Is the mitral valve passive flap theory overstated? An active valve is hypothesized.
The concept that the mitral valve of the heart is a passive flap that opens and closes like a barn door has been emphasized for decades by medical and biology professors to their students. But experimental findings, which are outlined in this report, support the theory of an active valve. We hypothesize that the two leaflets of the mitral valve are actively contractile; that physical forces generated in the valve itself may stabilize and add precision to the sum of forces that regulate valve movement. This precision could be of critical significance both in the moments preceding, and during, valve opening and closing. Evidence supporting our active valve hypothesis includes the profuse innervation of motor and sensory nerves that are present in the mitral valves of all animals studied. In addition, multiple contractile cell types have been found in the mitral valve, including cardiac muscle cells, smooth muscle cells, and cardiac valvular interstitial cells. In vitro work in our laboratories using the rat mitral valve shows that not only are the valves capable of contraction and relaxation, but that the contractions and relaxations are nerve-mediated. We theorize that the rich innervation and contractile cells in the mitral valve work together to modulate fine-tuning of valve movements and tone, thereby ensuring the integrity of the valve seal. Other investigators have reported that the mitral valve demonstrates contractile activity and that denervation localized to the mitral valve affects valve competence. The evidence for an active mitral valve presented by these and other experimental studies warrant a reexamination of the validity of the passive valve concept. An accurate and full understanding of the precise movements of the valve leaflets and the mechanisms that regulate these movements is likely to provide the information needed to understand and develop treatments for many different cardiac valve problems, including mitral valve diseases such as prolapse and myxomatous degeneration. In view of the available experimental evidence, the concept that the mitral valve functions only as a passive structure is challenged by numerous anomalies. A reinterpretation of the concept of valve function that incorporates active as well as passive roles for the valve leaflets and other components of the valve apparatus would have significant implications both for the directions taken in research involving the cardiac valves and for the approaches to treatment.
Williams
T H
TH
Department of Anatomy and Cell Biology, University of Iowa, 1-449 Bowen Science Building, Iowa City, IA 52242, USA. williamsthwillia@msn.com
Jew
J Y
JY
D000818:Animals; D015415:Biomarkers; D015740:Calcitonin Gene-Related Peptide / Q000378:metabolism; D006325:Heart Atria; D006352:Heart Ventricles; D006801:Humans; D007150:Immunohistochemistry; D018613:Microscopy, Confocal; D008943:Mitral Valve / Q000737:chemistry / Q000166:cytology / Q000201:enzymology / Q000294:innervation / Q000502:physiology*; D009046:Motor Neurons / Q000166:cytology; D009119:Muscle Contraction; D009126:Muscle Relaxation; D009129:Muscle Tonus; D009130:Muscle, Smooth / Q000166:cytology / Q000502:physiology; D032383:Myocytes, Cardiac / Q000166:cytology / Q000502:physiology; D009475:Neurons, Afferent / Q000166:cytology; D009478:Neuropeptide Y / Q000378:metabolism; D009638:Norepinephrine / Q000378:metabolism; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
D015415:Biomarkers; D009478:Neuropeptide Y; D014446:Tyrosine 3-Monooxygenase; D015740:Calcitonin Gene-Related Peptide; D009638:Norepinephrine