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Secondary Mitral Regurgitation Subtypes: Linking Etiology, Left Atrial Mechanics, and Clinical Phenotypes
Session:
SESSÃO DE POSTERS 31 - VALVULOPATIA MITRAL E TRICÚSPIDE - DIAGNÓSTICO E INTERVENÇÃO VALVULAR
Speaker:
Ricardo Carvalheiro
Congress:
CPC 2025
Topic:
F. Valvular, Myocardial, Pericardial, Pulmonary, Congenital Heart Disease
Theme:
15. Valvular Heart Disease
Subtheme:
15.1 Valvular Heart Disease – Pathophysiology and Mechanisms
Session Type:
Cartazes
FP Number:
---
Authors:
Ricardo Carvalheiro; Miguel Marques Antunes; Isabel Cardoso; José Miguel Viegas; Vera Vaz Ferreira; Pedro Rio; Ana Teresa Timóteo; Ana Galrinho; Rui Cruz Ferreira
Abstract
<p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong>Introduction: </strong>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.</span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong>Methods: </strong>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. </span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong>Results: </strong>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 cm<sup>2</sup>, p=<span style="color:black">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 </span>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.</span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif">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.</span></span></p> <p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong>Conclusions: </strong>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.</span></span></p>
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