Beyond mitral regurgitation reduction: Divergent hemodynamic and structural responses to transcatheter edge-to-edge repair in primary and secondary mitral regurgitation.

BACKGROUND

Severe mitral regurgitation is associated with reduced forward cardiac output. Transcatheter edge-to-edge repair reduces regurgitation severity, but its effects on resting systemic hemodynamics may differ according to etiology. This study evaluated changes in cardiac structure, cardiac output, and systemic oxygen transport six months after transcatheter edge-to-edge repair in patients with primary or secondary mitral regurgitation.

METHODS

We prospectively studied 195 patients with severe mitral regurgitation and low forward cardiac output undergoing successful transcatheter edge-to-edge repair. Echocardiography and non-invasive hemodynamic assessment by inert gas rebreathing were performed at baseline and at six months. Oxygen consumption and arteriovenous oxygen content difference were derived using the Fick principle.

RESULTS

At baseline, cardiac output was similar between groups, while arteriovenous oxygen content difference was higher in secondary mitral regurgitation (p < 0.05). In the overall cohort, cardiac output increased (p = 0.02) and arteriovenous oxygen content difference decreased (p = 0.03), with unchanged oxygen consumption. In secondary mitral regurgitation, cardiac output increased and arteriovenous oxygen content difference decreased, without changes in ventricular volumes or ejection fraction. In primary mitral regurgitation, ventricular volumes decreased and ejection fraction declined, with no significant changes in hemodynamics.

CONCLUSIONS

After transcatheter edge-to-edge repair, secondary and primary mitral regurgitation show distinct adaptive patterns at rest. Seconday mitral regurgitation is characterized by predominant peripheral remodeling with improved forward hemodynamics, whereas primary mitral regurgitation mainly shows central cardiac remodeling with stable global output, indicating heterogeneous physiological responses beyond mitral regurgitation reduction.