Open Access

The unique mechanism of functional mitral regurgitation in acute myocardial infarction: a prospective dynamic 4D quantitative echocardiographic study

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Date: 4 December 2018
Journal: European Heart Journal - Cardiovascular Imaging , Volume 20 , Issue 4 , Pages 396 - 406
Authors: T. Kimura , V. Roger , N. Watanabe , S. Barros-Gomes , Y. Topilsky , S. Nishino , Y. Shibata , M. Enriquez-Sarano

ESC Journals

AbstractAims

Mechanisms of chronic ischaemic mitral regurgitation (IMR) are well-characterized by apically tethered leaflet caused by papillary muscles (PMs) displacement and adynamic mitral apparatus. We investigated the unique geometry and dynamics of the mitral apparatus in first acute myocardial infarction (MI) by using quantified 3D echocardiography.

Methods and results

We prospectively performed 3D echocardiography 2.3 ± 1.8 days after first MI, in 174 matched patients with (n = 87) and without IMR (n = 87). 3D echocardiography of left ventricular (LV) volumes and of mitral apparatus dynamics throughout cardiac cycle was quantified. Similar mitral quantification was obtained at chronic post-MI stage (n = 44). Mechanistically, acute IMR was associated with larger and flatter annulus (area 9.29 ± 1.74 cm2 vs. 8.57 ± 1.94 cm2, P =0.002, saddle shape 12.7 ± 4.5% vs. 15.0 ± 4.6%, P =0.001), and larger tenting (length 6.36 ± 1.78 mm vs. 5.60 ± 1.55 mm, P =0.003) but vs. chronic MI, mitral apparatus displayed smaller alterations (all P <0.01) and annular size, PM movement remained dynamic (all P <0.01). Specific to acute IMR, without PM apical displacement (P >0.70), greater separation (21.7 ± 4.9 mm vs. 20.0 ± 3.4 mm, P =0.01), and widest angulation of PM (38.4 ± 6.2° for moderate vs. 33.5 ± 7.3° for mild vs. 31.4 ± 6.3° for no-IMR, P = 0.0009) wider vs. chronic MI (P <0.01).

Conclusions

3D echocardiography of patients with first MI provides insights into unique 4D dynamics of the mitral apparatus in acute IMR. Mitral apparatus remained dynamic in acute MI and distinct IMR mechanism in acute MI is not PM displacement seen in chronic IMR but separation and excess angulation of PM deforming the mitral valve, probably because of sudden-onset regional wall motion abnormality without apparent global LV remodelling. This specific mechanism should be considered in novel therapeutic strategies for IMR complicating acute MI.

About the contributors

Toshiyuki Kimura

Role: Author

Véronique L Roger

Rochester (Mayo Clinic)

Role: Author

Nozomi Watanabe

Role: Author