The influence of chest wall conformation on myocardial strain parameters in a cohort of mitral valve prolapse patients with and without mitral annular disjunction.

Purpose: To evaluate the possible influence of chest wall conformation on myocardial strain parameters in a cohort of mitral valve prolapse (MVP) patients with and without mitral annular disjunction (MAD).

Methods: All consecutive middle-aged patients with MVP referred to our Outpatient Cardiology Clinic for performing two-dimensional (2D) transthoracic echocardiography (TTE) as part of work up for primary cardiovascular prevention between March 2018 and May 2022, were included into the study. All patients underwent clinic visit, physical examination, modified Haller index (MHI) assessment (the ratio of chest transverse diameter over the distance between sternum and spine) and conventional 2D-TTE implemented with speckle tracking analysis of left ventricular (LV) global longitudinal strain (GLS) and global circumferential strain (GCS). Independent predictors of MAD presence on 2D-TTE were assessed.

Results: A total of 93 MVP patients (54.2 ± 16.4 yrs, 50.5% females) were prospectively analyzed. On 2D-TTE, 34.4% of MVP patients had MAD (7.3 ± 2.0 mm), whereas 65.6% did not. Compared to patients without MAD, those with MAD had: 1) significantly shorter antero-posterior (A-P) thoracic diameter (13.5 ± 1.2 vs 14.8 ± 1.3 cm, p < 0.001); 2) significantly smaller cardiac chambers dimensions; 3) significantly increased prevalence of classic MVP (84.3 vs 44.3%, p < 0.001); 4) significantly impaired LV-GLS (-17.2 ± 1.4 vs -19.4 ± 3.0%, p < 0.001) and LV-GCS (-16.3 ± 4.1 vs -20.4 ± 4.9, p < 0.001), despite similar LV ejection fraction (63.7 ± 4.2 vs 63.0 ± 3.9%, p = 0.42). A-P thoracic diameter (OR 0.25, 95%CI 0.10-0.82), classic MVP (OR 3.90, 95%CI 1.32-11.5) and mitral annular end-systolic A-P diameter (OR 2.76, 95%CI 1.54-4.92) were the main independent predictors of MAD. An A-P thoracic diameter ≤ 13.5 cm had 59% sensitivity and 84% specificity for predicting MAD presence (AUC = 0.81). In addition, MAD distance was strongly influenced by A-P thoracic diameter (r = - 0.96) and MHI (r = 0.87), but not by L-L thoracic diameter (r = 0.23). Finally, a strong inverse correlation between MHI and both LV-GLS and LV-GCS was demonstrated in MAD patients (r = - 0.94 and - 0.92, respectively), but not in those without (r = - 0.51 and - 0.50, respectively).

Conclusions: A narrow A-P thoracic diameter is strongly associated with MAD presence and is a major determinant of the impairment in myocardial strain parameters in MAD patients, in both longitudinal and circumferential directions.