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Tricuspid
Regurgitation

Tricuspid Regurgitation (TR) is a complex disease that has multiple causes, and is associated with high rates of morbidity and mortality.1,2 TR is highly prevalent, and among valve diseases, is one of the most undertreated.1,3 If left untreated, TR initiates a cascade of events that can lead to right-sided Heart Failure (HF) and death.4

TRICUSPID REGURGITATION

Tricuspid Valve Disease (TVD), including TR and tricuspid stenosis, is estimated to affect >70 million people worldwide.5 In Europe, the rate of moderate or greater TR is estimated to be 1.1% in patients aged ≥65 years, and the prevalence increases to 4.0% in patients aged ≥75 years.1

Moderate-to-severe TR is associated with increased mortality, and the risk of mortality increases with TR severity.1,6–12 Higher TR severity is independently associated with increased rates of all-cause mortality.6–12

The tricuspid valve is often referred to as the “forgotten valve”, as TVD was historically perceived to be less important than Left-Sided Heart Disease (LSHD) and was not normally considered for surgical treatment.13–16 In recent years, there is increasing focus on the tricuspid valve and diseases affecting its function, due to increased awareness and understanding of the adverse consequences associated with TVD.14,16,17 The tricuspid valve is located between the Right Atrium (RA) and the Right Ventricle,13 and controls the flow of blood between these two heart chambers.18

TR occurs when the tricuspid valve does not close sufficiently during ventricular contraction (systole), and consequently allows blood to flow backwards through the tricuspid valve from the right ventricle into the RA.19,20 TR places substantial strain on the heart, as the heart must work harder to pump blood into the right ventricle, against the backflow of blood regurgitating through the tricuspid valve.18

 

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TR can be classified as primary (e.g. degenerative) or secondary (functional), depending on the underlying cause of the condition, and some patients may present with a mixed aetiology, although this is uncommon.1,11,13,15,21 TR is commonly associated with HF, Atrial Fibrillation (AF), pulmonary hypertension, drug use, and cardiac device implantation (e.g. pacemaker leads).17, 20,22,23

CLASSIFICATION, CAUSES AND RISK FACTORS FOR TR


PRIMARY/DEGENERATIVE TR

  • Approximately 10–20% of cases are due to primary TR, which is diagnosed in the presence of abnormal tricuspid valve morphology.13,19
  • The causes of primary TR include congenital abnormalities, infection (i.e. endocarditis), rheumatic disease, chest cavity trauma, tumors, and intravenous drug use.13,17,20,22,23
  • Structural damage to the tricuspid valve during cardiac device implantation is another common cause of primary TR.22,23
     

SECONDARY/FUNCTIONAL TR

  • Secondary TR is the most common form, occurring in 80–90% of cases,13,19 and is diagnosed in the presence of normal tricuspid valve morphology.13
  • The causes of secondary TR include changes in the right ventricle or distortion of the tricuspid valve leaflets, annulus or chords.15
  • The condition typically occurs secondary to LSHD and/or Right Ventricular (RV) remodelling, Pulmonary Hypertension (HT), tricuspid annular dilation, AF or RV dysfunction.11,13–15,24 This can make it difficult to isolate the risk factors that contribute to secondary TR independently of comorbid or underlying cardiac disease(s).13,15
     

MIXED TR

  • Patients with primary TR aetiology may experience worsening of TR due to progressive cardiac remodelling and annular dilation, subsequently causing secondary TR.25


Abbreviations: AF, atrial fibrillation; HF, heart failure; HT, hypertension; LSHD, left-sided heart disease; RV, right ventricular; TR, tricuspid regurgitation.

Secondary TR arising from RV remodelling can be classified in three progressive stages26

PHASE 1

Initial RV dilation results
in tricuspid annulus (TA) dilation

PHASE 2

Initial RV dilation results
in TA dilation

PHASE 3

Initial RV dilation results
in TA dilation

Source: Taramasso et al., 2017.26{sup 26}

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References
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