The pathophysiological triad introduced for the mitral valve ( Chapter 6 ) is also relevant to the other valves, including the tricuspid valve. It provides an accurate description of the valve pathophysiology by a clear separation between etiology, lesions, and dysfunctions ( Table 18-1 ).
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ETIOLOGY
Tricuspid valve diseases are primarily divided into two etiological groups: functional and organic. The term “functional” tricuspid regurgitation (TR) is used with many different nosologic interpretations that require clarification ( Table 18-2 ). Since the qualifier “functional” is the opposite of organic, the most logical definition would be to use “functional tricuspid regurgitation” in the absence of well-identified valvular or myocardial lesions. The advantage of this nosologic distinction is emphasized by the fact that organic tricuspid regurgitation is irreversible whereas functional regurgitation is potentially reversible.
| Functional TR | Organic TR |
|---|---|
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Functional Tricuspid Regurgitation
“Functional” tricuspid valve regurgitation (i.e., tricuspid regurgitation without organic valvular or myocardial lesions) is by far the most frequent cause of tricuspid valve dysfunction. This condition is commonly observed in patients with mitral valve diseases. In one of our early studies of 150 patients presenting with mitro-tricuspid valve dysfunction, functional tricuspid regurgitation was present in 70% of the patients. Functional tricuspid regurgitation can also be observed in a variety of diseases producing pulmonary hypertension and/or right ventricular dysfunction . The high frequency of functional tricuspid regurgitation is explained by the peculiar sensitivity to loading conditions of the thin wall of the right ventricle. Volume overload (preload), right ventricular dysfunction, and increased afterload can all contribute to the onset of functional tricuspid regurgitation, a dysfunction that can be reversible if normal loading conditions and ventricular function are restored. The most important characteristic of functional tricuspid regurgitation is its variability in a given patient , depending upon cardiac output, ventricular contractility, blood volume, and medical treatment. This variability makes difficult the assessment of the severity of the regurgitation and therefore the decision to repair the regurgitation. A long-lasting evolution of functional tricuspid regurgitation creates the conditions of irreversible dysfunction and secondary organic lesions, a general observation applied to many functional disturbances as highlighted by René Leriche.
Organic Tricuspid Valve Regurgitation
Organic tricuspid valve regurgitation mainly results from primary involvement of the tricuspid valve by a variety of diseases ( Table 18-3 ). Rheumatic valvular disease is prevalent in developing countries whereas degenerative valvular diseases and bacterial endocarditis are more common in Western countries ( Fig. 18-1 ). Organic tricuspid valve regurgitation may also result from primary myocardial diseases such as myocardial infarction, dilated cardiomyopathy, or endomyocardial fibrosis. Severe adhesions between the right ventricle and the sternum after cardiac surgery have been reported as responsible for rare cases of tricuspid regurgitation attributable to the deformation of the annulus. The release of these adhesions corrects the regurgitation.
Primary valve diseases
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Secondary to myocardial diseases
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Other causes
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* Bacterial endocarditis may be a primary valve disease or may complicate the course of a pre-existing valve disease.
The determination of the etiology of tricuspid valve regurgitation is based on several considerations such as age, medical history, geographical considerations, socioeconomic conditions, and clinical presentation. In many cases, however, the etiology remains uncertain until echocardiography is performed or surgery is undertaken, both of which permit assessment of the characteristic gross morphology of the valve. Although often difficult, the etiological diagnosis is important because it determines the complexity of the operation and the long-term prognosis. The clinical and pathological characteristics of these different valvular diseases are extensively studied in Section 5.
LESIONS
Whatever the etiology, a disease can cause multiple lesions that may affect the different components of the valve ( Table 18-4 ). Annular dilatation is the most common cause of tricuspid regurgitation. A 20% increase in annular diameter creates a lack of leaflet coaptation and therefore a regurgitation.
| Annulus: | Dilatation |
| Abscess | |
| Leaflets: | Excess leaflet tissue |
| Thickening | |
| Vegetations | |
| Abscess, perforation | |
| Tear | |
| Commissures: | Fusion |
| Thickening | |
| Chordae: | Rupture |
| Elongation | |
| Thickening | |
| Shortening | |
| Fusion | |
| Papillary muscles: | Rupture |
| Elongation | |
| Ventricle: | Infarction |
| Fibrosis | |
| Dilatation |
A diameter of 40 mm in four-chamber view or 70 mm in transgastric view indicates significant annular dilatation.
During echocardiography ( Fig. 18-2 ), a significantly dilated annulus in the adult is indicated by a cut-off value of 40 mm in the four-chamber view (a) and 70 mm in the transgastric view (b) . The dilatation of the tricuspid annulus does not affect its four segments to the same degree. The difference depends upon the surrounding anatomical structure and the etiology of the regurgitation ( Fig. 18-3 ). In functional tricuspid regurgitation, the most severely dilated segment is the posterior segment of the annulus, which may increase its normal length by up to 80% (a) . The anterior and aortic segments are affected to a lesser degree, up to a 40% increase, followed by the septal segment, which displays moderate changes because of its tight relationship with the interventricular septum. Distension also affects the commissures, mainly the anteroposterior and posteroseptal commissures (up to 30%) and to a lesser degree the anteroseptal commissure. In rheumatic valvular disease, the degree of annular dilatation depends upon whether the regurgitation is isolated (b) or associated with a certain degree of stenosis (c) . In the latter case, the degree of annular dilatation is not limited by the commissural retraction. In all circumstances, the regurgitation is worsened by lesions involving other components of the valve such as leaflets, chordae, papillary muscles and the ventricular wall.
