP, Hartmann AF, Aker U, Schad N. Tricuspid valve
prolapse with late systolic tricuspid insufficiency. Radiology
1973: 107:309-11.
76. Rippe 1M, Angoff G, Sloss LJ, Wynne 1. Alpert IS. Multiple floppy
valves: an echocardiographic syndrome. Am 1 Med 1979;66:817-24.
77. Mary DA, Day JB, Pakrashi BC, lonescu MI. Isolated tricuspid in-
competence after penetrating trauma. Am 1 CardioI1973;31:792-5.
78. Watanabe T, Katsume H, Matsukubo H, Furukawa K, Ijichi H. Rup-
tured chordae tendineae of the tricuspid valve due to nonpenetrating
trauma. Chest 1981;80:751-3.
79. Brandenburg RO, McGoon DC, Campeau L, Giuliani ER. Traumatic
rupture of the chordae tendineae of the tricuspid valve. Am 1 Cardiol
1966;18:911-5.
80. Gerry JL, Bulkley BH, Hutchins GM. Rupture of the papillary muscle
of the tricuspid valve. Am 1 Cardiol 1977;40:825-8.
81. Mintz GS, Kotler MN, Segal BL, Parry WR. Two-dimensional echo-
cardiographic recognition of ruptured chordae tendineae. Circulation
1978:57:244-50.
82. Ports TA, Silverman NH, Schiller NB. Two-dimensional echocardio-
graphic assessment of Ebstein's anomaly. Circulation 1978;58:336-43.
83. Bharati S, Lev M. Congenital poly-valvular disease. Circulation
1973;47:575-86.
84. Strickman NE, Rossi PA, Massumkhani GA, Hall Rl. Carcinoid heart
disease: a clinical, pathological and therapeutic update. Curr Probl
Cardiol 1982;6:1-42.
85. Baker BJ, McNee VD, Scovil lA, Bass KM, Watson JW, Bissell JK.
Tricuspid insufficiency in carcinoid heart disease: an echocardio-
graphic description. Am Heart 1 1981;101:107-8.
86. Callahan lA, Wroblewski EM, Reeder GS, Edwards WD, Seward JB,
Tajik lA. Echocardiographic features of carcinoid heart disease. Am
J Cardiol 1982;50:762-8.
87. Howard Rl, Drobac M, Rider WD, et al. Carcinoid heart disease:
diagnosis by two-dimensional echocardiography. Circulation
1982:66: 1059-65.
88. DePace NL, Soulen RL, Kotler MN, Mintz GS. Two-dimensional
echocardiographic detection of intraatrial masses. Am 1 Cardiol
1981 ;48:954-60.
89, Siqueira-Filho AG, Cunha CLP, Tajik AJ, Seward JB. Schallenberg
TT, Guiliani ER. M-mode and two-dimensional echocardiographic
features in cardiac amyloidosis. Circulation 1981 ;63: 188-96.
90. Veyrat C, Kalmanson D, Farjon M, Manin IP, Abitbol G. Non-
invasive diagnosis and assessment of tricuspid regurgitation and ste-
nosis using one and two-dimensional echo-pulsed Doppler. Br Heart
J 1982;47:596-605.
Downloaded From: http://content.onlinejacc.org/pdfAccess.ashx?url=/data/Journals/JAC/22684/ on 12/03/2013