p.60 抽出テキスト

Otto et al 2020 ACC/AHA Guideline for the Management of Valvular Heart Disease

Circulation. 2021;143:e72–e227. DOI: 10.1161/CIR.0000000000000923 February 2, 2021 e131 CLINICAL STATEMENTS AND GUIDELINES

8 TRICUSPID VALVE DISEASE

8.1 Classification and Stages of TR

Trace to mild degrees of TR of no physiological consequence are commonly detected on TTE in subjects with anatomically normal valves. However, significant or worsening TR is associated with poor long-term outcomes.1–7 Primary disorders of the tricuspid apparatus that can lead to more significant degrees of TR include rheumatic disease, IE, congenital disease (Ebstein’s), myxomatous changes, and other problems affecting the tricuspid valve leaflets (blunt chest trauma, carcinoid, drugs, and radiation) (Table 19). A growing number of patients develop significant TR from iatrogenic etiologies (device leads and endomyocardial biopsies).8–10 Most cases of significant TR are secondary and related to tricuspid annular dilation and leaflet tethering in the setting of RV remodeling because of pressure or volume overload, as seen in patients with pulmonary hypertension (primary or secondary to left-sided heart disease) or dilated cardiomyopathies.11–13 In addition, 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 pressure and imaging evidence of significant TR. Symptomatic patients with severe TR (Stage D) have symptoms of fatigue, abdominal bloating, and peripheral 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 Diagnosis of TR

Recommendations for Diagnosis of TR COR LOE Recommendations

1 C-LD 1.  In patients with TR, TTE is indicated to evaluate the presence and severity of TR, determine the etiology, measure the sizes of the rightsided chambers and inferior vena cava, assess RV systolic function, estimate pulmonary artery systolic pressure, and characterize any associated left-sided heart disease.1,2

2a C-LD 2.  In patients with TR, invasive measurement of the cardiac index, right-sided diastolic pressures, pulmonary artery pressures, and pulmonary vascular resistance, as well as right ventriculography, can be useful when clinical and noninvasive data are discordant or inadequate.3–5 Synopsis

TTE can determine the etiology of TR and its effect on the RV. Cardiac catheterization is of clinical value if the information from TTE is inadequate or discordant with the clinical presentation.6–10

Recommendation-Specific Supportive Text

1.	 TTE can distinguish primary TR (abnormal valve leaflets) from secondary TR (normal valve leaflets), define any associated left-sided valvular or myocardial disease, and provide an estimate of pulmonary artery systolic pressure.11–15 Characterization of the severity of TR relies on an integrative assessment of multiple parameters, as recommended by the American Society of Echocardiography and European Association of Echocardiography,1,2 but many limitations remain. In patients with TR undergoing leftsided valve surgery, an annular diastolic diameter >40 mm (or >21 mm/m2) indicates an increased risk of persistent or progressive TR after isolated mitral valve surgery.13 Pulmonary artery systolic pressure is estimated from maximal TR velocity. Assessment of RV systolic function is challenged by geometric and image acquisition constraints, as well as by variability in RV loading condition.16,17 Normal RV systolic function is defined by several parameters, including tricuspid annular plane systolic excursion >16 mm, tricuspid valve systolic annular velocity >10.0 cm/s, and RV end-systolic area <20.0 cm2 or fractional area change >35%. Other imaging modalities, such as 3D TEE, magnetic resonance imaging, and CT scan, may provide more accurate information on the status of the RV. 2.	 When physical examination and TTE data on estimated pulmonary artery systolic pressure are either discordant or inadequate, invasive measurement of pulmonary artery pressures and pulmonary vascular resistance can be helpful to guide

Table 19.  Classification of TR

Primary Secondary Rheumatic Infective endocarditis Iatrogenic (device leads, endomyocardial biopsy) Congenital (eg, Ebstein’s, levotransposition of the great arteries) Other (eg, trauma, carcinoid, drugs, irradiation) Pulmonary hypertension with RV remodeling (primary or secondary to left-sided heart disease)

Dilated cardiomyopathy Annular dilation (associated with AF)* RV volume overload (shunts/high output)

*Isolated TR is associated with AF and has LVEF >60%, pulmonary artery systolic pressure <50 mm Hg, and no left-sided valve disease, with normalappearing tricuspid valve leaflets. AF indicates atrial fibrillation; LVEF, left ventricular ejection fraction; RV, right ventricular; and TR, tricuspid regurgitation.

Downloaded from http://ahajournals.org by on October 7, 2026