Tricuspid stenosis (TS), which is much less prevalent than mitral stenosis (MS) in North America and Western Europe, is generally rheumatic in origin, and is more common in women than men (Table 261-1). It does not occur as an isolated lesion and is usually associated with MS. Hemodynamically significant TS occurs in 5–10% of patients with severe MS; rheumatic TS is commonly associated with some degree of tricuspid regurgitation (TR). Nonrheumatic causes of TS are rare.
++ Table Graphic Jump Location TABLE 261-1Causes of Tricuspid Valve Diseases ||Download (.pdf) TABLE 261-1 Causes of Tricuspid Valve Diseases
|Valve Lesion ||Etiologies |
|Tricuspid stenosis ||Rheumatic |
|Tricuspid regurgitation ||Primary (organic) |
| Rheumatic |
| Endocarditis |
| Myxomatous (TVP) |
| Carcinoid |
| Radiation |
| Congenital (Ebstein’s) |
| Trauma |
| Papillary muscle injury (post-MI) |
|Secondary (functional) |
| RV and tricuspid annular dilatation due to multiple causes of RV enlargement (e.g., long-standing pulmonary HTN, remodeling post-RV MI, left-sided valve disease, cardiomyopathy, AF) |
| Chronic RV apical pacing |
A diastolic pressure gradient between the right atrium (RA) and right ventricle (RV) defines TS. It is augmented when the transvalvular blood flow increases during inspiration and declines during expiration. A mean diastolic pressure gradient of 4 mmHg is usually sufficient to elevate the mean RA pressure to levels that result in systemic venous congestion. Unless sodium intake has been restricted and diuretics administered, this venous congestion is associated with hepatomegaly, ascites, and edema, sometimes severe. In patients with sinus rhythm, the RA a wave may be extremely tall and may even approach the level of the RV systolic pressure. The y descent is prolonged. The cardiac output (CO) at rest is usually depressed, and it fails to rise during exercise. The low CO is responsible for the normal or only slightly elevated left atrial (LA), pulmonary artery (PA), and RV systolic pressures despite the presence of MS. Thus, the presence of TS can mask the hemodynamic and clinical features of any associated MS.
Because the development of MS generally precedes that of TS, many patients initially have symptoms of pulmonary congestion and fatigue. Characteristically, patients with severe TS complain of relatively little dyspnea for the degree of hepatomegaly, ascites, and edema that they have. However, fatigue secondary to a low CO and discomfort due to refractory edema, ascites, and marked hepatomegaly are common in patients with advanced TS and/or TR. In some patients, TS may be suspected for the first time when symptoms of right-sided failure persist after an adequate mitral valvotomy.
Because TS usually occurs in the presence of other obvious valvular disease, the diagnosis may be missed unless it is considered. Severe TS is associated with marked hepatic congestion, often resulting in cirrhosis, jaundice, serious malnutrition, ...