The most common cause of tricuspid insufficiency is the right ventricle and the valvular ring dilation causing secondary regurgitation (functional). It can occur as a complication of right ventricular decompensation from any cause. Secondary pulmonary hypertension can accompany any form of heart disease or lung, but most commonly in lesions of the mitral valve. In general, a right ventricular systolic pressure greater than 55 mmHg will cause functional tricuspid insufficiency. Other causes of tricuspid regurgitation may include heart congenital diseases (for example pulmonary stenosis, pulmonary hypertension in Eisenmenger syndrome), primitive pulmonary hypertension and chronic pulmonary. Right ventricular infarction may lead to either papillary muscle rupture or severe disorders of regional kinetic which prevents proper closing of the valves with a ‘tethering’ effect on them, causing regurgitation. Tricuspid regurgitation in children complicates the right ventricular insufficiency, secondary to the neonatal lung diseases and pulmonary hypertension with persistent fetal circulation. Marfan syndrome and Myxomatous degeneration that accompanies the mitral, chordae elongation occurs, their rupture and prolapsing valve incompetence.
A multitude of pathological processes directly affect the tricuspid valve apparatus and cause regurgitation primary. Such diseases are congenital including Ebstein’s anomaly, atrioventricular canal, corrected transposition of large vessels or may occur as a congenital isolated.
A multitude of pathological processes directly can affect the tricuspid valve apparatus and cause primary regurgitation. Such diseases are congenital including Ebstein’s anomaly, atrioventricular canal, corrected transposition of large vessels or may occur as a congenital isolated.
Rheumatic fever may directly affect the valve. When it occurs, it causes retraction valves and chordae tendineae, causing reduced impaired mobility isolated tricuspid or stenosis associated. Generally coexists with impaired rheumatic aortic or mitral valves. Tricuspid regurgitation with or without stenosis can occur in carcinoid syndrome which determines focal or diffuse deposits of fibrous tissue on the endocardium cusps and cardiac chambers, on the intima of large veins and coronary sinus.
Endomyocardial fibrosis with retraction of the cusps and chordae tendineae constitutes a common cause of tricuspid regurgitation in Africa. Insufficiency Tricuspid valve prolapse may occur through secondary myxomatous changes being commonly associated with the mitral valve damage and the presence of atrial septal defect.
Other causes of tricuspid insufficiency are: penetrant or non-penetrating traumatisms, dilated cardiomyopathy, endocarditis (especially the staphylococcal one at drug users), cardiac tumors (especially right atrial myxoma), repeated endomyocardial biopsies at cardiac transplantations, valvulopathy induced by methysergide, by the use of fenfluramine-phentermine, systemic lupus erythematosus. A rare cause of regurgitation is the peacemakers and implantable defibrillators whose probe passes from the right atrium to the right ventricle directly interfering with the valve flakes coaptation. In a recent report Kim et al, studied the effect of pacemaker and automatic implantable defibrillators at 248 subjects with echocardiography before and after implantation. The author has seen the worsening regurgitation by 1 degree or more up to 24.2 from implanted subjects, especially those with defibrillator. 17.8% of the initial tricuspid regurgitation patients developed mild moderate or severe regurgitation. It was also observed that five years from tricuspid repair, 42% of patients with a pacemaker had severe tricuspid insufficiency; the incidence is 2 times lower in those without pacemakers. Track the transtricuspid probe suggests that removing and replacing it with epicardial electrodes during surgery and surgical correction of tricuspid valve regurgitation may reduce the incidence of late.
Pathogenesis of tricuspid valve insufficiency
Tricuspid insufficiency pathogenesis is complex and multifactorial.
Most often IT is functional, secondary to dilatation and to the right ventricular dysfunction and tricuspid ring expansion. Mitral valvular disease increases right atrial pressure, and if it is sufficiently important causes pulmonary hypertension. This leads to right ventricular dysfunction and remodeling, tricuspid annular dilatation, papillary muscle displacement and tethering of the tricuspid valve with regurgitation appearance. Tricuspid insufficiency in turn emphasizes the right ventricular dilatation and dysfunction, dilated ring, tethering, increasing regurgitation. The right ventricle expands and decompensates determining the increase in diastolic blood pressure and shift to the left ventricle of the interventricular septum, due to the interdependence rate; it may compress the left ventricle with impaired diastolic filling and increasing pressure and the pressure in the lungs. This phenomenon has been called restriction – dilatation syndrome by Autunes and Barlow.
The increase in size of the left atrium, and pressure can cause atrial fibrillation which in turn causes the right atrial dilation and expansion of the tricuspid ring. Atrial fibrillation has been recognized as an important risk factor for the development of tricuspid insufficiency in patients with mitral valvular disease as the persistence or the emergence of mitral regurgitation after surgery or balloon valvuloplasty. Furthermore, patients who underwent successful Maze procedure during mitral valve surgery on tricuspid regurgitation were rare.
In patients with rheumatic valvular, organic modification of the valve can cause tricuspid regurgitation. Valvular thickening and restriction flakes were reported in one-third of patients with tricuspid insufficiency after mitral valve replacement, but the actual incidence of organic tricuspid valve damage is likely higher.
Tricuspid annular dilatation is probably the most important factor in the development of tricuspid insufficiency and constitutes also the target for intervention. Normal diameter measured by echocardiography in apical 4 rooms’ incidence is 28.5cm. Sugimoto et al. showed a good correlation between ring diameter and regurgitant volume. Reduced shortening of the ring seen in patients with severe annular dilatation and dysfunction in patients with right ventricular tricuspid regurgitation severity influences also.
The clinical picture of tricuspid valve insufficiency
For tricuspid regurgitation initial symptoms are fatigue and weakness secondary to decrease in cardiac output. Right heart failure leads to ascites, hepatosplenomegaly, pulsatile liver, peripheral edema and pleural overflow. In advanced stages patients are cachectic and cyanotic. Atrial fibrillation is common in right atrial dilatation. Listener can observe the emergence of noise 3 emphasized inspiration and Valsalva maneuver decreased, P2 increased in case of occurrence of pulmonary hypertension 12 and parasternal pansystolic murmur that increases in inspiration.
Chest X-ray reveales the presence of cardiomegaly, increased cavity diameter straight prominent azygos vein, possible pleural effusion.
Echocardiography allows identifying the presence of regurgitation, assessment of severity, degree of pulmonary hypertension and right ventricular dysfunction. Echocardiographic criteria for assessing the severity of impairment in the guide published European Society of Cardiology in 2006.
Inter-atrial septum’s bulging to the left and paradoxical movement of the septum are highly suggestive of right overloading. The Doppler exam pulsed and colored allows the identification of valvular regurgitation with revers flow in the inferior vena cava and hepatic veins. Sometimes it can be currently atrial septal defect or patent ovale foramen.
Lesions caused by endocarditis or vegetation’s may be visible by ultrasound; valve can be destroyed and septic pulmonary emboli are common. In carcinoid syndrome valves are thickened, retracted, fixed in a semi-open position throughout the cardiac cycle.
Cardiac catheterization shows increased atrial pressure and right ventricular telediastolic; permits quantification of pulmonary hypertension. A pulmonary arterial pressure above 60 mmHg is often caused by damage to the left heart and causes secondary tricuspid insufficiency.
Both the guidelines of the American College of Cardiology / American Heart Association and the European Society of Cardiology recommends tricuspid valve repair in patients with severe tricuspid regurgitation, in patients requiring mitral valve surgery (Class I recommendation). European guidelines considers recommendation of class II concomitant tricuspid valve repair in patients with mitral annulus diameter over 40mm or moderate regurgitation while the American College of Cardiology / American Heart Association considers a class II-B recommendation for intervention for all patients with moderate regurgitation.
It is also considered a class II-A recommendation tricuspid valve repair in symptomatic patients with isolated tricuspid regurgitation, left heart belatedly after surgery in the absence of left or right ventricular dysfunction without severe pulmonary hypertension. Surgery is not indicated for asymptomatic patients with severe tricuspid regurgitation that develops right ventricular dysfunction, in contrast to asymptomatic patients with severe aortic or mitral regurgitation, there is a clear indication of surgical correction in the presence of mild ventricular dysfunction. Tricuspid valve annuloplasty is an indication class II-B and III in subsets of patients with pulmonary hypertension.
Bibliography: 1. Braunwald's Heart Disease; 2. Harrison's Principles of Internal Medicine; 3. European Society of Cardiology - Clinical Practice Guidelines.