292 Mechanical stress, myocardial deformation abnormalities, and ventricular fibrosis: a fatal cascade in arrhythmic mitral valve prolapse patients
Authors: Cecere Annagrazia , De Lazzari Manuel , Cipriani Alberto , Brunetti Giulia , Graziano Francesca , Lorenzoni Giulia , De Conti Giorgio , Motta Raffaella , Iliceto Sabino , Marra Martina Perazzolo 
Published: December 2021

Aims

Arrhythmic mitral valve prolapse (MVP) is characterized by left ventricular (LV) fibrosis in the basal inferolateral wall and papillary muscles. We hypothesized that LV fibrosis are driven by excessive mechanical forces acting on myocardial susceptible cells, representing the last step in the MVP-induced myocardial stretch process. We evaluated the LV myocardial deformation, using strain assessed with cardiac magnetic resonance (CMR), in arrhythmic MVP patients with normal LV ejection fraction (LVEF) and absent/trivial mitral regurgitation (MR) and its correlation with the presence of LV fibrosis, detected by late gadolinium enhancement (LGE) in post-contrast CMR images.

Methods and results

We enrolled consecutive arrhythmic MVP patients with normal LVEF and no/trivial MR. Sixty-nine (39 female; median age: 40 years) patients without MVP, arrhythmias or cardiovascular history served as control group. All patients underwent CMR for identification of LGE and evaluation of LV myocardial deformation. A total of 66 patients were enrolled (47 female; median age: 44 years). In the overall MVP population, LGE was present in 41 patients (62.1%). MVP patients without LGE (25 patients, 37.9%) presented a higher global radial (median: 42.19 vs. 33; P &lt;0.0001) and higher global longitudinal strain (median: −21.61 vs. −18.10; P &lt;0.0001), compared to the control group. A reduction of regional basal posterolateral radial (BPL median: 50.60 vs. 67.30; P = 0.0015) and longitudinal strain (BPL median: −23.50 vs. −26.70; P = 0.0186) were observed in the MVP patients as compared with controls (Figures A–D). Conversely to the basal region, mid anterolateral and posterolateral region presented a higher radial (MAL median: 52.60 vs. 31.10; P &lt; 0.0001 and MPL median: 52.80 vs. 21.50; P &lt; 0.0001) and longitudinal strain (MAL median: −24.80 vs. −18.30; P &lt; 0.0001 and MPL median: −25.30 vs. −14.80; P &lt; 0.0001), when compared to control group. MVP patients with LGE had a lower global radial (median: 36.48 vs. 42.19; P &lt;0.0047), longitudinal (median: −19.18 vs. −21.61; P = 0.0013), and circumferential strain (median: −17.80 vs. −19.28; P =  0.0134) compared with those without fibrosis. According to MVP patients without LGE, the presence of fibrosis is associated with a lower regional radial (BAL median: 64.40 vs. 82.80; P = 0.0481; MAL median: 42.60 vs. 52.60; P = 0.0287) and circumferential strain (BAL median: −21.90 vs. −24.20; P = 0.0174; BPL median: −16.80 vs. −18.80; P = 0.0411; MPL median: −15.50 vs. −19.40; P = 0.0077) in the LV basal-mid lateral walls (Figures E–H). 292 Figures A–D and E-H 

Conclusions

Arrhythmic MVP patients with normal LV systolic function and absent/trivial MR presented an abnormal myocardial deformation pattern. The reduced strain in BPL wall of MVP patients without LGE could be considered as an early marker of MVP-induced myocardial stress, that could promote, time by time, LV fibrosis and arrhythmias in MVP patients.