Management of Tricuspid and Mitral Regurgitation with Normal Valve Morphology
When echocardiography demonstrates tricuspid and mitral regurgitation with structurally normal valves, this represents secondary (functional) regurgitation requiring identification and treatment of the underlying cause—most commonly left ventricular dysfunction, pulmonary hypertension, or atrial fibrillation—rather than primary valve intervention. 1
Understanding the Mechanism
Secondary regurgitation occurs due to ventricular remodeling and annular dilatation, not valve pathology itself:
Mitral regurgitation with normal leaflets results from left ventricular dilation causing papillary muscle displacement, leaflet tethering, and annular dilatation—the valve structure remains intact but cannot coapt properly due to geometric distortion 1
Tricuspid regurgitation with normal leaflets develops from right ventricular pressure/volume overload causing tricuspid annular dilatation (>40 mm or >21 mm/m²) and leaflet tethering, with tenting area >1 cm² indicating severe functional TR 1
Atrial fibrillation is present in 70-88% of patients with severe TR and causes progressive annular dilatation independent of ventricular dysfunction—AF-induced annular remodeling is a major determinant of secondary TR 1, 2
Initial Diagnostic Workup
Determine the severity and underlying etiology through systematic echocardiographic assessment:
Quantify mitral regurgitation severity using effective regurgitant orifice area (EROA ≥0.4 cm² = severe), regurgitant volume (≥60 mL = severe for primary MR, ≥30 mL for secondary MR), vena contracta width, and left atrial/ventricular dimensions 1
Quantify tricuspid regurgitation severity using vena contracta ≥7 mm, EROA ≥0.4 cm², regurgitant volume ≥45 mL, hepatic vein systolic flow reversal, and right heart chamber dilation 1, 2
Assess left ventricular function and dimensions to identify systolic dysfunction (LVEF <60%) or diastolic dysfunction as the primary driver of functional MR 1
Measure pulmonary artery systolic pressure to determine if pulmonary hypertension (PASP >35-40 mmHg) is driving the functional TR 1
Evaluate right ventricular function using TAPSE (<17 mm indicates dysfunction), tricuspid annular S' velocity (<10 cm/s indicates dysfunction), and RV free wall longitudinal strain 1, 2
Measure tricuspid annular diameter in diastole—dilatation ≥40 mm or ≥21 mm/m² indicates significant functional TR requiring consideration for intervention if left-sided surgery is planned 1, 2
Medical Management Strategy
Optimize guideline-directed medical therapy for the underlying condition before considering surgical intervention:
For secondary MR due to LV dysfunction: Initiate neurohormonal antagonists (ACE inhibitors/ARBs, beta-blockers, aldosterone antagonists), consider cardiac resynchronization therapy if appropriate, and pursue coronary revascularization if ischemic etiology—reassess MR severity after optimal medical therapy as it may improve significantly 1, 2
For functional TR with right heart failure: Use loop diuretics for symptom relief from congestion, add aldosterone antagonists for volume management, and implement rhythm control strategies if atrial fibrillation is present 2
Medical therapy should not delay surgical referral when intervention is already indicated based on severity criteria and symptoms, but it remains first-line treatment for isolated functional regurgitation 2
Critical Pitfall: Dynamic Nature of Functional Regurgitation
Secondary regurgitation severity varies with loading conditions and heart rhythm:
Color Doppler jet size alone is unreliable because jet momentum flux depends on velocity squared—two patients with identical-appearing jets can have vastly different EROA (0.30 cm² vs 0.08 cm²) based on peak velocity differences 1
Calculate left atrial pressure from systolic blood pressure minus peak MR gradient (from continuous wave Doppler velocity)—elevated LAP (>25-30 mmHg) with moderate EROA confirms hemodynamically significant MR despite "moderate" quantification 1
Irregular rhythms (atrial fibrillation) complicate assessment—average measurements over multiple beats and recognize that restoration of sinus rhythm may significantly reduce functional regurgitation severity 1
Timing of regurgitation matters—late systolic or biphasic jets require frame-by-frame analysis as single-frame PISA measurements will overestimate severity 1
Surgical Intervention Indications
Surgery for functional regurgitation follows different criteria than primary valve disease:
For Functional Mitral Regurgitation:
Severe secondary MR with symptoms (NYHA Class II-IV) despite optimal medical therapy warrants consideration for mitral valve surgery, though outcomes are less favorable than primary MR 1
Concomitant mitral intervention during CABG should be considered when severe secondary MR is present, though the threshold remains debated 1
For Functional Tricuspid Regurgitation:
Tricuspid valve repair is strongly recommended (Class I, Level B) for patients with mild, moderate, or greater functional TR undergoing left-sided valve surgery when either tricuspid annular dilation (≥40 mm or ≥21 mm/m²) or prior right heart failure is present 1, 2
Concomitant tricuspid annuloplasty prevents progression of TR after mitral surgery—without repair, 31% with no preoperative TR develop moderate or greater TR by 5 years, and 62% with moderate TR progress 1, 3
Isolated tricuspid valve surgery (Class IIa, Level C) is reasonable for symptomatic severe primary TR but has poor outcomes when performed late with established RV dysfunction—timing is critical 1
Rigid or semi-rigid ring annuloplasty is the gold standard technique for functional TR, superior to flexible bands which have higher recurrence rates 1, 2
When NOT to Operate
Avoid futile interventions in irreversible disease:
Do not perform tricuspid surgery in patients with tricuspid annular dilation but absent or only trace TR—annular size alone without regurgitation is not an indication 1, 2
Surgery is contraindicated in severe irreversible RV dysfunction or severe irreversible pulmonary hypertension where intervention is likely futile 1, 2
Isolated tricuspid valve surgery has poor outcomes when RV dysfunction has already occurred—the window for intervention closes once advanced RV remodeling develops 3
Monitoring and Follow-Up
Regular surveillance is essential as functional regurgitation is progressive:
Serial echocardiography every 6-12 months to assess progression of regurgitation severity, ventricular dimensions, and ventricular function 2
Monitor for development of symptoms (fatigue, dyspnea, peripheral edema, abdominal fullness) which change management strategy 4
Track tricuspid annular diameter progression—reaching ≥40 mm triggers consideration for intervention if left-sided surgery becomes necessary 2
Assess RV function deterioration using TAPSE, S' velocity, and RV free wall longitudinal strain as early markers of irreversible dysfunction 1, 2
Exercise stress echocardiography and cardiopulmonary exercise testing may be considered in asymptomatic patients for risk stratification 1, 2
Key Distinction from Primary Valve Disease
The management paradigm differs fundamentally from organic valve disease:
Primary regurgitation (flail leaflet, prolapse, endocarditis) has clear morphological abnormalities and warrants surgery based on severity, symptoms, or ventricular dysfunction regardless of medical therapy 1
Secondary regurgitation requires treating the underlying cause first—LV dysfunction, pulmonary hypertension, atrial fibrillation—and surgery is reserved for persistent severe regurgitation despite optimal medical management or when concomitant left-sided surgery is planned 1, 2
Normal valve morphology with regurgitation indicates the valve is a "victim" not the "culprit"—fixing the valve without addressing the underlying ventricular/atrial pathology leads to high recurrence rates 1