Tricuspid and Pulmonic Valve Disease

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7 Tricuspid and Pulmonic Valve Disease

Tricuspid Regurgitation

Scanning Issues

Required parameters to obtain from scanning include the following:

Valve and RV details to explain the cause of the tricuspid regurgitation (TR)

TR severity

• Hepatic venous systolic flow pattern

• Jet size, right atrium (RA) size, effective regurgitant orifice (ERO)

RV size and systolic function, and net forward cardiac index (CI) from the left ventricular outflow tract (LVOT)–velocity time interval (VTI) method

TR spectral profile

Scanning Notes

There are problems with color Doppler “quantification” of TR, as there are for color Doppler flow-mapping of any lesions of insufficiency: TR flow-mapping is dependent on gain, angle, position, and jet shape and orientation.

Retrograde hepatic venous systolic flow reliably establishes that TR is severe.

Obtain the complete TR profile by appropriate means, and measure in the center of the parabola. The single most common problem with TR spectral recording is not having enough signal to establish the true peak velocity. If the complete profile does not appear to be present, the cursor should be placed off to the side of the profile so that the reviewer is not swayed by the position of the cursor placed by the person recording the study.

Spectral profiles should be two-thirds the height of the display, and wide enough so that there are two or three per display.

Use zoom views liberally to identify the valve lesion responsible for TR.

Proximal isovelocity surface area (PISA) techniques are acceptable for severity assessment, but offer no more than does hepatic venous flow, and therefore are not required.

Reporting Issues

For any given size of tricuspid valve ERO, there is less regurgitant flow than with MR, as the usual RV–RA gradients are less than the usual left ventricular (LV)–left atrial (LA) gradients. Absence of hepatic venous flow reversal is associated with tricuspid valve EROs (<40 mm²) and therefore, in the final analysis, tricuspid valve–ERO generally adds little to hepatic flow profiling.¹

Although there is some correlation between TR and RVSP, an important minority of cases of severe pulmonary hypertension lack sufficient TR to be detected by Doppler interrogation.

Causes of Tricuspid Regurgitation

Congenital

Tricuspid valve dysplasia

• Thickened and shortened leaflets and chordae

Ebstein’s anomaly

Functional

“Functional” (i.e., intact leaflet/chordal/papillary components)

• RV annular dilation

• RV body dilation

“Organic”

Rheumatic

• Characterized by thickening, chordal thickening, commissural thickening, and sometimes by doming

• Thickening and roughness of the leaflet edges impair coaptation.

• Motion is reduced.

Carcinoid

• Characterized by thickening, chordal thickening, often frank immobility

• Doming is atypical.

• Stenosis usually is concurrent but regurgitation dominates.

• Leaflets typically are “fixed” partially open/partially closed.

Myxomatous tricuspid valve disease/tricuspid valve prolapse

• May be isolated

• Anterior and septal leaflets usually; therefore, seen on apical 4CV, RV inflow views

• More usually associated with other myxomatous findings (e.g., mitral valve prolapse, aortic root dilation)

RV papillary muscle rupture: post-infarction, post-trauma, post-biopsy, post–lead extraction

Pacemakers or implantable defibrillators

• Impinging on a leaflet

• Perforating a leaflet

Trauma

• Penetrating (e.g., endomyocardial biopsy)

• Blunt force trauma

Endocarditis

• Septic emboli to the lungs raise the pulmonary artery pressure, which increases the TR.

Estimation of Right Ventricular Systolic Pressure

The RV–RA gradient is calculated, and the right atrial pressure (RAP) is estimated: therefore, the RVSP is both calculated and estimated. Some TR is recordable in >95% of cases.

Potential problems in estimating the RVSP include the following:

No TR from which to determine RV–RA gradient

Insufficient TR from which to determine maximum RV–RA gradient

Incomplete TR profile (missing peak)

The RAP estimate is only that.

The TR gradient method to estimate RVSP is a clinical workhorse, not a racehorse. The overall correlation is very good, but there is a tendency to overestimate lower RVSP and to underestimate high RVSP.

Over-estimation of low RVSP

• Due to estimation of RAP as, for example, 10 mm Hg, which is higher than normal physiologic RAP (–2–8 mm Hg)

Underestimation of high RVSP

• Due to estimation of RAP as, for example, 10 mm Hg, which is lower than may occur in several disease states (RV infarction, restrictive cardiomyopathy, constrictive pericarditis, terminal cor pulmonale) where the RVSP may be 20 to 35 mm Hg

Inability to record the full TR profile due to inadequate signal

• As the echocardiography:catheterization relation demonstrates this tendency for echocardiography to overestimate RVSP at lower pressures, and to underestimate it at higher pressures when a “fixed” RAP of 10 mm Hg is added, use of 5, 10, and 15 mm Hg seems reasonable, at the operator’s discretion. The presence of extremely high RAPs will systematically lead to underestimation of the RVSP.

The correlation of RV:RA gradient is excellent (r = 0.95; SEE = 7 mm Hg)² (r = 0.96; SEE = 7 mm Hg),³ but the correlation of jugular venous pressure estimate to catheter RAP is less good (r = 0.80; SEE = 2.3 mm Hg). Clearly, clinical estimate of jugular venous pressure overestimates lower RAPs (<8 cm) and underestimates higher RAPs—sometimes by 40% when the true RAP is 20 mm Hg.

More patients with an elevated RVSP have analyzable TR spectral profiles than do patients (half) with normal RVSP.³ However, an important minority subset of patients with severely elevated RVSP (approximately 20–25% of cases of primary pulmonary hypertension) may not have associated TR to yield an analyzable (complete) TR spectral profile. Overall, the correlation of echocardiographic RVSP to catheter RVSP is quite good (r = 0.93; SEE = 8 mm), but remains influenced by the vagaries of estimating jugular venous pressure and RAP.²

Indications for the management and intervention in tricuspid regurgitation are listed in Boxes 7-1 and 7-2.

Tricuspid Stenosis

Scanning Issues

Required parameters to obtain from scanning include the following:

Valve morphology and motion (doming)

Mean gradient, spectral profile characteristics

• Measure three spectral profiles at a high sweep speed (100 mm/sec) if in sinus rhythm and five spectral profiles if in atrial fibrillation.

• Do not measure at inspiration; measure at end expiration.

RA size

As the tricuspid valve has three commissures, extensive disease must be present (at least two commissures) to cause stenosis. Echocardiographic features of tricuspid stenosis (TS) include the following:

Evidence of flow convergence across the tricuspid valve

Doming motion or frozen leaflets

Mean gradient ≥ 5 mm Hg

Marked prolongation of the pressure half time (PHT), and elevation of the end-diastolic velocity (PHT ≥ 190 msec)

Ancillary findings: dilated RA and inferior vena cava

Tricuspid Atresia

There is no continuity between the right atrial and right ventricular cavities. A thick barrier/band separates the two.

The right ventricle, without blood volume within it, is hypoplastic.

An anterior septal defect, with or without a ventricular septal defect, is present.

Transposition of the great arteries may be present.

Concerns

By definition, TS is present when there is a mean gradient of ≥5 mm Hg. The difference between normal tricuspid valve “gradient” by the modified equation (= 4 × V², = 4 × 0.7² = 2 mm Hg), where V is peak diastolic velocity across the tricuspid valve, and what constitutes significant TS (≥5 mm Hg) is a small difference.

Neither the modified Bernouilli relation nor the PHT relation is as accurate for the evaluation of most cases of TS as they are for most cases of MS.

The 220/PHT has not been validated for the tricuspid valve, and is essentially “borrowed” from the validation of MS with areas of 1.0 to 1.5 cm².

It is proposed by some that 190/PHT be used for the assessment of TS.

In TS, the RAP will be very elevated, confounding estimation of RVSP determination using usual estimated RAP.

Pulmonic Stenosis

Pulmonic stenosis is almost always a congenital lesion. It may be solitary at the valvar level, or made up of differing degrees of subvalvar narrowing, valvar narrowing, or supravalvar narrowing. Contrary to most other valve lesions, the severity of pulmonic stenosis is usually described by the peak gradient, which in the case of echocardiography will have to be the peak instantaneous gradient. The site and substrate of the gradient must be imaged, as well as the magnitude of the gradient being established. Balloon valvuloplasty, the usual treatment for severe pulmonic stenosis, achieves better results for thinner/doming leaflets than with thicker presumed dysplastic leaflets. Subvalvar stenosis is a surgical lesion. Sampling of gradients is easier in children than it is in adults. Posterior short-axis views in adults often fail to achieve optimal alignment for the purposes of Doppler sampling, and subcostal outflow views are less achievable as the distances increase with larger body size, even without abdominal obesity. Concurrent VSD jet turbulence in the right ventricular outflow tract may confound accurate sampling.

If the TR-derived RVSP exceeds significantly the PS gradient at the valve level, look for the presence of subvalvar and/or supravalvar stenosis.

The valvular diameter dimension is used to identify the optimal balloon size for dilation.

Grading of pulmonic stenosis

Indications for the evaluation of pulmonary stenosis are given in Box 7-3 and and indications for balloon valvulopathy are given in Box 7-4.

Pulmonic Insufficiency

A minor amount of pulmonic valve insufficiency is detected by transthoracic echocardiography in almost all normal individuals, occurring along the commissures rather than being central. As with other lesions of insufficiency, color Doppler flow mapping techniques do not “quantify” pulmonic insufficiency. Recognizing mild and moderate degrees of pathological insufficiency is less important than distinguishing severe insufficiency. Severe PI will invariably dilate the right ventricular cavity, although other lesions also do, such as severe tricuspid insufficiency. Severe PI jets will fill the right ventricular outflow tract with color signal, and the slope of the profile will be steep. As with severe AI, the gradient wanes as the right ventricular diastolic pressure rises and the pulmonary artery diastolic pressure decreases, and the two pressures approximate, leaving little driving pressure and, thereby, low velocity.

Summary

TS requires fusion of at least two commissures.

The 5-mm Hg gradient of significant TS is a problem for the modified Bernouilli equation.

Tricuspid insufficiency is readily detected by echocardiography, and its cause is usually apparent.

Alternate imaging modalities generally add little for the assessment of the tricuspid valve.

Conversely, cardiac magnetic resonance offers a robust means, and the only accurately quantitative means, to calculate pulmonic insufficiency volume, regurgitant fraction, right ventricular volume, and ejection fraction. Cardiac magnetic resonance also can more accurately depict the anatomy of the pulmonary subvalvar and supravalvar segments.

BOX 7-1 Management of Tricuspid Regurgitation: ACC/AHA 2006 Recommendations

Class I

Tricuspid valve repair is beneficial for severe tricuspid regurgitation (TR) in patients with mitral valve disease requiring mitral valve surgery. (Level of evidence: B)

Class IIa

Tricuspid valve replacement or annuloplasty is reasonable for severe primary TR when symptomatic. (Level of evidence: C)

Tricuspid valve replacement is reasonable for severe TR secondary to diseased/abnormal tricuspid valve leaflets not amenable to annuloplasty or repair. (Level of evidence: C)

Class IIb

Tricuspid annuloplasty may be considered for less than severe TR in patients undergoing mitral valve surgery when there is pulmonary hypertension or tricuspid annular dilatation. (Level of evidence: C)

Class III

Tricuspid valve replacement or annuloplasty is not indicated in asymptomatic patients with TR whose pulmonary artery systolic pressure is <60 mm Hg in the presence of a normal mitral valve. (Level of evidence: C)

Tricuspid valve replacement or annuloplasty is not indicated in patients with mild primary TR. (Level of evidence: C)

From ACC/AHA 2006 guidelines for the management of patients with valvular heart disease. J Am Coll Cardiol. 2006;48(3):e1–e148.

BOX 7-2 Indications for Intervention in Tricuspid Regurgitation: ACC/AHA 2006 Recommendations

Class I

1. Surgery for severe tricuspid regurgitation (TR) is recommended for adolescent and young adult patients with deteriorating exercise capacity (New York Heart Association [NYHA] functional class III or IV). (Level of evidence: C)

2. Surgery for severe TR is recommended for adolescent and young adult patients with progressive cyanosis and arterial saturation less than 80% at rest or with exercise. (Level of evidence: C)

3. Interventional catheterization closure of the atrial communication is recommended for the adolescent or young adult with TR who is hypoxemic at rest and with exercise intolerance due to increasing hypoxemia with exercise, when the tricuspid valve appears difficult to repair surgically. (Level of evidence: C)

Class IIa

1. Surgery for severe TR is reasonable in adolescent and young adult patients with NYHA functional class II symptoms if the valve appears to be repairable. (Level of evidence: C)

2. Surgery for severe TR is reasonable in adolescent and young adult patients with atrial fibrillation. (Level of evidence: C)

Class IIb

1. Surgery for severe TR may be considered in asymptomatic adolescent and young adult patients with increasing heart size and a cardiothoracic ratio of more than 65%. (Level of evidence: C)

2. Surgery for severe TR may be considered in asymptomatic adolescent and young adult patients with stable heart size and an arterial saturation of less than 85%, when the tricuspid valve appears repairable. (Level of evidence: C)

3. In adolescent and young adult patients with TR who are mildly cyanotic at rest but who become very hypoxemic with exercise, closure of the atrial communication by interventional catheterization may be considered when the valve does not appear amenable to repair. (Level of evidence: C)

4. If surgery for Ebstein’s anomaly is planned in adolescent and young adult patients (tricuspid valve repair or replacement), a preoperative electrophysiologic study may be considered to identify accessory pathways. If present, these may be considered for mapping and ablation either preoperatively or at the time of surgery. (Level of evidence: C)

From ACC/AHA 2006 guidelines for the management of patients with valvular heart disease. J Am Coll Cardiol. 2006;48(3):e1–e148.

BOX 7-3 Evaluation of Pulmonic Stenosis in Adolescents and Young Adults: ACC/AHA 2006 Recommendations

Class I

1. An ECG is recommended for the initial evaluation of pulmonic stenosis in adolescent and young adult patients, and serially every 5–10 years for follow-up examinations. (Level of evidence: C)

2. Transthoracic Doppler echocardiography is recommended for the initial evaluation of pulmonic stenosis in adolescent and young adult patients, and serially every 5–10 years for follow-up examinations. (Level of evidence: C)

3. Cardiac catheterization is recommended in the adolescent or young adult with pulmonic stenosis for evaluation of the valvular gradient if the Doppler peak jet velocity is >3 m/sec (estimated peak gradient >36 mm Hg), and balloon dilation can be performed if indicated. (Level of evidence: C)

Class III

Diagnostic cardiac catheterization is not recommended for the initial diagnostic evaluation of pulmonic stenosis in adolescents.

From ACC/AHA 2006 guidelines for the management of patients with valvular heart disease. J Am Coll Cardiol. 2006;48(3):e1–e148.

BOX 7-4 Balloon Valvotomy in Pulmonic Stenosis: ACC/AHA 2006 Recommendations

Class I

1. Balloon valvotomy is recommended in adolescent and young adult patients with pulmonic stenosis who have exertional dyspnea, angina, syncope, or presyncope and an RV–to–pulmonary artery peak-to-peak gradient >30 mm Hg at catheterization. (Level of evidence: C)

2. Balloon valvotomy is recommended in asymptomatic adolescent and young adult patients with pulmonic stenosis and RV–to–pulmonary artery peak-to-peak gradient >40 mm Hg at catheterization. (Level of evidence: C)

Class IIb

Balloon valvotomy may be reasonable in asymptomatic adolescent and young adult patients with pulmonic stenosis and an RV–to–pulmonary artery peak-to-peak gradient 30–39 mm Hg at catheterization. (Level of evidence: C)

From ACC/AHA 2006 guidelines for the management of patients with valvular heart disease. J Am Coll Cardiol. 2006;48(3):e1–e148.

BOX 7-5 Appropriateness Criteria and Indications for Cardiac Imaging Modalities for the Assessment of Tricuspid and Pulmonic Valve Disease

Transthoracic Echocardiography

ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography ⁵

Native Valvular Regurgitation or Stenosis with TTE

Routine surveillance of trace valvular regurgitationAppropriateness criteria: I; median score: 1

Routine surveillance (<3 yr) of mild valvular regurgitation or stenosis without a change in clinical status or cardiac examinationAppropriateness criteria: I; median score: 2

Routine surveillance (≥3 yr) of mild valvular regurgitation or stenosis without a change in clinical status or cardiac examinationAppropriateness criteria: U; median score: 4

Routine surveillance (<1 yr) of moderate or severe valvular regurgitation or stenosis without a change in clinical status or cardiac examinationAppropriateness criteria: U; median score: 6

Routine surveillance (≥1 yr) of moderate or severe valvular regurgitation or stenosis without change in clinical status or cardiac examinationAppropriateness criteria: A; median score: 8

ACC/AHA/ASE 2003 Guideline Update for the Clinical Application of Echocardiography

No specific entries

Transesophageal Echocardiography

ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography ⁵

TEE as Initial or Supplemental Test—Valvular Disease

Evaluation of valvular structure and function to assess suitability for, and assist in planning of, an interventionAppropriateness criteria: A; median score: 9

Cardiac Computed Tomography

ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/SCMR 2010 Appropriate Use Criteria for Cardiac CT ⁶

Characterization of native cardiac valves

Suspected clinically significant valvular dysfunction

Inadequate images from other noninvasive methodsAppropriateness criteria: A; median score: 8

Nuclear

ACCF/ASNC/AHA/ASE/SCCT/SCMR/SNM 2009 Appropriate Use Criteria for Cardiac Radionuclide Imaging ⁷

Evaluation of LV Function

Assessment of LV function with radionuclide angiography (ERNA or FP RNA)

In absence of recent reliable diagnostic information regarding ventricular function obtained with another imaging modality

Appropriateness criteria: A; median score: 8

Appropriateness criteria: A, appropriate; I, inappropriate; U, uncertain.

LV, left ventricular; TEE, transesophageal echocardiography; TTE, transthoracic echocardiography.

TABLE 7-1 Utility of Different Imaging Modalities and Cardiac Catheterization in the Assessment of Tricuspid Valve Disease

MODALITY	PROS	CONS/CAVEATS
Transthoracic Echocardiography	• For the detection of tricuspid valve infective endocarditis, TTE and TEE are nearly equivalent. • Use of hepatic systolic flow reversal as the sign of severe TR is reproducible.

• The characterization of TR in the mild/moderate range is imprecise.

• The modified Bernouilli equation functions poorly at the low gradients typical of TS.

Transesophageal Echocardiography

TEE is better able to image the tricuspid valve.

• TEE affords poor alignment for sampling of TS and most TR jets.

• Unless the transthoracic image quality is poor, TEE does not add much to the detection of tricuspid valve endocarditis.

Cardiac CT NA

• The role of cardiac CT for the assessment of tricupsid valve disease has not been determined.

Cardiac MRI

CMR is the best test to follow right ventricular volumes and systolic function, and tricuspid valve regurgitant volumes and fraction. SSFP sequences will determine the total RV stroke volume, velocity-encoded phase contrast sequences will determine the net forward stroke volume; the difference is the TR volume.

NA Nuclear

First-pass RNA is an accurate and reproducible test for serial following of changes in RVEF with chronic severe TR.

NA Chest Radiography

The chest radiograph has little to add to the evaluation of tricuspid valve disease other than some depiction of right atrial chamber size and pulmonary artery size.

NA Cardiac Catheterization

The role of cardiac catheterization for the assessment of tricuspid valve disease is limited to verification of right-sided pressures and delivery of balloon dilation for TS.

CMR, cardiac magnetic resonance; NA, not applicable; RVEF, right ventricular ejection fraction; SSFP, steady-state free precession; TEE, transesophageal echocardiography; TR, tricuspid regurgitation; TS, tricuspid stenosis; TTE, transthoracic echocardiography.

TABLE 7-2 Utility of Different Imaging Modalities and Cardiac Catheterization in the Assessment of Pulmonic Valve Disease

MODALITY	PROS	CONS/CAVEATS
Transthoracic Echocardiography	2D echocardiography • TTE is able to depict pulmonic valve morphology: • Thickening • Doming • Vegetations • For the detection of right-sided infective endocarditis, TTE and TEE are nearly equivalent.	• In adult patients, shadowing may impair visualization of the lateral aspect of the pulmonary valve and pulmonary artery. • Identification of concurrent subvalvar stenosis or supravalvar and peripheral pulmonic stenosis may be difficult.
	Doppler echocaradiography: TTE is able to assess both PS and PI in children and young adults, but views become more limited (and Doppler alignment less suitable) with age.	• Determination of PI severity by TTE is qualitative. • In adulthood, the assessment of PS, especially subvalvar PS, becomes less reliable.
Transesophageal Echocardiography	• TEE does not offer a better means to assess the severity of PI, but may offer a better understanding of the cause. • 70-degree views of the RVOT usually depict subvalvar lesions and obstruction. • Transgastric RV long-axis views may allow for accurate determination of RVOT and pulmonic gradients.	• Shadowing from any dense structure at the aortic valve level, (e.g., calcification, prosthesis), will be to the detriment of imaging the pulmonic valve.
Cardiac CT	Determination of RVOT dimensions and trabecular level obstruction should be feasible if systolic phase images are gathered.	• The contribution and role of ECG-gated cardiac CT in treatment of pulmonic valve disease is undefined. • No physiologic information (other than RVEF%) will be available by cardiac CT.
Cardiac MRI	SSFP sequences • The contribution of CMR toward pulmonic valve disease is significant: • No other imaging modality is as well suited to determine RV volumes and ejection fraction as is CMR. • Able to assess RVOT anatomy
	LGE sequences: NA	• Have little to offer the average case
	VEPC sequences • VEPC techniques are well-suited to assess the regurgitant volume and regurgitant fraction of PI, as the main pulmonary artery lends itself well to the technique. • VEPC techniques are reasonably well suited to assess the systolic gradient of PS.
Nuclear	RNA: First-pass RVEF calculation is accurate and reproducible, second in rank to CMR for assessment of RVEF.	NA
Chest Radiography	Chest radiography has relatively little to offer in the assessment of pulmonic valve disease, although pulmonic valve endocarditis with septic emboli to the lungs is often apparent, as is poststenotic dilation of the pulmonary artery.	NA
Cardiac Catheterization	Right heart catheterization is readily able to provide the gradients across the pulmonic valve and a vehicle for valvuloplasty and percutaneous valve delivery.	NA

CMR, cardiac magnetic resonance; ECG, electrocardiographic; LGE, late gadolinium enhancement; NA, not applicable; PI, pulmonary insufficiency; PS, pulmonary stenosis; RV, right ventricular; RVEF, right ventricular ejection fraction; RVOT, right ventricular outflow tract; SSFP, steady-state free precession; TEE, transesophageal echocardiography; TTE, transthoracic echocardiography; VEPC, velocity-encoded phase contrast.

Figure 7-1 Severe tricuspid regurgitation due to severe pulmonary hypertension. The jet of color Doppler flow mapping nearly fills the large right atrium, which, although not as specific a sign as hepatic systolic flow reversal, is almost as good. The spectral Doppler tracings of the tricuspid regurgitation reveal systemic levels of pressure gradient between the right ventricle and right atrium. If the respirometry tracing can be taken at face value, the right ventricular systolic pressure increases with inspiration—a sign of impaired right heart compliance.

Figure 7-2 Tricuspid regurgitation spectral profiles/atrial fibrillation. In this case, there is little variation of the tricuspid regurgitation velocity depending on R-R interval. When the peak part of the profile is ambiguous, additional height to the spectral display should be left to enable the reader to determine his or her sense of the peak. Similarly, the optimal place to mark with cross-hairs is beside the spectral profile, so as not to obscure the profile and to allow the reader to generate his or her own impression of the peak velocity.

Figure 7-3 Severe tricuspid regurgitation. Spectral tracings of superior hepatic venous flow in two patients, both with systolic flow reversal, which is the best (i.e., most specific) sign of severe tricuspid regurgitation.

Figure 7-4 Severe tricuspid regurgitation with volume overload findings of the right heart. The parasternal M-mode tracing demonstrates enlargement of the right ventricle with diastolic shift of the interventricular septum toward the left side of the heart due to right ventricle volume overload from tricuspid regurgitation. If there were a similar volume load on the left heart from mitral regurgitation, the septal position would be neutral—“two (equivalent and opposite) wrongs make a right.” In keeping with the right heart volume overload, the inferior vena cava is dilated and lacks respiratory variation in dimension.

Figure 7-5 Tricuspid stenosis. The color Doppler image reveals a large proximal isovelocity surface area and a well-formed diastolic jet. The spectral profiles reveal (the effect of atrial fibrillation) elevation of the peak and mean velocities, and prolongation of the deceleration time. As with mitral stenosis, the longer diastolic filling periods are associated with lower mean velocities but easier tracings to measure the deceleration time.

Figure 7-6 Carcinoid heart disease. The tricuspid leaflets and chordae are thickened, bright, and retracted open, resulting in severe tricuspid regurgitation. The pulmonary metastases were held to be responsible for the severe pulmonary hypertension.

Figure 7-7 Severe tricuspid regurgitation with two-dimensional signs of volume overload (diastolic shift toward the left side), hepatic venous systolic flow reversal, open retraction of the tricuspid leaflets, and a large color jet essentially filling the right atrium.

Figure 7-8 Tricuspid regurgitation spectral profiles and right ventricular pressures. The rhythm is sinus, eliminating much chance for RR variation effect on developed systolic pressures. The first spectral tracing is so incomplete that the determination of right ventricular systolic pressure (RVSP) is inconclusive. The second spectral profile is still incomplete with respect to depicting the parabolic outer shape, but the highest depicted aspect measures about 4.7 m/sec, demonstrating just how incomplete the first profile was. The biggest problem in determining RVSP is obtaining a meaningfully complete spectral profile. If it is not complete, reporting should emphasize that the determination of RVSP is inadequate. In this case the catheterization recorded RVSPs are commensurate with the echo determination of RVSP, with an estimated/guesstimated right atrial pressure of 10 mm Hg: 4 × 4.6² + 10 mm Hg = 95 mm Hg. Note the variation of RVSP and of right ventricular diastolic pressure (RVDP). The RVSP varies by 12%, whereas the RVDP varies by 75%. Although the right ventricular end-diastolic pressure is 10 to 14 mm Hg, the mean right ventricular diastolic pressure varies between approximately 4 and 10 mm Hg, revealing how difficult it is to assign a single pressure to the right atrium, and how averages of many cardiac cycles are always more representative of the variation and mean than are single measurements. In a helpful way, in the spectral display the cross-hairs were kept to the side of the observed peaks, rather than being placed onto the marginal quality tracings and imparting a bias.

Figure 7-9 Severe tricuspid regurgitation: tricuspid (TR) and hepatic venous spectral flow profiles. Right upper image: The TR spectral profile is nonparabolic, with the second half concave. Right middle image: The hepatic venous flow profile reveals a well-formed profile of systolic reversal. The lower image depicts superimposition of the two spectral tracings—the hepatic reversal profile completes the component missing on the TR profile. A recording of a nice V-wave would be usual in such a situation: as the right atrial pressure rises rapidly (into a large V-wave), the right ventricle-to-right atrium gradient diminishes, resulting in the trailing away of the latter aspect of the TR profile. Because the systolic V-wave in the right atrium exceeds the inferior vena cava pressure, there is systolic reversal of flow. The concave TR profile and hepatic venous systolic profiles are physiologically interlinked.

Figure 7-10 Tricuspid bioprosthesis obstruction from large vegetations. The prosthesis is slathered with bulky vegetations seen on both transthoracic and transesophageal two-dimensional imaging (which lends credence to the similar detection rate of right heart endocarditis lesions by transthoracic and transesophageal imaging). There is a very large diastolic proximal isovelocity surface area before the prosthesis orifice, and elevation of the flow velocities and shallow deceleration slope. In fact, the contour of the diastolic spectral profile of flow velocity across the bioprosthesis appears to be upward sloping, consistent with a dynamic and worsening orifice, probably because of the bulky vegetations approximating within the orifice through diastole. The lungs were heavily stained by septic embolism (Staphylococcus aureus).

Figure 7-11 Same patient as in Figure 7-10. The sternotomy wires are obvious, and the bioprosthesis stent wires can be seen. There is extensive patchy consolidation due to septic embolization of tricuspid valve vegetations into the lungs.