Left sided Wall Stress Causing Arrhythmia | 211 wall visualized in the 3-chamber long-axis view was found to be the only distinctive location for MAD between IVF patients and controls. In the other walls, gaps of 1-3 mm between the LV myocardium and the mitral annulus hinge points were frequently seen in both patients and controls. Where the 3-chamber view (or parasternal long-axis view in echo) is generally considered to be the most standardized for measurements of the mitral valve, the other views are less reproducible when it comes to measurements on the saddle shaped valve and might therefore be more subjected to errors.24,31 This might have contributed to our finding that the inferolateral wall was the only distinctive location for MAD between IVF patients and controls, which is in line with previous studies.8,9,25,32 Additionally, a recent study applying a comprehensive 3D analysis on cardiac computed tomography images of 98 structurally normal hearts also showed high prevalence of MAD in the anterior to anterolateral and inferior to inferoseptal segments (77.5% and 87.8%, respectively), while inferolateral MAD was less common in healthy subjects (11.2%).33 The cut-off to determine presence of MAD on CMR is another point of discussion. We considered longitudinal distances of >1 mm significant, given the spatial resolution of CMR18, but general consensus is lacking. The voxel size of cine sequences acquired in routine clinical care limits reliability of measurements below 1.5 mm. Besides, longitudinal distances measured by CMR and echocardiography cannot be used interchangeably, as shown by differences in measured distances by the two modalities in a previous study.8 Larger CMR based population studies are needed to determine the upper limit of normal. Mitral annulus disjunction and the relation to mitral valve prolapse The concept of MAD as an arrhythmic factor was introduced for the first time around the 1980s.11,12,34 Since then, it has been closely linked to MVP and other mitral valve disease.25 During the last years, MAD has regained interest and multiple reports indicate that MAD may also be present without MVP.8,35 This is in line with our findings, as 43% of IVF patients with MAD did not show MVP. The distinction between MAD and MVP can however be difficult, especially when determining the exact hinge point of a prolapsed mitral valve that parallels the atrial wall. If the prolapse distance is measured from the myocardial edge, MVP will always be found in presence of MAD.25 We measured longitudinal MAD distance from the myocardial edge to the annular hinge point and MVP beyond the annular hinge point, allowing a distinction between the two.8 Although the distinction between MAD and MVP can be challenging, the increased prevalence of both entities in IVF that was found in this study is remarkable. The pro-arrhythmic substrate The exact proarrhythmic mechanism of MAD is unknown. It has been hypothesized that hypermobility of the mitral valve causes mechanical stretch on the myocardial wall. This may directly induce ventricular ectopy which can potentially trigger VF. On the long term, mechanical stretch may also result in myocyte hypertrophy and fibrosis, creating another potential cause for myocardial electrical instability and arrhythmias.9,25 Previous studies related papillary muscle fibrosis to arrhythmic events in the presence of MAD and MVP, but severe arrhythmias were also observed in patients without visible papillary muscle fibrosis on CMR.8,14,25 In this study, we did not observe any papillary muscle fibrosis in IVF patients with MAD. However, we did observe more frequently ventricular ectopy and T-wave abnormalities in the inferolateral leads in MAD/MVP patients, which was also observed in previous studies.9,25 10
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