Ablation of mitral annular and leaflet muscle: effects on annular and leaflet dynamics

Timek, Tomasz A.; Lai, David; Dagum, Paul; Tibayan, Frederick A.; Daughters, George T.; Liang, David; Berry, Gerald J.; Miller, D. Craig; Ingels, Neil B.

doi:10.1152/ajpheart.00179.2003

Cited by 24 publications

(23 citation statements)

References 19 publications

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“…A key prediction of this hypothesis is that excitation can vary leaflet stiffness in the closed valve. 2) Leaflet excitation develops a brief twitch contraction to aid valve closure (7,32,33,41). A key prediction of this hypothesis is that leaflet stiffness is transiently increased during valve closure.…”

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confidence: 99%

Active stiffening of mitral valve leaflets in the beating heart

Itoh

Krishnamurthy²,

Swanson³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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The anterior leaflet of the mitral valve (MV), viewed traditionally as a passive membrane, is shown to be a highly active structure in the beating heart. Two types of leaflet contractile activity are demonstrated: 1) a brief twitch at the beginning of each beat (reflecting contraction of myocytes in the leaflet in communication with and excited by left atrial muscle) that is relaxed by midsystole and whose contractile activity is eliminated with β-receptor blockade and 2) sustained tone during isovolumic relaxation, insensitive to β-blockade, but doubled by stimulation of the neurally rich region of aortic-mitral continuity. These findings raise the possibility that these leaflets are neurally controlled tissues, with potentially adaptive capabilities to meet the changing physiological demands on the heart. They also provide a basis for a permanent paradigm shift from one viewing the leaflets as passive flaps to one viewing them as active tissues whose complex function and dysfunction must be taken into account when considering not only therapeutic approaches to MV disease, but even the definitions of MV disease itself.

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confidence: 99%

Active stiffening of mitral valve leaflets in the beating heart

Itoh

Krishnamurthy²,

Swanson³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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“…annular physiology; ventricular long-axis function; echocardiography; three dimension; four dimension THE MITRAL ANNULUS (MA) is a discontinuous fibrous ring and an essential component of the mitral valve/left atrial/left ventricular (LV) complex. It contributes to efficient valve closure as well as unimpeded LV filling (14,19,28,29). Many studies support the concept that the motion of the MA is dynamic throughout the cardiac cycle, yet the timing and extent of annular motion and shape variation remain incompletely understood (28,29).…”

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confidence: 99%

Contribution of mitral annular excursion and shape dynamics to total left ventricular volume change

Carlhäll

Wigström²,

Heiberg³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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The mitral annulus (MA) has a complex shape and motion, and its excursion has been correlated to left ventricular (LV) function. During the cardiac cycle the annulus' excursion encompasses a volume that is part of the total LV volume change during both filling and emptying. Our objective was to evaluate the contribution of MA excursion and shape variation to total LV volume change. Nine healthy subjects aged 56 Ϯ 11 (means Ϯ SD) years underwent transesophageal echocardiography (TEE). The MA was outlined in all time frames, and a four-dimensional (4-D) Fourier series was fitted to the MA coordinates (3-Dϩtime) and divided into segments. The annular excursion volume (AEV) was calculated based on the temporally integrated product of the segments' area and their incremental excursion. The 3-D LV volumes were calculated by tracing the endocardial border in six coaxial planes. The AEV (10 Ϯ 2 ml) represented 19 Ϯ 3% of the total LV stroke volume (52 Ϯ 12 ml). The AEV correlated strongly with LV stroke volume (r ϭ 0.73; P Ͻ 0.05). Peak MA area occurred during middiastole, and 91 Ϯ 7% of reduction in area from peak to minimum occurred before the onset of LV systole. The excursion of the MA accounts for an important portion of the total LV filling and emptying in humans. These data suggest an atriogenic influence on MA physiology and also a sphincter-like action of the MA that may facilitate ventricular filling and aid competent valve closure. This 4-D TEE method is the first to allow noninvasive measurement of AEV and may be used to investigate the impact of physiological and pathological conditions on this important aspect of LV performance. annular physiology; ventricular long-axis function; echocardiography; three dimension; four dimension THE MITRAL ANNULUS (MA) is a discontinuous fibrous ring and an essential component of the mitral valve/left atrial/left ventricular (LV) complex. It contributes to efficient valve closure as well as unimpeded LV filling (14,19,28,29). Many studies support the concept that the motion of the MA is dynamic throughout the cardiac cycle, yet the timing and extent of annular motion and shape variation remain incompletely understood (28,29). Assessment of the MA physiology has been important to the understanding of disorders of the mitral valve apparatus and LV dysfunction. The mechanisms of functional valve regurgitation in the setting of dilated cardiomyopathy and in the design of annuloplasty ring prostheses for valve repair (15,24,27) are two of many areas where MA physiology is a key issue.

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“…Finally, Timek et al (15) showed that ablation of leaflet myocytes in the annular region of the ovine anterior mitral leaflet slowed valve closure by some 35 ms relative to controls. This has been interpreted to suggest that the leaflet twitch may help close the valve, as suggested as a possibility by Curtis and Priola (3).…”

Section: Discussionmentioning

confidence: 99%

“…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).…”

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Electromechanical coupling between the atria and mitral valve

Swanson

Krishnamurthy

Kvitting

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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(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...

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Ablation of mitral annular and leaflet muscle: effects on annular and leaflet dynamics

Cited by 24 publications

References 19 publications

Active stiffening of mitral valve leaflets in the beating heart

Active stiffening of mitral valve leaflets in the beating heart

Contribution of mitral annular excursion and shape dynamics to total left ventricular volume change

Electromechanical coupling between the atria and mitral valve

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