Though tricuspid regurgitation is a common valvular abnormality on echocardiography rarely is it due to primary organic disease.Secondary or functional tricuspid regurgitation due to pulmonary hypertension of any cause, is much more common than primary tricuspid regurgitation. In these instances tricuspid valve structure is normal except for dilated tricuspid annulus. Right ventricular and right atrial dilatation further exaggerates this abnormality.
Primary causes or organic involvement of tricuspid regurgitation as opposed to its functional involvement are much less common. The common etiologies include rheumatic, traumatic,endocarditis, carcinoid, endomyocardial fibrosis and myxomatous valve prolapse. Rheumatic etiology is often accompanied by involvement of mitral valve. Similarly myxomatous degeneration is associated with mitral valve prolapse. Infective endocarditis is typically seen in drug addicts, but it is more commonly described with septic abortions and contaminated intra venous infusions in India. Endomyocardial fibrosis affecting right ventricular apex as well as mitral valve is confined to certain geographical regions. Tricuspid Regurgitation due to blunt injury chest can have a delayed presentation. Conduction abnormalities are often associated with traumatic tricuspid regurgitation. Ebstein’s anomaly, a congenital heart disease is often associated with varying degrees of tricuspid regurgitation. Carcinoid valve disease is rare, and tricuspidvalvular involvement is associated with hepatic metastasis only. Pulmonary valve also is often involved in this disease.
Pathophysiology
Tricuspid regurgitation is associated with prominent venous filling waves and elevated right atrial venous pressures. Hepatic and systemic venous congestion and low output state would result as a consequence. In the primary tricuspid regurgitation, right ventricular pressure is normal and the diseased tricuspid valve or right ventricle is the cause for tricuspid regurgitation. Since right ventricle can tolerate high volumes, it enlarges and symptoms would be manifested at an advanced stage of the disease. Secondary tricuspid regurgitation is due to elevated pressures inn right ventricle, which is more commonly due to elevated pulmonary artery pressures. Clinical features are predominantly due to disease processes causing elevation of pulmonary artery
pressures.
Clinical Features
Patients with severe primary tricuspid regurgitation will have symptoms of fatigue, dyspnoea and effort intolerance, abdominal fullness and distension. In the absence of left heart diseases leading to tricuspid regurgitation, orthopnoea and PND do not occur. Physical examination will show elevated mean jugular venous pressure with prominent ‘v’ waves and sharp v-y collapse in the absence of tricuspid stenosis. Pulsatile hepatomegaly is often noted. Pan systolic murmur of tricuspid regurgitation is heard at lower left sternal border and it typically increases with inspiration due to increased venous return. In about 20 per cent of patients the murmur may not be audible. Lateral head bobbing is sometimes obvious at bedside. This is in contrast to vertical head bobbing that may be seen in aortic regurgitation. The height of ‘v’ waves depends upon the compliance and size of right atrium and may not exactly reflect severity of regurgitation. Systolic murmurs of low pressure TR tend to be early systolic in contrast to those of high pressure TR.
This is because in the former, right atrial and right ventricular systolic pressure tend to equalize in early systole and regurgitation stops by mid systole. Intensity of murmur does not correlate with severity of regurgitation. Musical murmurs of TR may produce loud murmurs. In inspiration TR murmur typically increase due to increased venous return and this is called Carvello’s sign. This may not be seen in patients with right heart failure since failing right ventricle’s output cannot be increased further with inspiration.
Investigations
ECG in secondary TR shows evidence of right atrial overload and right ventricular hypertrophy with right axis QRS deviation. Chest X-ray shows evidence of right atrial enlargement and right ventricular type of cardiomegaly.
Echo Doppler Evaluation
Echocardiographic examination clarifies the diagnosis, etiology and severity of tricuspid regurgitation. Right atrial and ventricular dilatation depend upon severity of TR. High pressure TR may be associated with near normal size of RA and RV. Severe organic TR may be present with normal RV systolic pressure. In volume overload of RV, IVS shows a paradoxical motion in late systole while in pressure overload of RV, IVS motion is paradoxical in early systole. Inter atrial septum may be pushed to left side. There is no simple and reliable formula to calculate right ventricular ejection fraction and one has to depend upon suggestive visual impression. Color flow imaging shows the severity of TR and continuous wave Doppler imaging measures the TR jet velocity from which RV-RA systolic pressure gradient is calculated. Addition of estimated RA pressure to this gradient gives right ventricular systolic pressure. The following criteria suggest severe tricuspid regurgitation: A color flow regurgitant jet area > 30 per cent RA area, dense continuous wave Doppler signal annulus dilatation with incomplete leaflet coaptation, increased tricuspid inflow velocity [E-wave >1.0 m/sec], systolic flow reversal in the hepatic vein. Trivial to mild TR may be seen in echocardiogram of up to 65 per cent of normal subjects and these are of no clinical significance.
The etiology of TR is often clarified with echocardiogram. In Tricuspid Valve Prolapse it is often the myxomatous leaflets that prolapse, and is often present along with mitral valve prolapse.Ebsteins Anomaly has a characteristic appearance of attachment of septal leaflets. Carcinoid valve disease has typical appearance with shortened and thickened leaflets resulting in large area of incomplete coapatation. Rheumatic TR may be primary or secondary to thickened shortened leaflets with annular dilatation and associated mitral valve involvement is obvious. In the absence of pulmonary metastasis or PFO-left sided valves are not involved in carcinoid. With rheumatic etiology these are always involved.
HaemodynamicsRight Atrial pressure tracing shows a prominent ‘v’ wave and these cannot be appreciated in a patient with atrial fibrillation. RV angiography is never done to diagnose or assess severity of tricuspid regurgitation.
Natural History
Prognosis of the tricuspid regurgitation depends upon underlying cause, as most of the time tricuspid regurgitation is functional or associated with other valvular lesions.In-patients with severe mitral stenosis it is an independent predictor of poor late outcome. The 4 year survival rates for mild TR is 99 per cent, 90 per cent for moderate and 69 per cent for sever tricuspid regurgitation. In long term patients with severe tricuspid regurgitation develop signs and symptoms of systemic venous congestion and low output state.
Management
It depends upon the cause of tricuspid regurgitation. Specific therapy is directed towards the particular cause of pulmonary artery hypertension, which results in tricuspid regurgitation.Diuretics should be used with caution to relieve symptoms of venous congestion. Mean jugular venous pressure rather than top of ‘v’ wave should direct diuretic usage since inappropriate high dosage would result in low output state.
Tricuspid valve annuloplasty is often considered to decrease the severity of tricuspid regurgitation if the patient is undergoing surgery for associated left heart disease. This tends to reduce the severity of regurgitation but does not eliminate it. In patients with severe deformation replacement is needed. Complete heart block is an important potential complication. 5 and 10 year survival rates range from 55-80 per cent and 36-50 per cent respectively. Since mechanical valve have high risk of thrombogenicity, tissue prosthesis are preferred. However, in young patients and those who need anticoagulants for other reasons, mechanical valve may be considered.
Primary causes or organic involvement of tricuspid regurgitation as opposed to its functional involvement are much less common. The common etiologies include rheumatic, traumatic,endocarditis, carcinoid, endomyocardial fibrosis and myxomatous valve prolapse. Rheumatic etiology is often accompanied by involvement of mitral valve. Similarly myxomatous degeneration is associated with mitral valve prolapse. Infective endocarditis is typically seen in drug addicts, but it is more commonly described with septic abortions and contaminated intra venous infusions in India. Endomyocardial fibrosis affecting right ventricular apex as well as mitral valve is confined to certain geographical regions. Tricuspid Regurgitation due to blunt injury chest can have a delayed presentation. Conduction abnormalities are often associated with traumatic tricuspid regurgitation. Ebstein’s anomaly, a congenital heart disease is often associated with varying degrees of tricuspid regurgitation. Carcinoid valve disease is rare, and tricuspidvalvular involvement is associated with hepatic metastasis only. Pulmonary valve also is often involved in this disease.
Pathophysiology
Tricuspid regurgitation is associated with prominent venous filling waves and elevated right atrial venous pressures. Hepatic and systemic venous congestion and low output state would result as a consequence. In the primary tricuspid regurgitation, right ventricular pressure is normal and the diseased tricuspid valve or right ventricle is the cause for tricuspid regurgitation. Since right ventricle can tolerate high volumes, it enlarges and symptoms would be manifested at an advanced stage of the disease. Secondary tricuspid regurgitation is due to elevated pressures inn right ventricle, which is more commonly due to elevated pulmonary artery pressures. Clinical features are predominantly due to disease processes causing elevation of pulmonary artery
pressures.
Clinical Features
Patients with severe primary tricuspid regurgitation will have symptoms of fatigue, dyspnoea and effort intolerance, abdominal fullness and distension. In the absence of left heart diseases leading to tricuspid regurgitation, orthopnoea and PND do not occur. Physical examination will show elevated mean jugular venous pressure with prominent ‘v’ waves and sharp v-y collapse in the absence of tricuspid stenosis. Pulsatile hepatomegaly is often noted. Pan systolic murmur of tricuspid regurgitation is heard at lower left sternal border and it typically increases with inspiration due to increased venous return. In about 20 per cent of patients the murmur may not be audible. Lateral head bobbing is sometimes obvious at bedside. This is in contrast to vertical head bobbing that may be seen in aortic regurgitation. The height of ‘v’ waves depends upon the compliance and size of right atrium and may not exactly reflect severity of regurgitation. Systolic murmurs of low pressure TR tend to be early systolic in contrast to those of high pressure TR.
This is because in the former, right atrial and right ventricular systolic pressure tend to equalize in early systole and regurgitation stops by mid systole. Intensity of murmur does not correlate with severity of regurgitation. Musical murmurs of TR may produce loud murmurs. In inspiration TR murmur typically increase due to increased venous return and this is called Carvello’s sign. This may not be seen in patients with right heart failure since failing right ventricle’s output cannot be increased further with inspiration.
Investigations
ECG in secondary TR shows evidence of right atrial overload and right ventricular hypertrophy with right axis QRS deviation. Chest X-ray shows evidence of right atrial enlargement and right ventricular type of cardiomegaly.
Echo Doppler Evaluation
Echocardiographic examination clarifies the diagnosis, etiology and severity of tricuspid regurgitation. Right atrial and ventricular dilatation depend upon severity of TR. High pressure TR may be associated with near normal size of RA and RV. Severe organic TR may be present with normal RV systolic pressure. In volume overload of RV, IVS shows a paradoxical motion in late systole while in pressure overload of RV, IVS motion is paradoxical in early systole. Inter atrial septum may be pushed to left side. There is no simple and reliable formula to calculate right ventricular ejection fraction and one has to depend upon suggestive visual impression. Color flow imaging shows the severity of TR and continuous wave Doppler imaging measures the TR jet velocity from which RV-RA systolic pressure gradient is calculated. Addition of estimated RA pressure to this gradient gives right ventricular systolic pressure. The following criteria suggest severe tricuspid regurgitation: A color flow regurgitant jet area > 30 per cent RA area, dense continuous wave Doppler signal annulus dilatation with incomplete leaflet coaptation, increased tricuspid inflow velocity [E-wave >1.0 m/sec], systolic flow reversal in the hepatic vein. Trivial to mild TR may be seen in echocardiogram of up to 65 per cent of normal subjects and these are of no clinical significance.
The etiology of TR is often clarified with echocardiogram. In Tricuspid Valve Prolapse it is often the myxomatous leaflets that prolapse, and is often present along with mitral valve prolapse.Ebsteins Anomaly has a characteristic appearance of attachment of septal leaflets. Carcinoid valve disease has typical appearance with shortened and thickened leaflets resulting in large area of incomplete coapatation. Rheumatic TR may be primary or secondary to thickened shortened leaflets with annular dilatation and associated mitral valve involvement is obvious. In the absence of pulmonary metastasis or PFO-left sided valves are not involved in carcinoid. With rheumatic etiology these are always involved.
HaemodynamicsRight Atrial pressure tracing shows a prominent ‘v’ wave and these cannot be appreciated in a patient with atrial fibrillation. RV angiography is never done to diagnose or assess severity of tricuspid regurgitation.
Natural History
Prognosis of the tricuspid regurgitation depends upon underlying cause, as most of the time tricuspid regurgitation is functional or associated with other valvular lesions.In-patients with severe mitral stenosis it is an independent predictor of poor late outcome. The 4 year survival rates for mild TR is 99 per cent, 90 per cent for moderate and 69 per cent for sever tricuspid regurgitation. In long term patients with severe tricuspid regurgitation develop signs and symptoms of systemic venous congestion and low output state.
Management
It depends upon the cause of tricuspid regurgitation. Specific therapy is directed towards the particular cause of pulmonary artery hypertension, which results in tricuspid regurgitation.Diuretics should be used with caution to relieve symptoms of venous congestion. Mean jugular venous pressure rather than top of ‘v’ wave should direct diuretic usage since inappropriate high dosage would result in low output state.
Tricuspid valve annuloplasty is often considered to decrease the severity of tricuspid regurgitation if the patient is undergoing surgery for associated left heart disease. This tends to reduce the severity of regurgitation but does not eliminate it. In patients with severe deformation replacement is needed. Complete heart block is an important potential complication. 5 and 10 year survival rates range from 55-80 per cent and 36-50 per cent respectively. Since mechanical valve have high risk of thrombogenicity, tissue prosthesis are preferred. However, in young patients and those who need anticoagulants for other reasons, mechanical valve may be considered.
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