Dynamics of normal and diseased cardiac valves

Dynamics

of normal

and diseased

cardiac

valves

Elias Amador, M.D.* Wendell B. Thrower, M.D. &stave J. Dammin, M.D. Boston, Nass.

N

ormal cardiac valves offer minimal resistance to the forward flow of blood, and establish a unidirectional circulation by effectively preventing the backflow of ejected blood. When diseased, these valves may prevent complete emptying of the cardiac chambers or may permit reflux of ejected blood, thereby producing progressive cardiac dilatation with serious impairment of myocardial function. Postmortem observations, by disclosing pathologic valve structures, have played a basic role in the development and evaluation of heart surgery.’ The value of these observations has been increased by McMillan,2 who, in order to better correlate structure with function, designed the technique of cardiac pulse duplication for the study of normal and diseased valves. In the present communication, observations made with the technique of cardiac pulse duplication are correlated with previous work to explicate the structural factors essential for normal function of the cardiac valves, as well as the manner in which they are altered by disease. Previous reports have dealt with particular aspects of valve physiology or pathology, blit have not integrated the known facts into a single presentation. It is necessary to present these data in an integrated form since the clinical, radiologic, and From

hemodynamic manifestations of valvular disease are the direct result of the anatomic defect(s). Moreover, and most importantly, the type of anatomic lesion determines the corrective procedure to be employed. Hence, an understanding of the structure and function of normal and diseased cardiac valves is crucial in the selection of patients for cardiac surgery and in planning the therapeutic approach best suited for each patient. Historical

Late in the fifteenth century, Leonardo da Vinci studied the function of the aortic valve in beef hearts perfused with water.3 He observed that this valve has a triangular orifice during systole, and he assumed that the sinuses of Valsalva are held partially open by eddies of fluid. In 1669, Richard Lower described the function of atrioventricular valves in animal hearts, and concluded that valve motion was passive.4 Senac, in 1749, studied the motion of the atrioventricular valves in living animals by transatrial palpation.5 In 1848, Parchappe’j noted that contraction of the papillary muscles exerts tension on the chordae tendineae and prevents eversion of the leaflets. See? observed that during systole the septal leaflet of the mitral valve occludes most of the valve orifice. LianX

the Departments of Pathology and Surgery. Harvard Mass. This study was supported by Grant 248 from the Greater Received for publication Feb. 14, 1963. *Address: Peter Bent Brigham Hospital, 721 Huntington

777

review

Medical Lynn Ave.,

School Chapter

Boston

and

Peter

Bent

of the Massachusetts 15, Mass.

Brigham Heart

Hospital, Association,

Boston.

778

Amador,

Thrower,

Am. Heart f. December, 1963

and Dammin

observed that the sphincteric contraction of the ventricular myocardium furthers closure of the atrioventricular valves, an observation confirmed by Smith and coworkers in beating dog hearts.g Kantrowitz1° bypassed the left chambers of beating dog hearts and noted that, when the left ventricle is empty, the sphincteric action of the myocardium about the mitral annulus does not suffice to close this valve. Fluid-tight closure occurs only when fluid within the ventricle pushes up the leaflets and snaps them shut. Kantrowitz also found that during diastole the mitral leaflets are pulled open by the relaxing ventricle.*O With the cardiac pulse duplicator, McMillanl obtained cinematographic records of functioning cardiac valves, and for the first time was able to evaluate objectively the results of surgical correction of aortic stenosis.” He noted that attempted correction of aortic stenosis with a mechanical dilator produced torn and maximal restoration regurgitant valves; of valve function was obtained when the fused commissures were divided with a knife under direct vision. In the cardiac pulse duplicator designed by Davila and co-workers,12 water is drawn into the ventricle from the atrium, and expelled through the aorta by a piston pump connected to the ventricular apex. The forcible descent of the piston tends to snap open the mitral valve, and its ascent produces a paradoxical systolic expansion of the ventricle, but otherwise does not appear to affect significantly simulated valve function. The Davila cardiac pulse duplicator has been ingeniously modified by Hargett and Everest,13 who applied external cyclic pressure to the heart by surrounding it with a water jacket connected to a piston pump. With this external cardiac pulse duplicator, Frater14 has studied in detail the anatomy and function of the canine mitral valve. The McMillan cardiac pulse duplicator was modified by us in 1957, to permit the simultaneous study of the aortic and mitral valves; this modification was adopted by Kelley and co-workers,15 who determined forward and backward pressure gradients across stenotic aortic valves before and after surgical correction. Cardiac pulse

duplicators have been used extensively in the development and evaluation of prosthetic valves for cardiac surgery.“j In preliminary studies, cinefluorography coupled with angiocardiography has disclosed in detail the structure and function of cardiac valves in the living human being.17t18 Future developments of this technique would appear to require, as a standard of reference, correlated anatomic and physiologic studies of the type presented here. Materials

and methods

Fifty-two human hearts, obtained at autopsy, were perfused by means of a McMillan cardiac pulse duplicator2 modified to permit the simultaneous study of the mitral and aortic valves (Fig. 1). With it, fluid under pressure enters the left ventricle during simulated systole, closes the mitral valve, and leaves through the open aortic valve. During simulated diastole, fluid rapidly leaves the ventricle, opens the mitral valve, and snaps the aortic valve closed. The flow of fluid, delivered to the heart by a centrifugal pump, is controlled and “diastolic” solenoid by ‘Lsystolic” valves. The aortic outflow is provided with an air chamber to simulate arterial elasticity, and with a valve to control peripheral resistance and flow. Left atria1 filling and pressure are maintained by an independent reservoir placed above the atrium. The two solenoid valves are regulated by an electronic device which also controls heart rate and length of systole. Hearts were prepared by dividing the aorta 4.0 cm. above the aortic valve, and the other great vessels flush with the heart. The visceral pericardium was carefully perserved since it gives substantial mechanical support to the myocardium. Both coronary arteries were ligated to prevent leakage. The orifices of the pulmonary veins were joined by an incision, clots were washed out, and the atrium and mitral valve were inspected and palpated. A viewing chamber, placed immediately above the mitral annulus, was attached to the atrium with a lung tourniquet. A second viewing chamber was attached to the aorta with silk ligatures. An orifice made in the ventricular apex was cannulated with a flanged glass tube. Aortic outflow was

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Dynamics

of normal and diseased cardiac valves

779

E

Fig. 1. Modified McMillan cardiac pulse duplicator: A, water reservoir; B, centrifugal pump; C, systolic solenoid valve; D, inflow control valve, E, bubble trap; F, plastic viewing chamber for mitral valve, G, left auricle; H, left ventricle; I, plastic viewing chamber for aortic valve; J, closed chamber to simulate arterial elasticity; K, peripheral resistance control valve; L, open reservoir diastolic

to convert pulsatile flow solenoid valve; 0, diastolic

measured with a rotameter. Colored cinematographic records were obtained with a 16-mm. reflex camera operated at a shutter speed of 24 frames per second. Results Normal atrioventriculur valves. In 6 normal hearts the mitral and tricuspid valves opened and closed rapidly and completely during each cycle (Figs. 2 and 3). At the onset of systole the sharp rise in intraventricular pressure lifted the valve leaflets, brought their free edges together, and tightly sealed the inner third of their surfaces against each other. The chordae tendineae prevented the leaflets from everting into the atrium. In the mitral valve, the septal leaflet occluded most of the valve orifice, and was complemented by the mural leaflet and by the small anterior and posterior commissural leaflets (Fig. 2). In the tricuspid valve, the anterior leaflet occluded most of the valve orifice, and was

into continuous outflow control

flow; valve;

M,

flowmeter;

N,

P, manometers.

complemented by the posterior and septal leaflets and by one or two small commissural leaflets (Fig. 3). During diastole, fluid pressure within the atrium caused a wide separation of the leaflets. Free commissures and thin, supple chordae tendineae were essential for rapid and complete valvular opening. Diseased atrioventriculur valves. In 10 cases of rheumatic mitral stenosis,valvular opening was impaired by one or a combination of three lesions (Fig. 4). The first lesion was fusion of the leaflets with obliteration of the commissures and commissural leaflets, which, when extensive, greatly reduced the diastolic valvular orifice. The second lesion consisted of fibrosis and calcification of the leaflets, which transformed them into rigid shelves that occluded the mitral orifice. In the third lesion the chordae tendineae and papillary muscles were replaced by fibrous tissue, which transformed them into rigid pillars

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Amador, Thrower!

Am. Heart 1. December, 1963

and Dammin

Fig. 2. Cycle of a normal mitral valve. In systole the large septnl edges mold against each other, and the supple chordae tendineae patent commissures permit complete diastolic opening.

Fig. 3. Cycle of normal tricuspid valve. High perfusion mild insufficiency; this also occurs when the right heart

Fig. 4. “Fish creased.

mouth”

mitral

stenosis

after

valvuloplnsty;

Fig. 5. Mitral insufficiency produced by retraction the valve cannot close during systole.

leaflet occludes prevent leaflet

most of the orifice, the leaflet eversion. Flexible leaflets and

pressures have dilated the tricuspid ring and dilates secondarily to aortic or mitral disease.

opening

of the septal

is fully

leaflet

and

adequate

shortening

and insufficiency

of the chordae

produced

is not

tendineae;

in-

I’oltrme Nrrmber

66 6

Dynamics

that immobilized the leaflets. These fibrous pillars often narrowed the valvular channel and produced a second point of stenosis1 below the valve. When the fused chordae tendineae were separated, there was noticeable improvement in leaflet mobility. The effectiveness of mitral valvuloplasty in the treatment of mitral stenosis was evaluated in these hearts (Fig. 4). Complete separation of the commissures and freeing of the chordae tendineae often increased the diastolic mitral orifice up to

Fig.

6. Normal

aortic

Fig. 7. Bicuspid aortic competknt closure.

Fig.

8. The

same valve

valve

valve

after

cycle.

Each

resulting

splitting

cusp

from

is cup-shaped

fusion

of the fused

of normal and diseased cardiac valves

781

2.5 square centimeters, when estimated visually. Digital estimates of the same orifices were usually about twice as great. In 8 hearts, mitral insuiqiciency resulted from marked fibrous retraction of the valve leaflets. The effect on the septal leaflet was most significant (Fig. 5). These rigid and retracted leaflets closed slowly and could not seal off the atrioventricular orifice, thus permitting regurgitation during systole. Fibrous shortening of the chordae tendineae anchored the leaflets

and very

of one commissure;

commissures,

flexible;

the systolic

the flexible

. systolic

opening

orifice

is triangular.

free cusp permits

is visibly

improved.

opening

and

782

Amador,

Thrower,

Fig. 9. Calcific fused together,

aortic stenosis and insufficiency; the cusps and the commissures are obliterated.

in a semiopen position which produced marked mitral insufficiency. Rupture of two or more chordae tendineae, observed in 2 cases, produced marked mitral regurgitation by permitting systolic eversion of a leaflet into the atrium. In 3 hearts with severe mitral or aortic valvular disease there was dilatation of the tricuspid ring which impeded complete closure of the valves, and permitted regurgitation even though the valves were otherwise normal (Fig. 3). Normal semilunar valves. In 5 normal hearts the pulmonic and aortic valves opened when intraventricular pressure exceeded arterial pressure. During systole the valve cusps separated completely from each other, the sinuses of Valsalva remained partially open, and the normal valve orifice

Fig. 10. Rheumatic aortic traction of the cusps makes ble.

Am. Heart I. 1963 Dcccmber,

and Dammin

insufficiency; fibrous rediastolic closure impossi-

are retracted

and

was triangular (Fig. 6). At the end of systole, intraventricular pressure fell suddenly, and the cusps were snapped closed by the arterial pressure. All three semilunar cusps were essential for complete valve closure; small defects in any one of them allowed large volumes of fluid under high pressure to regurgitate into the ventricle. Flexibility of the free edges of the cusps allowed them to bend sharply at the center, thus sealing the center of the valve orifice (Fig. 6). The normal cup-shape of each cusp results from the high point of attachment of its free edge to the arterial wall. This point of attachment converts the free edge of the cusp into a suspension band for the valve cusp and permits it to support high pressures. When the point of attachment was cut, the cusp prolapsed into the ventricle, which resulted in marked insufficiency. Diseased aortic valves. In 7 hearts with aortic stenosis the principal lesion was fusion of the commissures, which varied in type and degree. Slight functional impairment resulted from fusion of the outer third of the commissures. Complete fusion of only one commissure produced a bicuspid valve, but only a moderate amount of stenosis resulted if the remaining cusp was flexible (Figs. 7 and 8). When two of the commissures were fused, the systolic blood was ejected through the remaining open commissure; the resulting stenosis varied in severity with the degree of flexibility of the cusp margins which formed this open commissure. When all three commissures were fused, the valve orifice was central and rigid, and concomitant insufficiency was

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Dynamics of normal and diseased cardiac valves

always present (Fig. 9) ; under such circumstances, marked calcification of the valve was the rule. In 6 additional hearts, large fibrocalcific deposits were present in all the sinuses of Valsalva, but the commissures and cusps were intact; the resulting stenosis was proportional to the size of these deposits. Careful debridement of these deposits produced remarkable improvement in valve function. In 6 hearts with rheumatic aortic insuficiency the most frequent lesion was fibrosis with retraction of the free cusp edges, which kept them from closing completely (Fig. 10). Retraction of even one valve cusp produced aortic insufficiency of 0.5 square centimeter or greater. Dilatation of the aortic annulus with separation of the commissures and sagging of the cusps was observed in hearts with rheumatic aortic insufficiency, and in 2 hearts with syphilis; unequal sagging of the cusps and slow diastolic closure due to fibrosis furthered the insufficiency. Direct surgical relief of aortic insufficiency was evaluated under direct vision. Circumclusion of the aortic annulus with a constricting silk band’ did not reduce the area of insufficiency. Plastic and silk stents of variable size and shape were placed in the insufficient orifice to provide a substitute for deficient valve substance; however, the stents always migrated to the periphery of the valve orifice without relieving the insufficiency. Prosthetic plastic valves with three cusps (designed by Dr. Vannevar Bush) functioned satisfactorily

Fig. Il. Aortic closure are fully

plastic valve adequate.

designed

783

when placed in the aortic annulus of several hearts (Fig. ll), as did ball valves of the caged ball type.16 Discussion

In the living organism, the blood propelled by myocardial contraction transmits to the cardiac valves the energy that opens and closes them. Contraction of the myocardium surrounding the mitral and tricuspid annuli also plays an important role in the systolic closure of these valves. Closure of the atrioventricular valves is completed when the leaflets are brought together by the protosystolic rise in intraventricular pressure, and is enhanced when the chordae tendineae are approximated by the contraction of the ventricles.rg Sphincteric contraction of the valvular annulus appears to be necessary for complete closure of the tricuspid valve, but is not essential for competent closure of the normal mitral valve. Flexible and sufficient leaflet substance and intact commissures are indispensable for normal function of the atrioventricular valves, as shown here and elsewhere.20 In mitral stenosis, visual evaluation of finger-fracture valvuloplasty’ confirmed that this procedure relieved the stenosis and rarely produced insufficiency when properly performed. Direct visual measurements indicated that after mitral valvuloplasty the valve orifice had been uniformly enlarged to greater than the functionally critical area of 1.5 square centimeters.21 Tricuspid insufficiency secondary to dila-

by

Dr.

Vannevar

Bush;

opening

and

784

Amador,

Thrower,

and Dammin

tation of the annulus was observed in 3 hearts with aortic or mitral vaivular disease and right ventricular dilatation. In 7 of 11 such hearts studied by Goodale and Shaw,22 dilatation of the triscupid annulus produced insufficiency in otherwise normal tricuspid valves. Retraction of the leaflets and shortening of the chordae tendineae were the major lesions which produced mitral insufficiency in the hearts studied here. Marked dilatation of the mitral annulus, and posterior herniation of this annulus with retraction of the mural leaflet away from the septal leaflet are aggravating lesionss3 Ensuing left ventricular dilatation pulls the chordae tendineae and leaflets into the ventricle, thus further increasing the insufficiency. Aortic stenosis was produced by fusion of the cusps at their commissures, and was proportional to the extent of fusion and to the degree of scarring of the cusps; stenosis produced by calcific deposits within the sinuses of Valsalva was less frequently observed. Loss of cusp sub: stance secondary to fibrous retraction, or to bacterial destruction, was the basic lesion in aortic insufficiency. Visual evaluation of corrective procedures for lesions of the aortic valve indicated that cusp substance must be carefully preserved, since even small areas of incompetence permit large volumes oi blood to regurgitate into the ventricle during diastole. 24Careful splitting of the fused commissures in calcific aortic stenosis, together with debridement of calcific masses, permitted the mobilized cusps to abut against each other without increasing any associated insufficiency. In aortic insufficiency, restoration of valve function appears to be feasible through the use of prosthetic ball vaIves.16 Summary

The function of normal and diseased cardiac valves was studied with a modified McMiIIan cardiac pulse duplicator. Opening of normal mitral and tricuspid valves depends on flexible valve leaflets and intact commissures; closure depends on sufficient leaflet substance to occlude the valve orifice, flexibility of the leaflet edges to permit fluid-tight seal, and intact chordae tendineae to prevent leaflet eversion.

Dcrmbcr, 1963 Am. Heart J.

Competent closure of the tricuspid valve necessitates contraction of the myocardium surrounding the valve annulus. In mitral stenosis, fibrous thickening and retraction of the leaflets, and fusion of the commissures are the basic lesions; they vary from tnild to moderate commissural fusion in some hearts to severe commissural fusion with thick, inflexible, and calcified leaflets in others. Associated fusion, shortening, and rigidity of the chordae tendineae further reduce leaflet mobility. Mitral valvuloplasty may significantly increase the area of the valve orifice, without significantly increasing any insufficiency already present. Opening of the semilunar valves depends on flexible cusps and intact commissures. Adequate closure depends on sufficient cusp substance, and on the cup-shape of the cusps which permits them to support high pressures without prolapsing. Aortic stenosis results from commissural fusion and/or from calcific deposits within the sinuses of Valsalva. Either splitting of the commissures or removal of the calcific deposits corrected this type of stenosis without leading to insufficiency. Aortic stenosis and insufficiency result from fusion and retraction of the valve cusps, with obliteration of the commissures and of the sinusesof Valsalva. Careful splitting of the residual commissures permitted the cusps to abut during diastole, and insufficiency was not increased. Aortic insufficiency commonly results from loss of cusp substance, aggravated by sagging of the cusps and by dilatation of the aortic ring. The use of aortic prosthetic valves appears to be the most promising tnethod for correction of this lesion. It is a pleasure to thank Dr. Jorge Benavides and Dr. Jorge Alberta1 for their generous collaboration; Dr. Harold D. Levine, Dr. Howard K. Thompson, Jr., Dr. Richard Gorlin and Dr. Warren E. C. Wacker for reviewing the manuscript; and Mr. I. K. R. McMillan, Dr. Stanley J. Sarnoff, and Dr. Dwight E. Harken for allowing us to use the cardiac pulse duplicator. Mr. John Rahilly lent valuable technical assistance. REFERENCES 1. klarken, D. E., and Black, H.: Improved valvuloplasty for mitral stenosis, with a discussion of multivalvular heart disease, New England J. Med. 253:669, 1955. 2. McMillan, I. K. R., Daley, R., and Matthews,

Dynamics

M. B.: The movement of aortic and pulmonary valves studied postmortem by colour cinematography, Brit. Heart J. 14:42, 1952. 3. Keele, K. D.: Leonardo da Vinci on the movement of the heart and blood, London, 1954, Harvey and Blythe, Ltd. 4. Lower, R.: Tractatus de Corde, Translated by K. J., Franklin, Oxford, 1932, Oxford University Press. 5.

Senac, J. D.: Paris, 1749.

Trait6

de la structure

J.

Biol.

Photogr.

Assoc.

tion

18.

19.

20. 21.

22. 23.

25:169,

14. Frater, R. W. M.: Mitral valve anatomy and prosthetic valve design, Proc. Staff Meet. Mayo Clin. 36:582, 1961.

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15. Kelley, R. R., Scannell, J. G., Shaw, R. S., Burke, J. F., Austen, W. G., and Villegas, A. H.: Aortic valvuloplasty under direct vision, New England J, Med. 262:492, 1960. 16. Harken, D. E., Taylor, W. J., Lefemine, A. A., Gupta, S. K., and Lunzer, S.: Partial and complete prosthesis in aortic insufficiency, J. Thoracic Surg. 40:744, 1960. 17. Sloman, G.: Cineaortography for the visualiza-

du coeur,

6. Parchappe, J. B. M.: Du coeur, de sa structure et de ses mouvements, Paris, 1848. 7. See, M.: Recherches sur l’anatomie et al physiologie du coeur, Paris, 1883, G. Masson. 8. Lian, C.: Contribution Q I’&ude de la physiologie de l’appareil valvulaire mitrale, J. physiol. 11597, 1909. 9. Smith, H. L., Essex, H. E., and Baldes, E. J.: A study of the movements of heart valves and heart sounds, Ann. Int. Med. 33:1357, 1950. 10. Kantrowitz, A., Hurwitt, E. S., and Hershovitz, A.: A cinematographic study of the function of the mitral valve in situ, Surg. Forum 2:204, 1951. 11. McMillan, I. K. R.: Aortic stenosis. A postmortem cinephotographic study of valve action, Brit. Heart J. 17:56, 1955. 12. Davila, J. C., Trout, R. G., Sumner, J. E., and Glover, R. P.: A simple mechanical pulse duplicator for cinematography of cardiac valves in action, Ann. Surg. 143:544, 1956. 13. Harpett. ., , G. K.. and Everest. F. A.: Photocraphy of heart valves with the cardiac pulse duplicator, 1957.

of normal and diseased cardiac valves

24.

of the aortic

valve

and

coronary

arteries,

Proc. Roy. Sot. Med. 52:460, 1959. Rafterv. E. B.. Humohries. A.. O’Neal. I.. Criley, J. M., and Ross, R. S.: Cineangiographic study of the diseased aortic valve. Abstracts of the 4th World Congress of Cardiology, Mexico City, 1962, p. 285. Harken, D. E., Dexter, L., Ellis, L. B., Farrand, R. E., and Dickson, J. F.: The surgery of mitral stenosis. III. Finger-fracture valvuloplasty, Ann. Surg. 134:722, 1951. Merendino, K. A., editor: Prosthetic valves for cardiac surgery, Springfield, Ill., 1960, Charles C Thomas, Publisher. Gorlin, R., and Gorlin, S. G.: Hydraulic formula for calculation of the area of the stenotic mitral valve, other cardiac valves and central circulatory shunts. I, AM. HEART J. 41:1, 1951. Goodale. F.. and Shaw. R. S.: Functional examination df the heart a; autopsy, New England J. Med. 253:719, 1955. Harken, D. E.: The surgical treatment of mitral insufficiency, In Lam, C. R., editor; International Symposium on Cardiovascular Surgery, Philadelphia, 1955, W. B. Saunders Company, p. 212. Gorlin, R., McMillan, I. K. R., Medd, W. E., Matthews, M. B., and Daley, R.: Dynamics of the circulation in aortic valvular disease, Am. J. Med. 18:855. 1955. <

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