From the Guidelines
The tricuspid valve appears normal with appropriate structure and function, and no intervention is required as all parameters are within physiological limits. The valve demonstrates normal respiratory variation of greater than 50%, which indicates proper right heart hemodynamics, as described in the 2014 AHA/ACC guideline for the management of patients with valvular heart disease 1. There is no evidence of tricuspid stenosis, and only trivial tricuspid regurgitation is present, which is considered a normal variant, corresponding to Stage A of TR as defined in Table 19 of the guideline 1. The inferior vena cava diameter measures 1.3 cm, which is within normal limits, suggesting normal right atrial pressures. This is confirmed by the measured right atrial pressure of 3 mmHg, which is in the normal range, and the tricuspid regurgitation velocity of 1.2 m/s is also normal, indicating normal pressure gradient between the right ventricle and right atrium during systole. Some key points to consider in this case include:
- The absence of significant tricuspid regurgitation, which is a key factor in determining the severity of TR, as outlined in the guideline 1
- The normal inferior vena cava diameter and right atrial pressure, which suggest that the right heart is functioning properly
- The normal tricuspid regurgitation velocity, which indicates a normal pressure gradient between the right ventricle and right atrium during systole Regular cardiac follow-up as part of routine health maintenance is sufficient, as the patient's tricuspid valve anatomy and function are within normal limits, and there is no evidence of significant pathology, as described in the guideline 1.
From the Research
Tricuspid Valve Structure and Function
- The tricuspid valve is a complex anatomical structure that incorporates a saddle-shaped annulus, asymmetric leaflets, the subvalvular apparatus, and the right ventricle and its loading conditions 2.
- The tricuspid valve apparatus consists of 3 leaflets (anterior, posterior, and septal) inserted in the fibrous tricuspid annulus and connected to the papillary muscle via the chordae tendinae 3.
Tricuspid Regurgitation
- Tricuspid regurgitation (TR) is present in 1.6 million individuals in the United States and 3.0 million people in Europe, with functional TR being the most common form caused by cardiomyopathies, LV valve disease, or pulmonary disease 4.
- TR is a progressive entity that worsens the prognosis of patients, regardless of its etiology, and its severity, mechanisms, and hemodynamic consequences must be taken into account 5.
- Functional TR is often a satellite of left-sided heart disease and/or elevated pulmonary artery pressure, and a particular form is characterized by TR worsening after left-sided valve surgery, which impairs patient prognosis 5.
Diagnosis and Treatment
- Echocardiography can assess the TR etiology/severity, measure RA and RV size and function, estimate pulmonary pressure, and characterize LV disease 4.
- Management of TR includes diuretics, ACE inhibitors, and aldosterone antagonists, while surgical annuloplasty or valve replacement should be considered in patients with progressive RV dilatation without severe LV dysfunction and pulmonary hypertension 4.
- Transcatheter repair/replacement is an emerging therapy for high-risk patients with TR who would otherwise have a dismal clinical prognosis, and multimodality imaging can help with the appropriate selection of patients for these procedures 4, 5, 3.
Imaging and Assessment
- Two and three-dimensional echocardiographic imaging of the TV using transthoracic and transesophageal windows can be used to assess TR and TV anatomy and function 2.
- Multimodality imaging, including cardiac magnetic resonance imaging and computed tomography scans, may add to two-dimensional transthoracic and transoesophageal echocardiographic data in the analysis of TR 5.
- A greater appreciation of normal and abnormal anatomy is important as new methods of treating TR are developed, and an understanding of TV anatomy and pathophysiology is essential to unraveling the pathophysiology of TR 6, 3.