Key result
Larger thoracic diameter linked to ~68% lower odds of reduced functional capacity per cm.
Why the study?
Exercise intolerance is frequently reported in patients with mitral valve prolapse despite preserved LV systolic function and non-severe mitral regurgitation, but its mechanisms remain incompletely understood.
Is antero-posterior thoracic diameter associated with reduced functional capacity in symptomatic individuals with mitral valve prolapse undergoing exercise stress echocardiography?
Observational (n=101)
No
Is antero-posterior thoracic diameter associated with reduced functional capacity in symptomatic individuals with mitral valve prolapse undergoing exercise stress echocardiography?
In symptomatic patients with MVP, reduced exercise capacity is driven by a smaller antero-posterior thoracic diameter rather than the MVP status itself, highlighting a distinct thoraco-cardiac phenotype.
Background: Exercise intolerance is frequently reported in patients with mitral valve prolapse (MVP) despite preserved left ventricular (LV) systolic function and non-severe mitral regurgitation, but its mechanisms remain incompletely understood. We investigated whether antero-posterior (A-P) thoracic diameter is associated with reduced functional capacity in symptomatic MVP and characterized exercise-related LV filling and forward-flow responses. Methods: In this prospective single-center study, 101 consecutive symptomatic individuals undergoing exercise stress echocardiography (ESE) were enrolled, including 58 with MVP and 43 symptomatic non-MVP controls. Resting and exercise assessment included indexed LV volumes, stroke volume index (SVi), cardiac index (CI), LV filling indices, and pulmonary pressures. Reduced functional capacity was prespecified as peak workload <100 W. Logistic regression and receiver-operating-characteristic analyses were performed to identify its determinants and evaluate A-P thoracic diameter. Results: Patients with MVP had a smaller A-P thoracic diameter and lower exercise capacity than controls, with more frequent exertional symptoms and greater exercise-induced ST-segment depression despite negative ESE for inducible wall-motion abnormalities. At rest, MVP patients exhibited smaller LV dimensions and volumes, lower LV mass and left atrial size, and lower SVi and CI despite comparable LVEF and E/e′. During exercise, LV contractile reserve and pulmonary pressure responses were comparable, whereas peak LVEDVi, LVESVi, SVi, CI, and E/e′ were lower in MVP patients. Exercise-induced increases in LVEDVi, SVi, CI, and E/e′ were also attenuated. After multivariable adjustment, female sex (adjusted OR 3.99, 95% CI 1.23–13.01; p=0.022) and A-P thoracic diameter (adjusted OR per 1-cm increase 0.32, 95% CI 0.17–0.58; p<0.001) remained independently associated with reduced functional capacity, whereas MVP did not. A-P thoracic diameter showed good discrimination (AUC 0.864), with an internally derived optimal cut-off ≤12.75 cm. Conclusions: Symptomatic MVP was characterized by reduced exercise capacity and a smaller, low-filling cardiac phenotype with limited forward-flow augmentation despite preserved LV contractile reserve. A smaller A-P thoracic diameter, rather than MVP status, remained independently associated with reduced functional capacity, supporting thoracic geometry as a component of a broader thoraco-cardiac functional phenotype. The identified threshold requires external validation.
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Sonaglioni et al. (2026) conducted an observational in Mitral valve prolapse (n=101). Antero-posterior thoracic diameter vs. Larger diameter (continuous variable) was evaluated on Reduced functional capacity (peak workload <100 W) (OR 0.32, 95% CI 0.17-0.58, p=<0.001). A smaller antero-posterior thoracic diameter (adjusted OR per 1-cm increase 0.32; 95% CI 0.17-0.58; p<0.001), rather than MVP status, was independently associated with reduced functional capacity.
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