Regional mitral leaflet opening during acute ischemic mitral regurgitation

Abstract

Background and aim of the study: Diastolic mitral valve (MV) opening characteristics during ischemic mitral regurgitation (IMR) are poorly characterized. The diastolic MV opening dynamics were quantified along the entire valvular coaptation line in an ovine model of acute IMR.

Methods: Ten radiopaque markers were sutured in pairs on the anterior (A1-E1) and corresponding posterior (A2-E2) leaflet edges from the anterior (A1/A2) to the posterior (E1/E2) commissure in 11 adult sheep. Immediately after surgery, 4-D marker coordinates were obtained before and during occlusion of the proximal left circumflex coronary artery. Distances between marker pairs were calculated throughout the cardiac cycle every 16.7 ms. Leaflet opening was defined as the time after end-systole (ES) when the first derivative of the distance between marker pairs was greater than a threshold value of 3 cm/s. Valve opening velocity was defined as the maximum slope of marker pair tracings.

Results: Hemodynamics were consistent with acute ischemia, as reflected by increased MR grade (0.5 +/- 0.3 versus 2.3 +/- 0.7, p < 0.05), decreased contractility (dP/dt(max): 1,948 +/- 598 versus 1,119 +/- 293 mmHg/s, p < 0.05), and slower left ventricular relaxation rate (dP/dt(min): -1,079 +/- 188 versus -538 +/- 147 mmHg/s, p < 0.05). During ischemia, valve opening occurred earlier (A1/A2: 112 +/- 28 versus 83 +/- 43 ms, B1/B2: 105 +/- 32 versus 68 +/- 35 ms, C1/C2: 126 +/- 25 versus 74 +/- 37 ms, D1/D2: 114 +/- 28 versus 71 +/- 34 ms, E1/E2: 125 +/- 29 versus 105 +/- 33 ms; all p < 0.05) and was slower (A1/A2: 16.8 +/- 9.6 versus 14.2 +/- 9.4 cm/s, B1/B2: 40.4 +/- 9.9 versus 32.2 +/- 10.0 cm/s, C1/C2: 59.0 +/- 14.9 versus 50.4 +/- 18.1 cm/s, D1/D2: 34.4 +/- 10.4 versus 25.5 +/- 10.9 cm/s; all p < 0.05), except at the posterior edge (E1/E2: 13.3 +/- 8.7 versus 10.6 +/- 7.2 cm/s). The sequence of regional mitral leaflet separation along the line of coaptation did not change with ischemia.

Conclusion: Acute posterolateral left ventricular ischemia causes earlier leaflet opening, probably due to a MR-related elevation in left-atrial pressure; reduces leaflet opening velocity, potentially reflecting an impaired left ventricular relaxation rate; and does not perturb the homogeneous temporal pattern of regional valve opening along the line of coaptation. Future studies will confirm whether these findings are apparent in patients with chronic IMR, and may help to refine the current strategies used to treat IMR.

Figure 1

Marker array used for the mitral leaflets and annulus. Leaflet markers were sutured as pairs along the anterior (#A₁-E₁) and corresponding posterior (#A₂-E₂) mitral leaflet edge from the anterior (ACOM, #16) to the posterior commissure (PCOM, #20) and on two second-order chordae insertion points of the anterior mitral leaflet (#SC_ant and #SC_post). Annular markers were sutured to the mid-septal annulus (#22), left fibrous trigone (#15), anterior commissure (#16), left lateral annulus (#17), mid-lateral annulus (#18), right lateral annulus (#19), posterior commissure (#20), and right fibrous trigone (#21).

Figure 2

Schematic to illustrate the calculation of (A) the onset of marker pair separation, and (B) maximum marker pair separation velocity (B). Distances between marker pairs (d) were plotted throughout the cardiac cycle. The curve shows the plotted distances between the mid-edge marker pair C₁/C₂ from one representative study under baseline conditions. To assess the time point of marker pair separation, the time point when the slope of this curve was greater than a threshold value of 3 cm/s was determined. Onset of marker pair separation was determined as time between this time point and the end of systole (ES). Maximum marker pair separation velocities were determined by assessing maximum slopes of the plotted curves.

Figure 3

Angle calculations performed to quantify anterior and posterior mitral leaflet (AML and PML, respectively) motion. A) AML edge motion was quantified by calculating α as the angle between the annular mid-septal-lateral diameter (line between #18 and #22) and marker #C₁. B and C) AML belly motion was quantified by calculating angles β (B) and γ (C): β was calculated as the angle between the anterior septal-lateral diameter (line between midpoints of markers #22 and #15 and markers #18 and #17) and the anterior strut chordal marker (#SC_ant); similarly, angle γ was calculated as the angle between the posterior septal-lateral diameter (chord between midpoints of markers #22 and #21 and markers #18 and #19) the posterior strut chordal marker (#SC_post).

Figure 4

Onset of marker pair separation (A), maximum marker pair separation (B) and maximum marker pair distances (C). Data are mean ± SD. *p <0.05 versus baseline, A, B, C, D, E = p <0.05 versus marker pair A₁/A₂, B₁/B₂, C₁/C₂, D₁/D₂ or E₁/E₂, respectively.

Figure 5

Plotted positions of mitral annular saddle horn (#22) and mid-lateral (#18) marker as well as anterior (A₁-E₁) and posterior (A₂-E₂) mitral leaflet edge markers from anterior commissure (A₁/A₂) to the posterior commissure (E₁-E2). Markers are plotted at end-systole (circles) and 102 ms after end-systole (triangles) under baseline conditions (closed symbols) and during acute ischemia (open symbols) in the X-Y plane. Details of the reference coordinate system are provided in Materials and methods. All data are mean ± SEM.

Figure 6

Plotted positions of mitral annular saddle horn (#22) and mid-lateral (#18) marker as well as anterior (A₁-E₁) and posterior (A₂-E₂) mitral leaflet edge markers from anterior commissure (A₁/A₂) to posterior commissure (E₁-E₂). Markers are plotted at end-systole (circles) and 102 ms after end-systole (triangles) under baseline conditions (closed symbols) and during acute ischemia (open symbols) in the X-Z plane. Details of the reference coordinate system are provided in Materials and methods. All data are mean ± SEM.