ATRIAL VS VENTRICULAR SECONDARY MITRAL REGURGITATION
Mechanisms, Echocardiographic Features, and Clinical Implications
INTRODUCTION
Secondary (functional) mitral regurgitation (SMR) occurs due to distortion of left heart geometry rather than primary mitral valve leaflet disease. Traditionally linked to left ventricular (LV) dysfunction, it is now clear that a distinct entity—atrial secondary mitral regurgitation (ASMR)—exists, driven predominantly by left atrial (LA) and mitral annular remodeling. Differentiating atrial from ventricular SMR is essential because mechanisms, prognosis, and management strategies differ significantly.
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1. DEFINITIONS
Atrial Secondary Mitral Regurgitation (ASMR)
Mitral regurgitation caused by left atrial enlargement and mitral annular dilatation, with preserved or near-normal LV systolic function and minimal leaflet tethering.
Ventricular Secondary Mitral Regurgitation (VSMR)
Mitral regurgitation resulting from left ventricular dilatation and dysfunction, leading to papillary muscle displacement, leaflet tethering, and incomplete leaflet coaptation.
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2. PATHOPHYSIOLOGY
Atrial Secondary MR
Chronic atrial fibrillation
Long-standing diastolic dysfunction
Heart failure with preserved ejection fraction (HFpEF)
Aging-related atrial remodeling
Key mechanism:
Mitral annular dilatation (especially posterior annulus)
Reduced annular contraction
Loss of atrioventricular coupling
Minimal leaflet tethering
Ventricular Secondary MR
Ischemic cardiomyopathy
Dilated cardiomyopathy
Heart failure with reduced ejection fraction (HFrEF)
Key mechanism:
LV remodeling → papillary muscle displacement
Apical and lateral leaflet tethering
Reduced closing forces
Increased tenting height and area
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3. ECHOCARDIOGRAPHIC DIFFERENCES
Atrial SMR
Normal or mildly reduced LVEF
Marked left atrial enlargement
Dilated mitral annulus (often circular)
Minimal leaflet tethering
Central MR jet common
Normal LV size or mild concentric remodeling
Ventricular SMR
Reduced LVEF
Dilated LV with spherical remodeling
Increased tenting height and tenting area
Posteriorly directed or eccentric MR jets
Displaced papillary muscles
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4. HEMODYNAMIC AND CLINICAL PROFILE
Feature Atrial SMR Ventricular SMR
LV systolic function Preserved Reduced
Primary driver LA / annulus LV remodeling
Common rhythm Atrial fibrillation Sinus rhythm or AF
Heart failure type HFpEF HFrEF
Pulmonary pressures Often elevated Often elevated
Prognostic driver Atrial disease burden LV dysfunction
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5. MANAGEMENT IMPLICATIONS
Atrial Secondary MR
Aggressive rhythm control (AF ablation, cardioversion)
Optimization of diastolic function
Blood pressure control
Consider mitral annuloplasty or transcatheter edge-to-edge repair (TEER) in selected patients with refractory symptoms
Restoration of sinus rhythm may significantly reduce MR severity
Ventricular Secondary MR
Guideline-directed medical therapy for HFrEF
Cardiac resynchronization therapy when indicated
Transcatheter mitral valve repair (e.g., TEER) in symptomatic patients despite optimal medical therapy
Surgical intervention reserved for selected cases
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6. PROGNOSIS
Atrial SMR: Prognosis closely linked to atrial fibrillation burden, pulmonary hypertension, and HFpEF progression. MR may improve with rhythm control.
Ventricular SMR: Prognosis primarily driven by LV dysfunction and adverse remodeling; MR often reflects advanced myocardial disease.
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7. KEY TAKE-HOME POINTS
Atrial and ventricular secondary MR are distinct pathophysiological entities.
ASMR is driven by left atrial and annular remodeling, not LV dysfunction.
VSMR results from LV dilation and papillary muscle displacement.
Echocardiography is central to differentiation.
Management strategies differ and should target the primary remodeling chamber.
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