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Ann Thorac Surg 2004;77:857-858
© 2004 The Society of Thoracic Surgeons


Original articles: cardiovascular

Invited commentary

Tomasz A. Timek, MD

Department of Cardiothoracic Surgery, Stanford University, CVRB Building, 2nd Floor, 300 Pasteur Dr, Stanford, CA 94305, USA

D. Craig Miller, MD

Department of Cardiothoracic Surgery, Falk Cardiovascular Research Center, Stanford University School of Medicine, Stanford, CA 94305-5247, USA

e-mail: kotek1{at}stanford.edu
e-mail: dem{at}stanford.edu

The mitral annulus is a discontinuous fibromuscular ring circumscribing the valve orifice, which has a poorly defined anatomical boundary and incompletely understood physiology. Since the pioneering canine experiments of Tsakiris et al in the 1960's, the sphincteric action of the mitral annulus has been thought to have important effects on valve performance by aiding both mitral valve closure and ventricular filling by virtue of its dynamic area change during the cardiac cycle. The current ovine data reported by Gorman and colleagues further elucidate the sphincteric action of the mitral annulus and emphasize its dynamic physiology.

In this elegantly designed sheep experiment, these investigators showed that the inotropic state of the myocardium directly affects the size of the mitral orifice, an effect beyond that exerted by faster heart rate alone. These experimental findings have important clinical implications, especially since the reduction in mitral annular area was found to be greatest at end-diastole, ie during the end of mitral valve closure when minimal orifice size would facilitate subsequent leaflet coaptation during systole. As the authors suggest, inotropic stimulation may be a possible therapy for some patients with compromised left ventricular (LV) function and functional mitral regurgitation (FMR) or ischemic mitral regurgitation (IMR). This highlights the well-known clinical observation that the amount of FMR and IMR is less when inotropic drugs are administered, eg dobutamine stress echocardiography, due to the smaller end-diastolic LV volume (and presumably smaller end-diastolic mitral annular size) achieved.

The hypothesis the authors present, however, is predicated on the assumption that it is the ventricular myocardium which modulates the size of the mitral annulus during the cardiac cycle, yet some clinical and experimental data suggest a closer link exists between left atrial myocardial contractile state and mitral annular size change, especially in early diastole. Most mitral annular area reduction in sheep occurs prior to end-diastole and is dependent on the strength and timing of atrial contraction. Echocardiographic studies have also confirmed the presence of presystolic mitral annular area reduction in healthy human volunteers, suggesting an "atriogenic" mechanism of mitral annular reduction. Thus, atrial rather than ventricular inotropic state may be more important for mitral annular sphincter function, although both probably contribute.

Perhaps the most important message of this manuscript is the reconfirmation that the mitral annulus is a very dynamic structure with an approximate 22% orifice area reduction under maximum inotropic stimulation compared to baseline control conditions. These data also beg the question of the adequacy of currently available prosthetic annuloplasty rings in terms of preserving dynamic annular motion. Ring design should strive to preserve normal annular dynamics, optimize valve competency, and maximize repair durability; yet, experimental data suggest that neither complete, partial, semirigid, nor flexible annuloplasty rings are able to imitate Nature's design satisfactorily.

Doctor Gorman and his collaborators should be congratulated for this carefully-performed work which adds to our basic understanding of mitral valve dynamics, proposes a novel therapeutic alternative in patients with FMR or IMR, and also forces us to ponder the physiologic consequences of all surgical interventions which affect the mitral annulus.





This Article
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D. Craig Miller
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Right arrow Articles by Timek, T. A.
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Right arrow Cardiac - physiology


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