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Tricuspid Regurgitation: Noninvasive Techniques for DeterminingCauses and SeverityNICHOLAS 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, FACCPhiladelphia Pennsylvania

Tricuspid regurgitation is often not apparent on physicalexamination and several methods are now available toaid in this difficult assessment. Cardiac catheterizationusing right ventriculography, previously considered thediagnostic standard, has several limitations. Currentlyavailable noninvasive tools such as Mmode and two-

Tricuspid regurgitation, first formally recognized in 1836(1), was described in greater detail the following year byKing (2). Duroziez (3) is credited with the description ofthe physical findings.Normal closure of the tricuspid valve depends on complex integrated functions of the leaflets, chordae tendineae,papillary muscles and the adjacent right ventricular myocardium. Malfunction of anyone of these components mayresult in tricuspid regurgitation. Tricuspid regurgitation canbe classified as pr imary when it is due to intrinsic abnormality in the valve apparatus or secondary (functional) whenit is due to right ventricular pressure or volume overload.Several factors have made possible and necessary a morecareful clinical evaluation of tricuspid regurgitation: 1) advances in surgical management with anuloplasty or valvereplacement; 2) improved medical management with vasodilators (4); and 3) recognition that residual unrecognizedtricuspid regurgitation contributes to surgical morbidity andmortality.

Clinical recognition of mild to moderate tricuspid regurgitation is often difficult (5,6). Several techniques canaid in the diagnosis, but some may not be more valuablethan careful clinical evaluation. The purpose of this reviewis to evaluate the value and limitations of current nonin-

From the Likoff Cardiovascular Institute of the Hahnemann UniversityHospital, Philadelphia, Pennsylvania. Manuscript received July II , 1983;revised manuscript received January 10, 1984, accepted January 19, 1984.Address for reprints: Joel Morganroth, MD, Likoff CardiovascularInstitute. Hahnemann University Hospital, 230 North Broad Street, Philadelphia. Pennsylvania 19102. 1984 by the American College of Cardiology

dimensional echocardiography (with or without contrast), Doppler techniques and even radionuclide cardiologic imaging have added significantly to the preciseassessment of the presence and severity of tricuspid regurgitation. This review examines the comparative useand limitations of these various techniques.

vasive techniques in determining the presence, causes andseverity of tricuspid regurgitation.

Tricuspid Valve MorphologyDetails of the morphologic features of the tricuspid valve

may be found in the excellent review by Silver et al. (7).

Diagnosis and Quantitation ofTricuspid RegurgitationPhonocardiography. Phonocardiography is useful in

demonstrating the increase in the systolic murmur of tricuspid regurgitation with inspiration, passive leg raising orany maneuver that augments right heart filling. Intracardiacphonocardiography reveals that the murmur originates inthe right ventricular inflow tract, and augmentation of themurmur with inspiration can thereby be documented (8-11).This method, however, is not frequently used. The stethoscope still remains an important clinical tool for detectionof the murmur.

Echocardiography (Table 1). M mode echocardiog-raphy The normal tricuspid valve has a pattern of motionsimilar to that of the mitral valve on M-mode echocardiography (Fig. I) (12). The posterior cusp is difficult tovisualize. In normal subjects, it is usually difficult to recordthe entire motion of the tricuspid valve. If the tricuspid valveis recorded easily, this generally indicates right ventricularenlargement. The diastolic (EF) slope of the tricuspid valveis of little value in determining whether tricuspid regurgi-

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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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Figure I . M-mode echocardiogram of the normal tricuspid valve(TV). ECG = electrocardiogram.

is considered specific for this condition (Fig. 3). 2) An Awave synchronous pattern in which the contrast echo enteredthe inferior vena cava during atrial contraction. This patternwas seen in conditions associated with forceful right atrialcontraction, such as pulmonary and tricuspid stenosis andpulmonary hypertension. 3) A random pattern in which contrast echoes were recorded in the inferior vena cava randomly with no relation to the cardiac cycle. This patterncould be due to inappropriate transducer position. at orabove the inferior vena cava-right atrial junction. and thusmay be seen in normal subjects.Mintz et a . (23) analyzed the severity of tricuspid regurgitation by measuring the amplitude of V waves on theinferior vena cava echocardiogram. A V wave 140% orgreater of the end-diastolic inferior vena cava dimensionwas observed in 75% of patients with severe tricuspid regurgitation. However. dilation of the inferior vena cava canalso he seen in patients with heart failure, constrictive pericarditis or cardiac tamponde. In another contrast echocardiographic pattern reported by Tei et a . (24) using the Mmode technique. linear contrast echoes were seen passingposteriorly through the tricuspid valve in systole, a rathercharacteristic pattern for tricuspid regurgitation.Two-dimensional echocardiography. With contrast twodimensional echocardiography. a back and forth motion

+

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A. M-Mode Echoeardiography

B. Two-Dimensional Echocardiography

Specificity

Right ventricular enlargementParadoxical septal motionDiastolic fluttering of the tricuspid valveContrast caval echogram showing V

wave synchronous patternAmplitude of V wave of inferior vena

caval echogram

tation is present. Right ventricular diastolic volume overloadis common but not specific for tricuspid regurgitation (13-17)and is suggested by two indexes: I) increased right ventricular index (right ventricular end-diastolic dimension/body surface area; normal, 0.3 to 1.1 c m / m ~ ; mean0.7), and 2) paradoxical septal motion, a nonspecific findingthat reflects right ventricular dilation of any origin (Fig. 2).The inference can be made that the midpoint of the septummoves during systole toward the center of the ventricularmass, whether the stimulus to dilation is volume or pressureoverload (18).

Using contrast echocardiography, one can visualize echoesmoving 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 subcoastaltechnique, the echoes emanating from the lungs and boneswill not interfere. The inferior vena cava can be recognizedin a nonnal subject as an echo-free space, slightly to theright of the midline at a depth range of 6 to 15 cm fromthe abdominal wall. The normal inferior vena cava echogram reveals A and V pulsations: the A pulsation is slightlymore prominent than the pulsation, and there is a characteristic inspiratory collapse (21).

Contrast echocardiographv Meltzer et a . (22) usedcontrast echocardiography in three groups of patients: patients with clinical tricuspid regurgitation, patients with conditions that may be associated with tricuspid regurgitationand normal subjects. Several patterns of contrast echoes inthe inferior vena cava were noted: I) A V wave synchronouspattern, indicating the appearance of contrast echoes in theinferior vena cava only during systole. This pattern wasseen only in patients with tricuspid regurgitation and, thus.

Table I. Echocardiographic Features inDiagnosing Regurgitation


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-

~ _ ~ ._ . = ~ ; ; : - . ~ . _Figure 2. Paradoxical septal motion(arrow) in a patient with right ventricular volume overload and tricuspidregurgitation. ECG = electrocardiogram; LY = left ventricle; PW = posterior left ventricular wall; RY = rightventricle.

of contrast echoes across the tricuspid valve can be visualized in patients with tricuspid regurgitation (25). Systolicmicrocavitation in the inferior vena cava appears to be asensitive marker for tricuspid regurgitation (Fig. 4), especially if the echocardiogram is performed during a Yalsalvamaneuver with the injectant being delivered immediately

Figure 3. Subcostal M-mode echocardiographic view during saline ejection in a patient with tricuspid regurgitation. Contrastbubbles appear just during systole (arrows) in the inferior venacava (IYC), a specific sign of tricuspid regurgitation. ECG =electrocardiogram.II11 \ \1111 1 I I 1 111 I I I' 1111111111P111/1 1 11/1 '1'1

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Figure 4. SlIbcostal two-dimensional viewof the inferiorvena cava lye) in a patientwith tricuspid regurgitation. The hepaticvein (HY) is at a right angle. Top left,before contrast injection; top right, aftercontrast injection. (Note the microcavitations 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 thatfor the diagnosis of tricuspid regurgitation, the microcavitations should be visualized in both the inferior vena cavaand hepatic veins for at least three consecutive cardiac cycles.There is no correlation between the persistence or intensityof microcavitation and the severity of tricuspid regurgitation.

The diameter of the right superior hepatic vein, whenvisualized by the subcostal technique, may provide an appropriate assessment of central venous pressure and the severity of tricuspid regurgitation. A maximal transverse diameter of at least 1.8 cm was found to be highly sensitiveand specific for tricuspid regurgitation in a study of 55patients with and 18 subjects without tricuspid regurgitation(28). Similarly, a diameter of more than 1.5 cm predictedan elevated central venous pressure > 6 mm Hg) in 87%of these patients. This technique is not useful if other causesof hepatic vein enlargement, such as intrahepatic disease,are present.

Distortion of the shape and motion of the interatrial septum has also been reported in tricuspid regurgitation (29).In normal subjects, the interatrial septum is slightly convextoward the left atrium at end-diastole. In patients with tricuspid 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 expansionindex (end-systolic volume - end-diastolic volume), measured with a computerized light pen system in a four chamber apical view, was useful in differentiating patients withsevere tricuspid regurgitation from patients with mild or notricuspid regurgitation.

Tei et al. (31) observed that the tricuspid anular circumference was significantly larger in patients with tricuspidvalve prolapse than in normal subjects. Also, the percentof anular reduction from diastole to systole was significantlylower in patients with tricuspid valve prolapse than in normalsubjects.

Doppler echocardiography. In the early 1970s, Benchimol et al. (32,33) detected tricuspid regurgitation withthe use of a catheter-tipped Doppler ultrasonic flowmeterpositioned in the right atrium or the superior vena cava. Bymeans of an external Doppler flowmeter probe (which measures jugular-subclavian venous flow velocity transcutaneously), Benchimol et al. (34) found that peak systolic todiastolic wave ratio was less than I in patients with andmore than I in patients without tricuspid regurgitation. However, peak systolic to diastolic rat io of less than I could


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Figure 5. Four chamber two-dimensional echocardiographic viewin a patient with tricuspid regurgitation and mitral stenosis. Note themarkedly enlarged right atrium (RA)encroaching on the left atrium (LA).The bottom panels show the rightatrium and right ventricle (R Y) aftercontrast injection, outlining thecavities.

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also be seen in conditions such as sinus bradycardia, atrioventricular block, junctional rhythm (35,36), obstructivecardiomyopathy of the right side and ventricular septal defect (37). The use of a bidirectional Doppler flowmeter maybe more useful than a single directional probe, because thedepth of the negative systolic wave was found to correlatewith the severity of tricuspid regurgitation (38,39).

Waggoner et al. (40) studied six open chest mongrel dogswith surgically created tricuspid regurgitation and were ableto detect tricuspid regurgitation by means of pulsed Dopplerechocardiography in all six. Turbulent flow in the rightatrium during systole was found in 61 of 101 patients examined by the pulsed Doppler technique, although only 18patients had clinically evident tricuspid regurgitation. Unfortunately, right ventriculography was performed in only21 patients.

Garcia-Dorado et al. (41) found the two-dimensionalechocardiographic pulsed wave Doppler ultrasound technique to be sensitive in detecting tricuspid regurgitationwhen the sample volume was placed behind the tricuspidvalve in the parasternal short-axis or four chamber apicalview in systole. The diagnosis of tricuspid regurgitation inthese patients was confirmed by right ventriculography. Itsseverity was assessed by: 1) the systolic turbulence in the

right atrium, and 2) the ratio of maximal systolic velocityto maximal diastolic velocity in the superior vena cava.

Miyatake et al. (42), using pulsed Doppler gated withtwo-dimensional echocardiography, reported pansystolicabnormal Doppler signals in the right atrial cavity in 58 of62 patients with suspected tricuspid regurgitation. The tricuspid regurgitation was graded on a scale of I to 4 + onthe basis of the distance traveled by the abnormal signalsfrom the tricuspid orifice toward the posterior right atrialwall. The right ventriculograms were also graded on a 4point scale. Grades matched exactly in 36 patients but differed by I point in 23 and by 2 points in 3 patients. Thus,it may be concluded that the pulsed Doppler technique isthe most rel iable noninvasive method for assessing the severity of tricuspid regurgitation (Fig. 6), and that it is usefuleven in patients with atrial fibrillation, congestive heart failure or right ventricular pressure overload.

Nuclear imaging. Equilibrium radionuclide gated angiography provides a noninvasive method for evaluatingaortic or mitral insufficiency. There are only a few reportsof investigators using scintigraphic techniques in the diagnosis and quantitation of tricuspid regurgitation. In two suchstudies (43,44), when the radionuclide was injected into aperipheral vein, radioactivi ty was detected in the inferior


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Figure 6. Pulsed mode Doppler wave tracings with sampled volume in the lower rightatrium in a patient with significant tricuspidregurgitation secondary to multiple thrombiin 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); amplitudetracing of the Doppler signal showing tricuspid valve closure (TVC); spectral Doppler signal showing the direction and concentration of red blood cells from the baseline([ +] = positive flow toward the Dopplertransducer, [] == negative flow away fromthe Doppler transducer). A and E = AandEpoint, respectively, of the tricuspid valve;TR = tricuspid regurgitation of negativeflow in the right atrium away from the transducer. Calibration of flow velocity = 2mls..:',.

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confirm the diagnosis. Therefore, it is difficult to be certainif the reflux in these patients was indeed secondary to tricuspid regurgitation.

Noninvasive Diagnosis of Etiology ofTricuspid RegurgitationThe causes of organic tricuspid regurgitation are listed

in Table 2.Rheumatic heart disease. Rheumatic heart disease maycause tricuspid regurgitation by primary involvement of thevalve (organic) (Fig. 7) or by secondary involvement (functional or nonorganic) as a result of pulmonary hypertensionthat is generally secondary to mitral valve disease. Rheumatic tricuspid regurgitation is almost always associatedwith mitral valve disease (47). Tricuspid stenosis is alsopresent in 4 to 33% of the patients, depending on the methodof diagnosis, the lower valve probalby being more reflective

Common

Table 2. Causes and Origins of OrganicTricuspid RegurgitationRare

Ruptured chordae tetltlineaeCongenital tricuspid

dysplasia (dysgenesis)Endocardial cushion defectsAmyloid heart diseaseEosinophilic endomyocardial

diseaseEndocardial fibroelastosisTrauma

Rheumatic valvular diseaseTricuspid valve prolapseEbstein's anomalyCarcinoid heart diseaseBacterial endocarditis

vena cava in the presence of tricuspid regurgitation, after ithad entered the right ventricle. Handler et al. (45) computeda regurgitant index (the ratio of left ventricular stroke countsto right ventricular stroke counts) and found the ratio to beless in patients with tricuspid regurgitation than in normalsubjects. They found the ratio to be 0.7 0.1 in 9 patientswith clinical significant tricuspid regurgitation and 1.4 ::t0.1 in 39 patients without tricuspid regurgitation. Timeactivity variation over the liver was used to compute thehepatic expansion fraction, which was significantly higherin patients with tricuspid regurgitation than in control subjects. Fourier analysis of time-activity variation in each pixelwas used in generating amplitude and phase images. Allpatients with tricuspid regurgitation had more than 100 pixels over the liver automatically retained by the computer,whereas only I of 39 patients without tricuspid regurgitationhad pixels retained by the computer. However, the resultsof these techniques in patients with severe right heart failureand hepatic congestion but without tricuspid regurgitationwere not compared. Also, because no standard was availablefor assessing tricuspid regurgitation, data on sensitivity andspecificity of this method are lacking. Further work is neededto determine whether this method will allow quantificationof the severity of the lesion.Winzelberg et al. (46) examined the areas above andbelow the right atrium for tracer reflux in the right brachiocephalic vein, hepatic veins and inferior vena cava duringventricular systole. Tracer reflux was observed in 25 of 37patients, including all 10 patients who had clinically evidenttricuspid regurgitation. Many patients wtih reflux did not,however, have clinically diagnosed tricuspid regurgitation.Unfortunately, right ventriculography was not performed to


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of the incidence (16,47-51). Doming of the tricuspid valveon the two-dimensional echocardiogram is believed to be aspecific sign of concomitant tricuspid stenosis (48,49). Thetypical two-dimensional and M-mode echocardiographicfindings of rheumatic mitral disease have been described(52).

Previous classification of tricuspid regurgitation of rheumatic origin into functional and organic categories was basedon the presence and degree of pulmonary hypertension (53).This categoriZation, however, is riot precise. We observedpatients with pulmonary hypertension who had echographicfeatures of organic tricuspid valve disease; thus, organic andfunctional factors may coexist in some patients (54). In alarge series of patients with rheumatic mitral valve disease55), 60 0 had evidence of organic tricuspid valve disease

by two-dimensional echocardiography and cardiac catheterization could not differentiate orgnic from nonorganiccauses.Endocarditis. Infective endocarditis may produce vegtations on one or more of the leaflets (56,57), varying innumber, shape and size. Occasionally, the abnormal echoesare seen anter ior to the tricuspid valve in the right ventricularinflow or outflow tract, or multiple-layered echoes may beseen posterior to the tricuspid valve, resembling atrial myxomaon M-mode echocardiography (58).

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A~Figure 7. Echocardiographic and hemodynamic findings in patients with rheumatic trisucpid valve disease. Panel A (top left).M-mode findings of a decreased tricuspid valve EF slope, whichis consistent with but not specific for the presence of tricuspidstenosis. TV = tricuspid valve, Panel B. Simultaneous right atrialand right ventricular pressure tracings in a patient with mixedtricuspid valve disease. The pressure curves show elevated rightventricular and right atrial pressures. A large V wave in the rightatrial pressure tracing is the result of tricuspid regurgitation. Inaddition, a small end-diastolic gradient is noted (scale 0 to 40 mmHg). RA = right atrium; RV = right ventricle. Panel C , Twodimensional echocardiographic parasternal view of a right ventricular inflow tract, showing thickened anterior and posterior tricuspid valve leaflets in a patient with organic tricuspid regurgitationand stenosis. The right atrium is enlarged. Doming of the tricuspidleaflets 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 = rightventricle; Sup = superior. Panel D, Four chamber apical twodimensional echocardiographic view in same patient as in C, showing thickening of the anterior (ATL) and septal (STL) tricuspidleaflets with restricted motion and doming in diastole (r ight side).The anterior mitral valve leaflet and posterior mitral leaflet arealso thickened and restricted in motion, reflecting rheumatic involvement of both anterior valves. AML = anterior mitral leaflet;L = \eft; LA = left atrium; LV = left ventricle; PML = posteriormitral leaflet; RA = right atrium; RV = right ventricle.


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Two-dimensional echocardiography permits assessmentof the size and extent of vegetations and can identify complications of endocarditis, such as valve ring abcesses (59),and is more valuable than M-mode echocardiography forthis pUrPOse (60,61). Vegetations may decrease in size ordisappear in most of these ptients in the follow-up period(62-64).Tricuspid valve prolapse. Tricuspid valve prolapse seenin association with mitral valve prolapse (65) is caused bymyxomatous degeneration, resulting in redundancy of theleaflets. The diagnosis can be made by M-mode echocardiography, which demonstrates findings similar to those ofmitral valve prolapse (Fig. 8) (66-75).The two-dimensional echocardiographic features of prolapse of the tricuspid valve include visualization of one ormore leaflets prolapsing beyond the atrioventricular ring intothe right atrium (Fig. 8). The parastemallong-axis approachmay be preferred over the apical four chamber view forvisualization of the prolapse (72,73). In some patients, thesubxiphoid approach may show the prolapse when the otherapproaches fail (74). Between 3 and 52% of patients withmitral valve prolapse may have associated tricuspid valveprolapse (65,68,72,73,75,76). An association between tricuspid prolapse and atrial septal defect has been noted (69).Occasionally, aortic valve prolapse may be seen in association with mitral and tricuspid valve prolapse, that is, the floppy valve syndrome (72,73,76).The incidence of tricuspid regurgitation in patients withtricuspid valve prolapse has not been clearly defined, buthas been reported to be as high as 48% (29,75). Occasionally, tricuspid valve prolapse has been reported withoutassociated mitral valve prolapse (69,76).Papillary muscle rupture or dysfunction and ruptureof chordae tendineae. Ruptured chordae tendineae maycause tricuspid regurgitation (77-79). Rupture of the papillary muscle as a result of direct chest trauma (for example,during cardiopulmonary resuscitation or as a complicationof acute infarction) or as a consequence of endocarditis mayalso cause tricuspid regurgitation (80). Papillary muscle discontinuity is a potential complication of endomyocardialbiopsy.

The two-dimensional echocardiographic features of flailtricuspid valve were first reported by Mintz et al. (81). Thediagnostic criteria include systolic motion of the flail leafletbeyond the closure line into the right atrium, with loss ofthe usual coaptation point (43,78).Congenital heart disease. The most common cause ofcongenital tricuspid regurgitation is Ebstein's anomaly, whichcan be readily diagnosed by two-dimensional echocardiography (52). I f one measures the length (in em) from theapex of the left ventricle to the mitral valve ring in the apicalfour chamber view, and compares it with the ratio from theapex of the right'ventricle to the septal tricuspid valve ring,a ratio of these lengths greater than 2: 1 is diagnostic ofEbstein's disease (82). The clinical severity of this diseasedepends on the degree of tricuspid valve displacement, thesize of the atrialized right ventricle, the size and functionalcapacity of the true right ventricle, the severity of tricuspidregurgitation and the presence of associated abnormalitiessuch as atrial septal defect. Several other congenital anomalies can produce tricuspid regurgitation, for example, congenital tricuspid dysplasia (dysgenesis) (83).Carcinoid heart disease. The carcinoid syndrome is mostcommon in patients with metastatic ileocecal carcinoid tucmors (84). Cardiac involvement occurs as a late complication in approximately 50% of these patients; such complications include pulmonary regurgitation, tricuspidregurgitation and pulmonary stenosis. The echocardiographic features include right ventricular overload; thickening and restriction of the tricuspid valve valve motion,which stays in a half-open position (Fig. 9) and thickeningand restriction of the pulmonary valve (85-87). Doming ofthe tricuspid valve, which may be seen in rheumatic heartdisease, is not a feature of carcinoid heart disease (84).Other causes. Myxomas of the right atrium may producetricuspid regurgitation and can be detected by two-dimensional echocardiography (88). Other rare causes includeamyloid heart disease, which can affect the tricuspid valveand produce thickening (89) and can be readily detected onthe two-dimensional echocardiogram. Eosinophilic endomyocardial disease and endocardial fibroelastosis have rarelybeen reported to involve the tricuspid valve (90).

Figure 8. Echocardiographic features in patientswith tricuspid valve prolapse. The left panel is anM-mode echocardiogram of the tricuspid valve withsystolic prolapse (black arrow). The right panelis an apical four chamber two-dimensional view ina patient with combined mitral valve (open arrow)and tricuspid valve (closed arrow) prolapse. LA= left arium; LV = left ventricle; TV = tricuspidvalve.

. . ' f ..


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F ig ur e 9. Echocardiographic findings in a patient with carcinoid heartdisease. The top panel is a two-dimensional echocardiographic parasternal view of the right ventricularinflow tract in a pat ient wi th carcinoid heart disease. Note the thickened tricuspid valve with reducedmotion from systole to diastole. Inaddition. systolic coaptation is notmaintained. The bottom panel is anapical four chamber view in the samepatient, detailing a thickened tricuspid valve and an enlarged right atrium.TV = tricuspid valve.

SummaryTricuspid regurgitation is often not apparent on physical

examination, but several methods are available for its diagnosis. Cardiac catheterization with right ventriculographyhas been the historical diagnostic standard for all cardiovascular diagnoses. However, the need to place a catheteracross the right-sided valves has limited its usefulness inthe diagnosis of tricuspid and pulmonary valve regurgitationbecause valvular insufficiency may be produced by the catheter distorting the valve it traverses. Currently availablenoninvasive tools, such as M-mode and two-dimensionalechocardiography (with or without contrast), Doppler techniques and radionuclide cardiologic imaging, have madepossible the evaluation of tricuspid regurgitation without theneed to invade the patient. Contrast M-mode echocardiography is now the diagnostic standard to detect the presenceof tricuspid regurgitation. However, this technique is nottotally noninvasive as it is necessary to perform a veni

P ~ n c t u ~ e in a d d i ~ i o ~ one cannot ascertain the severity oftncuspld regurgitatIOn. Two-dimensional echocardiography, when employed with the M-mode technique in apatient with suspected tricuspid regurgitation, can be usedto evaluate the severity of tricuspid regurgitation by notingthe size and expansion of the right atrium, inferior vena

cava and hepatic veins. In addition, the cause of tricuspidregurgitation can be best discerned using two-dimensionalechocardiography. Radionuclide cardiac imaging tech

~ i q ~ e s .require a venipuncture and are not available in manymstltutlOns. Further work is needed to determine this tool'svalue in the assessment of tricuspid regurgitation. The Doppler technique may be the most sensitive tool to detect thepresence of tricuspid regurgitation and define its severity.The combination of Doppler study with two-dimensionalechocardiography (for guiding where to sample blood flow)will probably become the method of choice for the diagnosisand assessment of tricuspid regurgitation once the combinedmethod becomes standardized and more readily available.

ReferencesI. 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 ventricleot the human heart and on the gradation of function in warm bloodedanimals. Guys Hosp Rep 1837;2:104-78.3. Duroziez M. Du Retrecissement de la Tricuspide. Gaz Hop Paris1868;41 :310.4. Chatterjee K. Parmley WW . The role of vasodilator therapy in heartfailure. Prog Cardiovasc Dis 1977; 19:301-25.


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