ESSENTIALS OF DIAGNOSIS
Prominent v wave in jugular venous pulse.
Systolic murmur at left lower sternal border that increases with inspiration.
Characteristic Doppler echocardiographic findings, including right ventricular (RV) volume overload (RV enlargement, paradoxical septal motion, and diastolic flattening of the interventricular septum), right atrial enlargement, and systolic turbulence in the right atrium.
Prominent a wave and reduced y descent in jugular venous pulse.
Diastolic murmur at left lower sternal border that increases with inspiration.
Characteristic Doppler echocardiographic findings, including a thickened and domed valve with restricted motion, right atrial enlargement, and increased diastolic velocity across the tricuspid valve.
Clinical interest in tricuspid valve disorders has increased because of several distinct but interrelated events in clinical cardiology. First, high-resolution, noninvasive imaging techniques have been developed and validated, allowing clinicians to easily assess the morphology and function of the tricuspid valve. Second, the frequency of tricuspid valve endocarditis has increased significantly, owing largely to an increasing population of injection drug users, patients with implanted cardiac devices or long-term central venous catheters, and, to a lesser extent, a growing number of immunocompromised patients. Third, several reparative percutaneous and surgical techniques with acceptable morbidity and mortality rates now exist. In addition, investigations in both animals and humans have demonstrated the influence of right-heart disease on cardiovascular performance vis-á-vis series and parallel interactions with the left ventricle.
Staging Valvular Heart Disease
Valvular heart disease (VHD) progresses through stages A to D. Stage A is defined by the possession of risk factors for the development of VHD; stage B is defined as progressive VHD (asymptomatic mild to moderate severity); stage C is defined as asymptomatic severe disease, and is subcategorized into those with (C1) and without (C2) ventricular compensation; and stage D is defined by severe, symptomatic VHD.
Pathophysiology & Etiology
The tricuspid valve has three leaflets that are unequal in size (anterior > septal > posterior). The papillary muscles are not as well defined as those of the left ventricle and are subject to considerable variation in both their size and leaflet support. Like the mitral valve, the leaflets, annulus, chordae, papillary muscles, and contiguous myocardium contribute individually to normal valve function and can be altered by pathophysiologic processes (Table 21–1).
Table 21–1.Causes of Tricuspid Valve Disease ||Download (.pdf) Table 21–1. Causes of Tricuspid Valve Disease
|Tricuspid Regurgitation ||Tricuspid Stenosis |
|Functional (structurally normal tricuspid valve) ||Rheumatic |
|Rheumatic ||Carcinoid heart disease |
|Infective endocarditis ||Tumors |
|Congenital (eg, tricuspid valve prolapse, Ebstein anomaly) ||Congenital (eg, Ebstein anomaly) |
|Carcinoid heart disease ||Systemic lupus erythematosus |
|Systemic lupus erythematosus ||Whipple disease |
|Catheter-induced ||Fabry disease |
|Trauma ||Infective endocarditis |
|Tumors ||Endomyocardial fibrosis |
|Orthotopic heart transplantation ||Endocardial fibroelastosis |
|Endomyocardial fibrosis ||Methysergide therapy |
|Antiphospholipid syndrome ||Antiphospholipid syndrome |