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Effects of acute ischemic mitral regurgitation on three-dimensional mitral leaflet edge geometry

^a Department of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, CA, United States
^b Laboratory of Cardiovascular Physiology and Biophysics, Research Institute of the Palo Alto Medical Foundation, Palo Alto, CA, United States

Received 24 September 2007; accepted 31 October 2007.

^_* Corresponding author. Address: Department of Cardiothoracic Surgery, Falk Cardiovascular Research Center, Stanford University School of Medicine, Stanford, CA 94305-5247, United States. Tel.: +1 650 725 3826; fax: +1 650 725 3846. (Email: dcm{at}stanford.edu).

Background: Improved quantitative understanding of in vivo leaflet geometry in ischemic mitral regurgitation (IMR) is needed to improve reparative techniques, yet few data are available due to current imaging limitations. Using marker technology we tested the hypotheses that IMR (1) occurs chiefly during early systole; (2) affects primarily the valve region contiguous with the myocardial ischemic insult; and (3) results in systolic leaflet edge restriction. Methods: Eleven sheep had radiopaque markers sutured as five opposing pairs along the anterior (A₁–E₁) and posterior (A₂–E₂) mitral leaflet free edges from the anterior commissure (A₁–A₂) to the posterior commissure (E₁–E₂). Immediately postoperatively, biplane videofluoroscopy was used to obtain 4D marker coordinates before and during acute proximal left circumflex artery occlusion. Regional mitral orifice area (MOA) was calculated in the anterior (Ant-MOA), middle (Mid-MOA), and posterior (Post-MOA) mitral orifice segments during early systole (EarlyS), mid systole (MidS), and end systole (EndS). MOA was normalized to zero (minimum orifice opening) at baseline EndS. Tenting height was the distance of the midpoint of paired markers to the mitral annular plane at EndS. Results: Acute ischemia increased echocardiographic MR grade (0.5 ± 0.3 vs 2.3 ± 0.7, p < 0.01) and MOA in all regions at EarlyS, MidS, and EndS: Ant-MOA (7 ± 10 vs 22 ± 19 mm², 1 ± 2 vs18 ± 16 mm², 0 vs 17 ± 15 mm²); Mid-MOA (9 ± 13 vs 25 ± 17 mm², 3 ± 6 vs 21 ± 19 mm², 0 vs 25 ± 17 mm²); and Post-MOA (8 ± 10 vs 25 ± 16, 2 ± 4 vs 22 ± 13 mm², 0 vs 23 ± 13 mm²), all p < 0.05. There was no change in MOA throughout systole (EarlyS vs MidS vs EndS) during baseline conditions or ischemia. Tenting height increased with ischemia near the central and the anterior commissure leaflet edges (B₁–B₂: 7.1 ± 1.8 mm vs 7.9 ± 1.7 mm, C₁–C₂: 6.9 ± 1.3 mm vs 8.0 ± 1.5 mm, both p < 0.05). Conclusions: MOA during ischemia was larger throughout systole, indicating that acute IMR in this setting is a holosystolic phenomenon. Despite discrete postero-lateral myocardial ischemia, Post-MOA was not disproportionately larger. Acute ovine IMR was associated with leaflet restriction near the central and the anterior commissure leaflet edges. This entire constellation of annular, valvular, and subvalvular ischemic alterations should be considered in the approach to mitral repair for IMR.

Key Words: Acute myocardial ischemia • Ischemic mitral regurgitation • Mitral orifice area • Radiopaque markers • Ovine model