Tricuspid regurgitation (TR)

Learning objectives

Tricuspid regurgitation (TR) occurs when the tricuspid valve does not close properly, causing a reversal of blood flow through the valve
TR can be of primary or secondary origin:
- Primary (organic) TR: Pathology of the tricuspid valve complex, may be of rheumatic, degenerative, congenital, infectious, traumatic, or iatrogenic origin
- Secondary (functional) TR: Related to right ventricular dilatation and/or dysfunction, annular dilatation, and leaflet tethering, usually secondary to left-sided valvular heart disease, atrial fibrillation or pulmonary hypertension

Often clinically silent and symptoms usually relate to concomitant left-sided valvular heart disease
General fatigue and reduced exercise capacity
Upper abdominal pain
Peripheral lower limb edema
Systolic jugular distension
Pulsatile hepatomegaly
Ascites, liver failure, and cachexia may be observed in end-stage disease
Electrocardiogram frequently shows right bundle branch block and atrial fibrillation reflects disease evolution.

	Parameters	Mild	Moderate	Severe
Qualitative	TV morphology	Normal/abnormal	Normal/abnormal	Abnormal/flail/large coaptation defect
	Color flow TR jet	Small, central	Intermediate	Very large central jet or eccentric wall impinging jet
	CW signal of TR jet	Faint/parabolic	Dense/parabolic	Dense/triangular with early peaking (peak <2 m/s in massive TR)
Semi-quantitative	VC width (mm)	Not defined	<7	>7
	PISA radius (mm)	≤5	6–9	>9
	Hepatic vein flow	Systolic dominance	Systolic blunting	Systolic flow reversal
	Tricuspid inflow	Normal	Normal	E-wave dominant (≥1 m/s)
Quantitative	EROA (mm2)	Not defined	Not defined	≥40
	R Vol (ml)	Not defined	Not defined	≥45

Tricuspid regurgitation is most commonly secondary to other morbidities, which might require further attention.