Electromechanical coupling between the atria and mitral valve

Abstract

(AL) stiffening during isovolumic contraction (IVC) may aid mitral valve closure. We tested the hypothesis that AL stiffening requires atrial depolarization. Ten sheep had radioopaque-marker arrays implanted in the left ventricle, mitral annulus, AL, and papillary muscle tips. Four-dimensional marker coordinates (x, y, z, and t) were obtained from biplane videofluoroscopy at baseline (control, CTRL) and during basal interventricular-septal pacing (no atrial contraction, NAC; 110 -117 beats/min) to generate ventricular depolarization not preceded by atrial depolarization. Circumferential and radial stiffness values, reflecting force generation in three leaflet regions (annular, belly, and free-edge), were obtained from finite-element analysis of AL displacements in response to transleaflet pressure changes during both IVC and isovolumic relaxation (IVR). In CTRL, IVC circumferential and radial stiffness was 46 Ϯ 6% greater than IVR stiffness in all regions (P Ͻ 0.001). In NAC, AL annular IVC stiffness decreased by 25% (P ϭ 0.004) in the circumferential and 31% (P ϭ 0.005) in the radial directions relative to CTRL, without affecting edge stiffness. Thus AL annular stiffening during IVC was abolished when atrial depolarization did not precede ventricular systole, in support of the hypothesis. The likely mechanism underlying AL annular stiffening during IVC is contraction of cardiac muscle that extends into the leaflet and requires atrial excitation. The AL edge has no cardiac muscle, and thus IVC AL edge stiffness was not affected by loss of atrial depolarization. These findings suggest one reason why heart block, atrial dysrhythmias, or ventricular pacing may be accompanied by mitral regurgitation or may worsen regurgitation when already present. markers; stiffness MITRAL VALVE CLOSURE MAY BE aided by a brief contraction of myocytes in the annular third of the anterior leaflet (AL) (15). This contraction is also believed to be the cellular basis for the substantial AL stiffening observed during isovolumic contraction (IVC) (5). Such stiffening, observed primarily as a stiffening transient in the annular third of the AL (8), subsides by isovolumic relaxation (IVR) (9). Thus the AL stiffens at the onset of each beat then relaxes back to IVR stiffness values as left ventricular (LV) ejection proceeds.Electrophysiological studies have shown that the AL is in electrical continuity with the left atrium (LA) (4,16,17) and likely depolarizes with each beat as a consequence of left atrial depolarization (3). Without a properly timed sequence of atrial and ventricular excitation (such as with heart block, arrhythmias, or LV pacing), AL stiffening may be perturbed, potentially resulting in abnormal valve function. Thus the present study tested the hypothesis that AL IVC stiffening is abolished when atrial depolarization does not precede ventricular systole in the beating ovine heart. Although a new cohort of animals was used in this experiment, the methodology used has been previously described (6, 8) and thus will only be b...

Mitral Valve Mechanics

“…Further analysis by Swanson et al 11 of these CTRL and NAC data during the four time intervals defined in Figure 29.7 showed that total leaflet stiffness (Figure 29.9, red bars) is the sum of the leaflet early systolic stiffening twitch and a constant, steady-state baseline leaflet "tone" (Figure 29.9, blue bars) throughout systole. If total leaflet stiffness is the sum of leaflet twitch plus leaflet tone, the question arises "do leaflet twitch and tone arise from a single mechanism with multiple responses, or multiple mechanisms with independent responses?"…”

“…In order to test this postulate, Swanson et al 11 utilized highseptal left ventricular pacing to create ventricular beats that were not preceded by atrial depolarization. Figure 29.8 from this study (control run datasets provided in Appendix A) demonstrates that the leaflet stiffening twitch requires atrial excitation.…”

“…We interpret this positional stability as reflecting the importance of all chordae in guiding the exact positions of all portions of the leaflet at the moment of closure, with subsequent rigidity attributable to additional aspects of valve geometry and mechanics discussed in Chapters 9, 10, 11, 13, 22, 29, and 41. 3,5), P2 edge (#5, 6,8,9,11), P3 edge (#11, 12,14), and anterior leaflet edge (#2, 1,4,7,10,13,14) 3,5), P2 edge (#5, 6,8,9,11), P3 edge (#11, 12,14), and anterior leaflet edge (#2, 1,4,7,10,13,14) 3,5), P2 edge (#5, 6,8,9,11), P3 edge (#11, 12,14), and anterior leaflet edge (#2, 1,4,7,10,13,14) 3,5), P2 edge (#5, 6,8,9,11), P3 edge (#11, 12,14), and anterior leaflet edge (#2, 1,…”

“…In support of this notion, direct measurements by Nielsen et al 8 have shown that leaflet edge chords exhibit a maximum tension of about 0.3N, even less than the strut chords maximum tension of about 0.7N, both being very small forces. Also in support of this notion, Guo et al 9 found ) that this force is applied to the mitral annulus throughout systole primarily to contribute to LV ejection, a proposal that finds support in both basic studies 10 and the finding, originally by Lillehei et al 11 but validated many times since, that clinical outcomes are improved by chordal preservation during mitral valve replacement. The importance of this 12N (2x6N) papillary muscle force measured by Askov et al 3 can be put into perspective.…”

“…We have been studying the 4-D dynamics of the heart using biplane radiography of surgically implanted radiopaque markers for the past forty years, 1 with emphasis on the mitral and aortic valves during the past 20 years, [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16] and dense leaflet and annular marker arrays during the past several years. [17][18][19][20][21][22][23][24][25][26][27] Data from the control runs in these studies comprise the substrate for this book.…”