Tricuspid Regurgitation Flashcards
Summarise tricuspid regurgitation
Usually presents with fatigue, dyspnoea, and lower extremity oedema. Additional complaints may include abdominal distension and early satiety.
Mild or moderate tricuspid regurgitation without abnormal valve anatomy, ventricular function, or pulmonary artery pressure is not necessarily abnormal but is estimated to be present in over 50% of asymptomatic young adults.
The clinically most important form is secondary to left-sided cardiac disease, with tricuspid annular dilation.
The affected valve may be repaired or replaced; similar to mitral surgery, surgical repair is preferred over replacement.
Operative risk for tricuspid valve operation depends on extent of right ventricular dysfunction and concomitant disease. Re-operation for severe tricuspid regurgitation after left-sided valve surgery carries a high risk. Therefore, correction of tricuspid regurgitation should be considered at the time of initial surgery.
The disease has largely been ignored and its impact is under appreciated.
Define tricuspid regurgitation
Tricuspid regurgitation (TR) occurs when blood flows backwards through the tricuspid valve. In the vast majority of patients, this occurs during systole, but severely elevated right ventricular filling pressure can be associated with diastolic TR. TR can be primary (abnormal valve morphology) or secondary (normal valve morphology). Some degree of valvular regurgitation is a quite common accidental finding in colour Doppler imaging. In fact, two-dimensional echocardiography has demonstrated that 50% to 60% of asymptomatic young adults exhibit mild tricuspid regurgitation.[1] A smaller proportion, up to 15%, have moderate tricuspid regurgitation.
Describe the epidemiology of TR
Some degree of valvular regurgitation is a quite common accidental finding in colour Doppler imaging. In fact, two-dimensional echocardiography has demonstrated that 50% to 60% of asymptomatic young adults exhibit mild tricuspid regurgitation.[1] A smaller proportion, up to 15%, have moderate tricuspid regurgitation. It is most often found secondary to, or in association with, left-sided cardiac pathology in the form of advanced mitral, aortic, or left ventricular myocardial disorders. In developed countries, the most commonly associated conditions include ischaemic or degenerative mitral regurgitation; however, in developing countries, the association is with rheumatic heart disease. Rarely does TR present as an isolated disease process
Describe the aetiology of TR
TR occurs with abnormal (primary) or normal (secondary, functional) valve morphology. Causes of primary valve dysfunction are uncommon, and include congenital aetiologies such as cleft valve in association with AV canal defect and Ebstein’s anomaly; acquired aetiologies include rheumatic valvulitis, endocarditis, or scarring from carcinoid heart disease. Less commonly, TR occurs with rheumatoid arthritis, Marfan’s syndrome, pacemaker lead entrapment, and tricuspid valve prolapse (sometimes in association with myxomatous mitral valve disease), or following trauma (such as blunt force trauma or repeated endomyocardial biopsies), radiotherapy, and toxin exposure (phentermine-fenfluramine [Phen-Fen] or methysergide). However, the most clinically significant form of TR is secondary in nature, commonly due to left-sided cardiac pathology in the form of advanced mitral, aortic, and left ventricular myocardial disorders
Describe the pathophysiology of TR
Normal tricuspid valves develop dysfunction with elevation of right ventricular systolic and/or diastolic pressure, right ventricular cavity enlargement, or tricuspid annular dilation with leaflet tethering.[1][5] The pathological consequences of advanced TR are related to a reduced cardiac output and elevated right atrial pressure, which, if long-standing, leads to atrial distension with reduced contractile reserve and atrial fibrillation.[6] Often, patients with chronic severe TR will present with ascites from advanced liver disease from chronic congestion or fibrosis (cardiac cirrhosis), gut congestion with symptoms of dyspepsia or indigestion, and fluid retention with leg oedema
Describe the classification of TR severity based on annular diameter
TR severity as determined by echocardiographic measurement of annular diameter
Normal tricuspid valve annulus diameter in adults is 28 mm (± 5 mm) in the 4 chamber view. Significant tricuspid annular dilation is defined by a diastolic diameter of over 40 mm (absolute value) or 21 mm/square metre of body surface area.[2] A correlation exists between tricuspid annulus diameter and TR severity: a systolic tricuspid diameter >3.2 cm or a diastolic tricuspid annulus diameter >3.4 cm are often markers of more significant TR
Describe the classification of TR severity based on vena contracta width measurement
Severe TR is defined as vena contracta (the narrowest central flow region of a jet that occurs at, or just downstream to, the orifice of a regurgitant valve) width >0.7 cm.
In case of multiple jets, the respective values of the vena contracta width are not additive
Describe echocardiography measurement of TR
Proximal isovelocity surface area (PISA) radius of 1 mm to 4 mm suggests mild TR, 5 mm to 8 mm moderate TR, >9 mm severe TR, at an aliasing velocity setting (the velocity of a flow that exceeds the colour Doppler scale) of approximately 40 cm/second. An effective regurgitant orifice area ≥40 mm² or a regurgitant volume of ≥45 mL indicates severe TR. The PISA method may underestimate the severity of TR; it is less accurate in multiple jets.[3] Quantification is important, as there is great variability in interpreting TR severity based on semi-quantitative indexes alone
Describe doppler colour flow jet measurement of TR
The colour flow area of the regurgitant jet is not recommended to measure the severity of TR. Colour flow imaging should only be used for diagnosing TR. A more quantitative approach is required when more than a small central TR jet is observed
Describe the IVC flow reversal measurement of TR
The systolic hepatic flow reversal is specific for severe TR.
It represents the strongest additional parameter for evaluating the severity of TR.[3] Concomitant presence of atrial fibrillation or right ventricular pacing reduces the specificity of this finding.
Describe a typical case history for TR
A 78-year-old man was diagnosed with left-sided systolic heart failure 14 years ago. He was subsequently found to have atrial fibrillation, and underwent atrioventricular node ablation and pacemaker placement 10 years ago that resulted in an improvement in his left ventricular ejection fraction from 35% to 50%. He did extremely well over the years and was extremely active; 3 years ago he completed a 210-mile bike ride across the Netherlands. Four months ago, however, he started developing chest tightness and back tightness when pulling his cart during golfing sessions. In addition, he developed significant dyspnoea with activity and his symptoms have worsened. Now, he says his quality of life is extremely poor. He has problems walking up one flight of stairs where he experiences significant shortness of breath; even walking half a block causes shortness of breath and chest tightness. He has also noticed increased abdominal girth, early satiety, and easy fatigue.
Describe a second case history for TR
A 73-year-old woman presented for the first time 5 years ago with worsening shortness of breath and lower extremity oedema. On clinical examination, she has a laterally displaced apical impulse, with a loud 3/6 holosystolic murmur at the apex. Jugular veins are distended to the angle of the jaw. Lung examination shows some bibasilar crackles. There is 2-3+ pitting edema in both lower extremities. Echocardiography shows a reduced left ventricular ejection fraction (40%), hypokinesis of the inferior and lateral walls, ischaemic mitral regurgitation (severe), and mild TR.
Describe some other typical presentations of TR
A spectrum exists such that TR may not be associated with any symptoms until a late stage of the disease involving progressive right ventricular dysfunction.[1] In some patients, moderate or severe TR may be present without the classic clinical complaints. The symptoms of left-sided cardiac disease predominate in most patients with secondary TR. The symptoms specific to advanced tricuspid valve disease are related to a reduced cardiac output and elevated right atrial pressure. Effort intolerance or dyspnoea reflects the limited cardiac reserve. Long-standing relevated right atrial pressure leads to atrial distension with reduced contractile reserve and atrial fibrillation. Often, patients with chronic severe TR will present with ascites from advanced liver disease from chronic congestion or fibrosis (cardiac cirrhosis), bowel congestion with symptoms of dyspepsia or indigestion, and fluid retention with leg oedema
What is TR often secondary too
TR is most often found secondary to, or in association with, left-sided cardiac pathology in the form of advanced mitral, aortic, or left ventricular myocardial disorders.[1] The most commonly associated conditions include ischaemic or degenerative mitral regurgitation. Other associated factors include a history of rheumatic heart disease, constrictive pericarditis, and permanent pacemaker placement. TR may be a consequence of endocarditis or carcinoid syndrome. Rarely, TR presents as an isolated disease process.
What are the pathological consequences of TR related to
The pathological consequences of advanced TR are related to a reduced cardiac output and right atrial hypertension. The clinical sequelae include atrial fibrillation, findings of advanced liver disease from chronic congestion or fibrosis (cardiac cirrhosis), and findings of congestive heart failure.
What does the clinical evaluation of TR begin with
The clinical evaluation begins with a review of the patient’s history for conditions associated with tricuspid regurgitation, including left-sided heart failure, rheumatic heart disease, permanent pacemaker, endocarditis, and carcinoid heart disease.
The symptoms of left-sided cardiac disease predominate in most patients with secondary TR and include fatigue, effort intolerance, or dyspnoea. Patients may describe palpitations due to atrial fibrillation or flutter.
Describe how right heart failure can also be associated with TR
Right heart failure can also be associated with TR. The clinical presentation involves exercise limitation, fatigue, and evidence of systemic venous congestion.[13] Additional signs and symptoms associated with right-sided heart failure include abdominal distension from ascites; liver pulsation due to advanced liver disease from chronic congestion or fibrosis (cardiac cirrhosis); gut congestion with symptoms of early satiety, dyspepsia, or indigestion; and fluid retention with leg swelling
What may you find on the physical exam in patients with TR
The physical examination may note the following.
Irregular pulse.
Abnormal and prominent v wave in the jugular venous pulse.[5]
Lower left parasternal systolic murmur (holosystolic or less than holosystolic, depending on the severity of haemodynamic derangement).[5] Increased systolic murmur on inspiration (Carvallo’s sign) may be present.
Peripheral oedema.
Pulsatile liver
Describe how a diagnosis of TR is reached
Diagnosis of TR is most often made with a transthoracic echo, which assesses the structure and motion of the tricuspid valve, measures annular size, and identifies other cardiac abnormalities that might influence tricuspid valve function. Systolic pulmonary artery pressure >55 mmHg is likely to cause TR with anatomically normal tricuspid valves, whereas TR occurring with systolic pulmonary artery pressures <40 mmHg is likely to reflect a structural abnormality of the valve apparatus.[5] Functional or secondary TR is characterised by annular dilation, the extent of which may determine its severity.[1] Doppler echocardiography permits estimation of the severity of TR and right ventricle systolic pressure. A transoesophageal echocardiogram can be performed if the transthoracic approach does not yield adequate quality images for accurate assessment.
