However, significant or worsening TR is associated with poor long-term Primary disorders of the tricuspid appa- ratus that can lead to more significant degrees of TR include rheumatic disease, IE, congenital disease (Eb- stein s), myxomatous changes, and other problems af- fecting the tricuspid valve leaflets (blunt chest trauma, carcinoid, drugs, and radiation) (Table 19). A growing number of patients develop significant TR from iatro- genic etiologies (device leads and endomyocardial biop- Most cases of significant TR are secondary and related to tricuspid annular dilation and leaflet tether- ing in the setting of RV remodeling because of pressure or volume overload, as seen in patients with pulmo- nary hypertension (primary or secondary to left-sided heart disease) or dilated cardiomyopathies.11 13 In addi- tion, there appears to be a subgroup of patients with significant isolated TR attributable primarily to annular dilation, usually associated with AF in the absence of pulmonary hypertension or LV systolic dysfunction.2,14 18 Table 20 shows the stages of TR as defined for other valve lesions. Asymptomatic patients with severe TR (Stage C) present with an elevated central venous pres- sure and imaging evidence of significant TR. Symptomatic patients with severe TR (Stage D) have symptoms of fatigue, abdominal bloating, and periph- eral edema. End-organ damage, such as hepatic failure and renal failure, is an adverse consequence of Stage D TR that markedly affects survival.19 23 The severity of TR can be dynamic and dependent on changes in preload and pulmonary pressure. 8.2. Tricuspid Regurgitation 8.2.1. 