6.9: Tricuspid Regurgitation
- Page ID
- 42759
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\(\newcommand{\avec}{\mathbf a}\) \(\newcommand{\bvec}{\mathbf b}\) \(\newcommand{\cvec}{\mathbf c}\) \(\newcommand{\dvec}{\mathbf d}\) \(\newcommand{\dtil}{\widetilde{\mathbf d}}\) \(\newcommand{\evec}{\mathbf e}\) \(\newcommand{\fvec}{\mathbf f}\) \(\newcommand{\nvec}{\mathbf n}\) \(\newcommand{\pvec}{\mathbf p}\) \(\newcommand{\qvec}{\mathbf q}\) \(\newcommand{\svec}{\mathbf s}\) \(\newcommand{\tvec}{\mathbf t}\) \(\newcommand{\uvec}{\mathbf u}\) \(\newcommand{\vvec}{\mathbf v}\) \(\newcommand{\wvec}{\mathbf w}\) \(\newcommand{\xvec}{\mathbf x}\) \(\newcommand{\yvec}{\mathbf y}\) \(\newcommand{\zvec}{\mathbf z}\) \(\newcommand{\rvec}{\mathbf r}\) \(\newcommand{\mvec}{\mathbf m}\) \(\newcommand{\zerovec}{\mathbf 0}\) \(\newcommand{\onevec}{\mathbf 1}\) \(\newcommand{\real}{\mathbb R}\) \(\newcommand{\twovec}[2]{\left[\begin{array}{r}#1 \\ #2 \end{array}\right]}\) \(\newcommand{\ctwovec}[2]{\left[\begin{array}{c}#1 \\ #2 \end{array}\right]}\) \(\newcommand{\threevec}[3]{\left[\begin{array}{r}#1 \\ #2 \\ #3 \end{array}\right]}\) \(\newcommand{\cthreevec}[3]{\left[\begin{array}{c}#1 \\ #2 \\ #3 \end{array}\right]}\) \(\newcommand{\fourvec}[4]{\left[\begin{array}{r}#1 \\ #2 \\ #3 \\ #4 \end{array}\right]}\) \(\newcommand{\cfourvec}[4]{\left[\begin{array}{c}#1 \\ #2 \\ #3 \\ #4 \end{array}\right]}\) \(\newcommand{\fivevec}[5]{\left[\begin{array}{r}#1 \\ #2 \\ #3 \\ #4 \\ #5 \\ \end{array}\right]}\) \(\newcommand{\cfivevec}[5]{\left[\begin{array}{c}#1 \\ #2 \\ #3 \\ #4 \\ #5 \\ \end{array}\right]}\) \(\newcommand{\mattwo}[4]{\left[\begin{array}{rr}#1 \amp #2 \\ #3 \amp #4 \\ \end{array}\right]}\) \(\newcommand{\laspan}[1]{\text{Span}\{#1\}}\) \(\newcommand{\bcal}{\cal B}\) \(\newcommand{\ccal}{\cal C}\) \(\newcommand{\scal}{\cal S}\) \(\newcommand{\wcal}{\cal W}\) \(\newcommand{\ecal}{\cal E}\) \(\newcommand{\coords}[2]{\left\{#1\right\}_{#2}}\) \(\newcommand{\gray}[1]{\color{gray}{#1}}\) \(\newcommand{\lgray}[1]{\color{lightgray}{#1}}\) \(\newcommand{\rank}{\operatorname{rank}}\) \(\newcommand{\row}{\text{Row}}\) \(\newcommand{\col}{\text{Col}}\) \(\renewcommand{\row}{\text{Row}}\) \(\newcommand{\nul}{\text{Nul}}\) \(\newcommand{\var}{\text{Var}}\) \(\newcommand{\corr}{\text{corr}}\) \(\newcommand{\len}[1]{\left|#1\right|}\) \(\newcommand{\bbar}{\overline{\bvec}}\) \(\newcommand{\bhat}{\widehat{\bvec}}\) \(\newcommand{\bperp}{\bvec^\perp}\) \(\newcommand{\xhat}{\widehat{\xvec}}\) \(\newcommand{\vhat}{\widehat{\vvec}}\) \(\newcommand{\uhat}{\widehat{\uvec}}\) \(\newcommand{\what}{\widehat{\wvec}}\) \(\newcommand{\Sighat}{\widehat{\Sigma}}\) \(\newcommand{\lt}{<}\) \(\newcommand{\gt}{>}\) \(\newcommand{\amp}{&}\) \(\definecolor{fillinmathshade}{gray}{0.9}\)Functional tricuspid regurgitation results from distortion of the architecture and coordinated actions of the tricuspid leaflets, annulus, chords, papillary muscles, and right ventricular (RV) wall. This distortion is most commonly caused by right ventricular dilation and dysfunction from left sided heart disease with pressure/volume overload conditions.
Pressure volume overload conditions cause enlargement of the tricuspid annulus and the saddle shape becomes more circular. The normal annular excursion can be reduced by 50% in severe tricuspid regurgitation.[55] Functional tricuspid regurgitation is a marker of poor prognosis in patients with left ventricular cardiomyopathy. Pure tricuspid regurgitation may result from rheumatic fever, infective endocarditis, carcinoid causes, rheumatoid arthritis, radiation therapy, anorectic drugs, trauma, Marfan’s syndrome, tricuspid valve prolapse, papillary muscle dysfunction, or congenital disorders.
Right ventricular infarction with severe regional wall motion abnormality or disruption of the papillary muscle may cause regurgitation. Right ventricular dilatation with annular enlargement and valvular incompetence can be seen in Eisenmenger syndrome and pulmonary hypertension.
Clinical Presentation
A reduction in cardiac output related to tricuspid regurgitation, may cause symptoms of fatigue and weakness. Right-sided heart failure may cause ascites, congestive hepatosplenomegaly, pulsatile liver, pleural effusions, and peripheral edema.
With progression of the disease, patients become cachexic, cyanotic and jaundice may be present. A parasternal pansytolic murmur increasing on inspiration may be appreciated on auscultation(Carvallo’s sign). An S3, increasing with inspiration and decreasing with a Valsalva maneuve may be audible, as well as an increased P2 if pulmonary hypertension has developed.
Diagnostic Options
Chest Radiography
Cardiomegaly, increased right atrial and ventricular size and a prominent azygous vein can be demonstrated on chest x-ray. Chest Radiography may reveal pleural effusion, and ascites by upward diaphragmatic displacement.
Echocardiography
The tricuspid valve structure and function can be assessed echocardiographically and specific abnormalities can be identified. Distinction between primary and functional forms of tricuspid regurgitation can be made with echocardiography. The annular size can be measured. This imaging modality is used to evaluate the degree of regurgitation, pressures and ventricular function. Severe regurgitation is characterized by systolic flow reversal in the hepatic veins and a vena contracta diameter of more than 7 mm.
Cardiac catheterization
Cardiac catheterization is not necessary to diagnose tricuspid regurgitation. Increased right atrial and right ventricular end-diastolic pressures and the degree of pulmonary artery hypertension can be evaluated by catheterization. Pulmonary artery pressures of over 60 mmHg are usually due to left-sided lesions leading to secondary tricuspid regurgitation.
Treatment
Treatment strategy for tricuspid regurgitation is dictated by the etiology and the underlying cause of the disease and the overall condition of the patient. Primary tricuspid regurgitation has a poor prognosis without treatment. Functional tricuspid regurgitation may improve following treatment of its cause. Correction of concomitant mitral regurgitation may worsen tricuspid regurgitation. Risk factors for persistence or worsening of tricuspid regurgitation are reduced right ventricular function and the diameter of tricuspid annulus.
Medical
When pulmonary hypertension is the underlying cause of tricuspid annular dilation, medical management alone may minimize the need for surgical intervention
Surgical
Surgical treatment can be recommended for primary tricuspid regurgitation, when there is pulmonary hypertension, important dilatation of the annulus (diameter >40mm or >21mm/m2).
Surgical options for tricuspid regurgitation include annuloplasty or valve replacement with a mechanical valve or bioprosthesis. Functional tricuspid regurgitation may be repaired by suture annuloplasty (De Vega procedure) or by ring annuloplasty. Long-term outcomes of ring annuloplasty are superior to those of suture annuloplasty. Annuloplasty can be optimized by the use of intraoperative transesophageal echocardiography. Bioprostheses are generally preferred above mechanical prostheses for the tricuspid position, as mentioned in the section about tricuspid stenosis.