CHAPTER SUMMARY AND CENTRAL ILLUSTRATION
This chapter reviews the prevalence, etiology, clinical presentation, diagnosis, and management of tricuspid regurgitation (TR) and tricuspid stenosis. The tricuspid valve (TV) regulates the blood flow between the right atrium and the right ventricle. During ventricular systole, the TV leaflets coapt to seal the valve orifice, whereas during diastole, they open to allow blood to flow into the right ventricle. Its function as check-valve depends on the integrated and synchronous interplay among the three leaflets, the tricuspid annulus, the subvalvular apparatus, and the surrounding myocardium. The prevalence of clinically significant (ie, moderate or severe) TR in the general population is around 0.5% to 0.8% and the condition is more common in women and in the elderly (see Fuster and Hurst’s Central Illustration). Although minimal or trivial TR may be considered a normal variant in structurally normal TVs, moderate and severe TR is associated with increased cardiac and all-cause mortality, independently from pulmonary artery pressure and left and right ventricular function. Moreover, a clear relationship exists between outcome and the severity of TR, making it mandatory to assess TR severity to properly address patients’ management. Conversely, tricuspid stenosis is an uncommon valvular abnormality that is usually found in combination with TR and/or other valve lesions.
eFig 31-01 Chapter 31: Acquired Tricuspid Valve Diseases
Tricuspid valve (TV) function depends on the integrated and synchronous interplay among the three leaflets, the tricuspid annulus (TA), the subvalvular apparatus, and the surrounding myocardium. By far, the most frequent acquired TV disease is regurgitation that can be detected in 65% to 85% of the general population.1 Mild tricuspid regurgitation (TR) in the setting of a structurally normal TV apparatus is usually considered a normal variant and benign. Conversely, moderate or severe TR is associated with leaflet abnormalities and/or annular dilation, it is a pathologic condition, and it has been shown to be an independent predictor of both morbidity and mortality.2 Approximately 5% to 10% of all acquired TR are organic (or primary) and are caused by abnormalities of one or more components of the tricuspid apparatus (Table 31–1). However, the large majority of TR is functional or secondary to conditions that cause right ventricular (RV) and/or right atrial (RA) dilatation/dysfunction, including left-sided heart disease, lung diseases, and chronic atrial fibrillation.
TABLE 31–1.Etiology of Acquired Tricuspid Valve Disease ||Download (.pdf) TABLE 31–1. Etiology of Acquired Tricuspid Valve Disease
Structural abnormality of the tricuspid valve apparatus (20% of patients)
Rheumatic disease (usually with left-sided disease)
Carcinoid disease, serotonin active drugs
Traumatic (blunt chest injury, laceration)
- Pacemaker/defibrillator lead interference
- Right ventricular biopsy
- Drugs (eg, exposure to fenfluramine-phentermine, or methysergide)
- Radiation therapy of the mediastinum
Functional regurgitation ...