neduri vinod kumar, 73B, internal medicine, tricuspid regurgitation ppt.pptx

tricuspid regurgitation, internal medicine

1. INTERNAL MEDICINE Professor: романова валентівна олександрівна

2. TRICUSPID REGURGITATION (Tricuspid Insufficiency; Tricuspid Incompetence) Presented by:  Neduri vinod kumar 73B

3. Introduction Tricuspid regurgitation (TR) is insufficiency of the tricuspid valve causing blood flow from the right ventricle to the right atrium during systole. Tricuspid regurgitation most frequently occurs with a structurally normal tricuspid valve (functional tricuspid regurgitation), which is the result of a dilated right ventricle and tricuspid annulus and papillary muscle dysfunction. Tricuspid regurgitation (TR) occurs in 65–85% of the population. Thus, mild TR in the setting of a structurally normal tricuspid valve (TV) apparatus can be considered a normal variant. Moderate or severe TR is usually associated with leaflet abnormalities and/or annular dilation and is usually pathologic. Primary tricuspid regurgitation occurs in  15 to 30% of patients due to the direct involvement of the tricuspid valve  and is the result of congenital heart disorders such as Ebstein's anomaly, or acquired disorders or diseases of the TV, such as myxomatous degeneration of the tricuspid valve, endocarditis, carcinoid.

4. Anatomy, overview & function of tricuspid valve The tricuspid valve (TV) is a complex anatomical structure that incorporates a saddle-shaped annulus, asymmetric leaflets, the subvalvular apparatus and the right ventricle and its loading conditions. The tricuspid valve is located between the right lower heart chamber (right ventricle) and the right upper heart chamber (right atrium). It’s positioned vertically (up and down). The tricuspid valve is made of three thin but strong flaps of tissue. They’re called leaflets or cusps. The leaflets are named by their positions: anterior, posterior and septal. They attach to the papillary muscles of the ventricle with thin, strong cords called chordae tendineae. With every heartbeat, those leaflets open and close. The sounds of the heart valves opening and closing are the sounds you hear in a heartbeat. The tricuspid valve ensures that blood flows from the right atrium to the right ventricle. It also prevents blood from flowing backward between those two chambersWhen the right atrium fills, the tricuspid valve opens, letting blood into the right ventricle. Then the right ventricle contracts to send blood to the lungs. The tricuspid valve closes tightly so that blood does not go backward into the right atrium.

5. Etiology and classification Primary (organic), anatomically abnormal valve TR: It can be inherited or acquired, and accounts for 10% of cases of TR in adults. Inherited causes include Ebstein’s anomaly, atrioventricular defects, and myxomatous prolapse. Acquired primary TR can be caused by rheumatic disease, carcinoid syndrome, infective endocarditis, cardiac implantable electronic device leads, trauma (for example, from repeated endomyocardial biopsies after cardiac transplantation, or from blunt trauma with papillary muscle rupture), drugs, and endomyocardial fibrosis.

6. Functional (secondary),  d ilated Annulus  anatomically normal valve TR: constitutes approximately 90% of TR and is due to a heterogenous group of etiologies that cause right atrial (RA) or right ventricular (RV) dilation.  This results in annular dilation and tethering of the TV leaflets. Common causes of RV/RA dilation include pulmonary hypertension (PH), longstanding atrial fibrillation, left-sided heart failure, mitral regurgitation or stenosis (MR or MS), and significant left-to-right shunting. the presence of severe TR was associated with decreased survival after adjusting for PH and ejection fraction  mortality in patients with greater than or equal to moderate isolated TR was higher than in the matched cases with trivial TR (P=0.0014; matching for age, sex, atrial fibrillation, ejection fraction, comorbidity index) In a retrospective analysis by Chorin , hazard ratio for overall mortality was 1.15 for moderate TR [95% confidence interval (CI), 1.02–1.30, P=0.024] and 1.43 for severe TR (HR 1.43; 95% CI, 1.08–1.88, P=0.011) when compared to no or minimal TR.

7. mechanisms Rheumatic tricuspid regurgitation:  It always coexists with mitral valve involvement and is aggravated by associated pulmonary hypertension. Although two-thirds of patients with rheumatic mitral valve disease have pathologic evidence of tricuspid valve involvement, clinically significant tricuspid disease, which generally affects young and middle-aged women, is much less common.  Rheumatic tricuspid involvement is usually mild and generally is manifested clinically as pure regurgitation or mixed regurgitation and stenosis, caused by the fibrosis of the valve leaflets and chordae tendineae. Contracture of the leaflets and commissural fusion, produce regurgitation and stenosis, respectively .

8. Tricuspid valve endocarditis; occurs primarily in injection drug users and patients with chronic intravascular hardware, left-to-right shunts, burns, and immunocompromised states. Infective endocarditis is more common in injecting drug users who are HIV positive than in HIV negative. It is caused by  virulent pathogens that infect structurally normal valves like Staphylococcus aureus, streptococci and enterococci. Fungal endocarditis should be considered when vegetations are large; they occasionally cause obstruction.  Abscesses may involve the annulus and septum, and chordal rupture or valve perforations may cause tricuspid regurgitation. 

9. Carcinoid tumors: rare cause of both tricuspid and pulmonic valve disease. The vasoactive substances (principally serotonin) produced by these tumors are believed to be causal, and patients with carcinoid valvular disease have higher serum levels of serotonin and increased urinary excretion of its metabolite, 5-hydroxyindoleacetic acid (5-HIAA), than those without cardiac disease. Left-sided valve involvement is seen in patients with right-to-left shunts or bronchial tumors. The valve exhibits pathognomonic plaque-like deposits of fibrous tissue (which may also deposit on the endocardium); leaflet distortion leads to regurgitation, stenosis, or both. Tricuspid regurgitation is the most common lesion and is detected by echocardiography in virtually all patients with carcinoid tricuspid valve disease. Surgery like tricuspid valve replacement

10. Tricuspid valve prolapse: It is owing to myxomatous degeneration, is seen almost exclusively in patients with mitral valve prolapse and occurs in as many as 50% of cases.  Anterior leaflet prolapse is most common, followed by septal and posterior leaflet prolapse.  The associated tricuspid regurgitation is usually mild.  Although tricuspid valve prolapse may be a marker of generalized connective tissue disease and a poor prognostic indicator in patients with mitral valve prolapse, its clinical significance remains undefined. Like mitral valve prolapse, the precise incidence of tricuspid valve prolapse is difficult to determine because of inconsistent clinical, echocardiographic, and angiographic definitions. 

11. Ebstein anomaly: TR is a frequent component of Ebstein anomaly of the tricuspid valve because of the apical displacement of septal and posterior tricuspid leaflets. This results in “ atrialization ” of a variable portion of the right ventricle and a range of abnormalities involving the anterior leaflet and atrial septum. The downward displacement of the tricuspid valve frequently causes a tricuspid regurgitant murmur (heard best in the apical area).  This uncommon congenital abnormality is associated with rightto -left intra-atrial shunting, RV dysfunction, supraventricular arrhythmias, and sudden death. systemic lupus erythematosus: TR of at least moderate severity may complicate as many as 25% of cases of SLE. significant tricuspid regurgitation is usually due to the pulmonary hypertension produced by lupus pulmonary disease. Libman-Sacks endocarditis that involves the tricuspid valve is far less common. Libman-Sacks endocarditis has been associated with antiphospholipid antibodies, which has been shown to cause valvular thickening, isolated tricuspid involvement, and the development of nonbacterial vegetations. 

12. Most patients present with combined tricuspid regurgitation and stenosis, and the regurgitation is typically moderate or severe. Pulmonary hypertension is usually present and contributes to the valvular dysfunction.  catheter-induced TR: occurs in approximately 50% of cases with catheters across the valve, the regurgitation is quantitatively small, clinically unimportant, and usually disappears when the catheter is removed. late complication of successful mitral valve replacement(MVR): In one series, Doppler-detected moderate-to-severe regurgitation occurred in two-thirds of patients at a mean of over 11 years following MVR; over one-third of these patients had clinically evident tricuspid regurgitation. . Other causes include blunt and penetrating trauma (rupture of papillary muscles, chordal disruption or detachment, leaflet rupture, complete valve destruction), primary or secondary cardiac tumors, right ventricular biopsy, and endomyocardial fibrosis.

13. Signs and symptoms Isolated TR is usually well tolerated When TR and pulmonary hypertension coexist, cardiac output declines and patients may manifest symptoms of right heart failure. Thus the symptoms of TR result from a reduced cardiac output and from ascites, painful congestive hepatomegaly, and massive edema. Occasionally, patients exhibit throbbing pulsations in the neck, which intensify on effort and are caused by JVD, and systolic pulsations of the eyeballs also have been described. In the many patients with TR who have mitral valve disease, the symptoms of the latter usually predominate. Symptoms of pulmonary congestion may abate as TR develops but are replaced by weakness, fatigue, and other manifestations of a depressed cardiac output. 

14. Physical Examination In patients with severe TR, evidence of weight loss and cachexia, cyanosis, and jaundice are often present on inspection. AF is common. JVD also is evident, the normal x and x′ descents disappear, and a prominent systolic wave—a c-v wave (or s wave)—is apparent. The descent of this wave, the y descent, is sharp and becomes the most prominent feature of the venous pulse, except with coexisting TS, in which case it is slowed. A venous systolic thrill and murmur in the neck may be present in patients with severe TR. Systolic pulsations of an enlarged tender liver are frequently present.  However, in patients with chronic TR and congestive cirrhosis, the liver may become firm and nontender. Ascites and edema are common.

15. auscultation  A holosystolic murmur that is best heard at the right or left midsternal border, but when the right ventricle is markedly dilated, the location of the murmur may move toward the left and suggest mitral regurgitation. auscultatory hallmark of tricuspid regurgitation is an inspiratory augmentation from increased systemic venous return and tricuspid valve flow. Under such circumstances as severe tricuspid regurgitation, markedly increased RA pressures, and RV systolic failure, the murmur may not increase with inspiration. Although usually described as holosystolic, the timing of the murmur may be early, mid, or late systolic. The murmur may be decrescendo when tricuspid regurgitation is severe and acute, and its character reflects the presence of a giant c-v wave; there may be a middiastolic flow rumble that resembles tricuspid stenosis. An S3 , which can vary in intensity and with inspiration, is often associated with an extremely dilated right ventricle. An S4 may also be heard if there is significant RV hypertrophy. 

16. Diagnostic Studies Electrocardiography:  When pulmonary hypertension is the cause of TR, the ECG may show evidence of RV hypertrophy with right axis deviation and tall R waves in V1 to V2 and RA enlargement.  Atrial fibrillation is also common, and incomplete right bundle branch block and Q waves in V1 are occasionally seen. Preexcitation frequently accompanies Ebstein anomaly. Chest radiography: cardiomegaly from RA and RV enlargement; pleural effusions and elevated diaphragms from ascites may be seen. In general, a dilated heart in the absence of pulmonary congestion or pulmonary hypertension should suggest either tricuspid valve disease or pericardial effusion.  Massive RA enlargement suggests Ebstein anomaly. 

17. Echocardiography: The goal of echocardiography is to estimate the severity of TR and assess pulmonary artery pressure (PAP) and RV function. In patients with TR secondary to dilation of the tricuspid annulus, the right atrium, right ventricle, and tricuspid annulus all usually are greatly dilated on echocardiography. There is evidence of RV diastolic overload with paradoxical motion of the ventricular septum similar to that observed in ASD. Exaggerated motion and delayed closure of the tricuspid valve are evident in patients with Ebstein anomaly. Prolapse of the tricuspid valve caused by myxomatous degeneration may be evident on echocardiography. A similar appearance of the tricuspid valve may be seen in patients who have used drugs that increase serotonin levels or simulate its effect on serotonin receptors. In patients with TR caused by endocarditis, echocardiography may reveal vegetations on the valve or a flail valve. TEE enhances detection of TR. Doppler echocardiography is a sensitive technique for visualizing the TR jet. The magnitude of TR can be quantified using techniques similar to those used to evaluate MR.

18. Two-dimensional echocardiography: Leaflet thickening may be seen in TR due to rheumatic or carcinoid disease. In functional TR, the leaflets usually appear normal. Tricuspid prolapse often occurs in patients with MV prolapse and may cause significant TR. In Ebstein’s anomaly, the septal leaflet of the TV is displaced apically. Vegetations are evident with endocarditis, and a flail valve leaflet may be seen with iatrogenic damage (e.g., after endomyocardial biopsy) or following papillary muscle rupture with right ventricular infarction. With moderate to severe TR, a right ventricular volume overload pattern is seen, characterized by right ventricular enlargement, ventricular septal flattening or shift to the left in diastole, and paradoxical motion in systole. There is often associated dilation of the right atrium and inferior vena cava (IVC).

19. The echocardiographic assessment of severe tricuspid regurgitation (TR). (A) The right heart chambers are both dilated, with apical tethering of the tricuspid leaflets and central coaptation gap ( arrowhead ). Vena contracta width (B) and proximal isovelocity surface area (PISA) radius (C) are indicative of severe TR; (D) the continuous wave Doppler demonstrates a dense, triangular waveform, and there is evidence of systolic flow reversal in the hepatic veins (E).

20. Doppler analysis: Assessment of TR involves incorporation of all of the Doppler information obtainable: size of the color jet, presence or absence of a proximal convergence zone (on the right atrial side of the valve), velocity profile, and eccentricity of theTR jet. Eccentric, wall-hugging jets should be typically upgraded by one grade, as is done for mitral regurgitation, because these are generally not visualized fully by echocardiography. TR direction and severity are assessed with color-flow Doppler. The severity of TR is estimated in several ways, including: Jet area: This measure is highly dependent on echocardiographic settings, particularly the pulse repetition frequency, and the direction and eccentricity of the jet. b)   Vena contracta width: The narrowest portion of the jet just downstream from the valve orifice gives a rough estimate of the effective orifice area. A jet width of >0.7 cm suggests severe TR.

21. c) Proximal flow convergence d) CW Doppler: The signal intensity and contour of the TR jet on CW Doppler can help define TR severity. Severe TR produces a dense spectral recording along with a triangular, early peaking velocity. e) Hepatic vein flow: Systolic flow reversal in the IVC or hepatic veins is consistent with severe TR. The RVSP is estimated using the modified Bernoulli equation after measuring the peak TR jet velocity by CW Doppler. In the absence of pulmonic stenosis, the pulmonary artery systolic pressure (PASP) can then be estimated as PASP = RVSP + RAP.  Cardiac catheterization: In the presence of moderate to severe TR, right heart catheterization will show a dominant v wave in the RAP curve, an RAP curve resembling that of the right ventricle, increased right ventricular end-diastolic pressure, and low cardiac output by thermodilution and Fick techniques.

22. management TR in the absence of pulmonary hypertension usually is initially well tolerated and may not require surgical treatment but may require chronic diuretic therapy.However , if TR is severe and sustained, eventually right-sided heart failure will ensue; thus appropriate consideration of and timing for surgery are indicated. When pulmonary arterial pressures increase, cardiac output falls, leading to symptoms of right-heart failure (edema, fatigue, dyspnea). Restriction of sodium and the use of potent loop diuretics to decrease RA pressure are indicated. Medical therapy is also aimed at the cause of pulmonary hypertension Functional TR in the setting of pulmonary hypertension is associated with heart failure and poor survival.

23. Surgery on the tricuspid valve may involve repair, reconstruction, excision, or replacement with a prosthetic valve. The surgeon must determine whether the regurgitation is functional or organic ( ie , associated with a structurally normal or abnormal tricuspid valve), and if it is functional, the response of the pulmonary arterial pressure to the primary procedure should be anticipated. For example, repair may be unnecessary for functional tricuspid regurgitation if there is a high likelihood of a postoperative fall in pulmonary arterial pressure. In addition, repair of the functionally regurgitant tricuspid valve in patients with severe right ventricular dysfunction is unlikely to improve their status.

24. because “functional” tricuspid regurgitation may be due to unrecognized annular involvement and because annular dilation may be progressive, “prophylactic” tricuspid annuloplasty has been recommended when the annular diameter exceeds 21 mm/m2 . Interestingly, in patients with chronic pulmonary thromboembolic disease, pulmonary thromboendarterectomy dramatically reduces functional tricuspid regurgitation without a change in tricuspid annular diameter. Annuloplasty procedures correct dilatation of the tricuspid valve annulus. The dilatation, which is not symmetric, typically involves the annulus around the anterior and posterior leaflets (posterior more than anterior)

25. When the tricuspid valve cannot be repaired and replacement is necessary, a bioprosthesis is often used because of the lower risk of thrombosis, although recent changes in valve design have significantly lowered the risk of thrombosis with mechanical prostheses. Successful percutaneous balloon valvuloplasty has been reported for native valve tricuspid stenosis and stenotic bioprosthetic tricuspid valves, but experience is limited. In selected patients with failing bioprostheses , preliminary data suggest that percutaneous tricuspid valve-in-valve implantation is feasible and effective. Initial tricuspid valve replacement with percutaneously delivered stent-mounted bioprostheses is under development.