Secondary mitral regurgitation subtypes: linking etiology, left atrial mechanics, and clinical phenotypes

Abstract Introduction Secondary mitral regurgitation (SMR) arises from diverse mechanisms impacting the mitral apparatus. Ventriculogenic SMR (SMR-V) is driven by left ventricular (LV) dysfunction or dilation, whereas atriogenic SMR (SMR-A) stems from atrial remodeling, frequently linked with atrial fibrillation (AF) or HFpEF. We aimed to characterize SMR patients and compare clinical and echocardiographic features, focusing on left atrial (LA) mechanics, diastolic parameters, and survival outcomes between SMR-V and SMR-A groups. Methods We retrospectively examined 96 pts with SMR diagnosed with transesophageal echocardiogram in a single tertiary center between 2018 and 2023. Pts were categorized as having SMR-V if they showed LV dilation or systolic dysfunction, and as having SMR-A otherwise. Results Of 96 pts (mean age 67 ± 14 years, 62% female), 73 (76%) presented SMR-V and 23 (24%) SMR-A. Pts with SMR-A were less symptomatic (mean NYHA 2 vs 3, p=0.043) and had less severe MR by EROA (24.7 vs 33.9 cm2, p=0.016), although there were no differences in regurgitant volume (41.3 vs 47.0 mL, p=0.23). Pts were more frequently female (p=0.003), with a higher prevalence of atrial fibrillation (65 vs 22% p=0.001). They had lower E/e' (10.0 vs. 15.5, p = 0.015) and a longer deceleration time (169.0 vs. 144.5 ms, p = 0.028), suggesting less severe diastolic dysfunction. They had higher conduit LAS (10.0% vs. 7.0%, p = 0.001) and a trend towards higher reservoir strain (11.0% vs. 9.0%, p = 0.078), along with significantly lower LA stiffness (0.8 vs. 1.7, p = 0.002). In multivariate analysis, patient rhythm didn’t account for the differences shown in LA strain. Overall survival over 60 months did not differ between the SMR-V and SMR-A groups (p = 0.391), despite slightly higher mean survival estimates in the SMR-A group (47.98 vs. 42.63 months). Notably, although pts with SMR-A seemed to have less severe mitral regurgitation, EROA alone did not fully explain the differences found in LA strain and mortality trends in multivariate analysis, suggesting other pathophysiological factors underlie the divergent LA mechanics and prognosis. Conclusions In our cohort, while patients with SMR-A presented with less symptomatic disease, lower EROA, and more favorable diastolic parameters, they ultimately shared similar long-term survival with SMR-V patients. Recognizing the distinct remodeling pathways of pts with SMR may aid in clarifying the prognosis for the different subtypes.