Aorto-mitral annular dynamics

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Aorto-mitral annular dynamics Tomasz A. Timek, G. Randall Green, Frederick A. Tibayan, David T. Lai, Filiberto Rodriguez, David Liang, George T. Daughters, Neil B. Ingels, Jr and D. Craig Miller Ann Thorac Surg 2003;76:1944-1950

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The Annals of Thoracic Surgery is the official journal of The Society of Thoracic Surgeons and the Southern Thoracic Surgical Association. Copyright © 2003 by The Society of Thoracic Surgeons. Print ISSN: 0003-4975; eISSN: 1552-6259.

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Aorto-Mitral Annular Dynamics CARDIOVASCULAR

Tomasz A. Timek, MD, G. Randall Green, MD, Frederick A. Tibayan, MD, David T. Lai, FRACS, Filiberto Rodriguez, MD, David Liang, MD, PhD, George T. Daughters, MS, Neil B. Ingels, Jr, PhD, and D. Craig Miller, MD Department of Cardiothoracic Surgery, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, Department of Surgery, Loma Linda University Medical Center, Loma Linda, and Laboratory of Cardiovascular Physiology and Biophysics, Research Institute of the Palo Alto Medical Foundation, Palo Alto, California

Background. The aortic and mitral valves are coupled through fibrous aorto-mitral continuity, but their synchronous dynamic physiology has not been completely characterized. Methods. Seven sheep underwent implantation of five radiopaque markers on the left ventricle, 10 on the mitral annulus, and 3 on the aortic annulus. One of the mitral annulus markers was placed at the center of aorto-mitral continuity (mitral annulus “saddle horn”). Animals were studied with bi-plane videofluoroscopy 7 to 10 days postoperatively. Total circumference and lengths of mitral fibrous annulus, mitral muscular annulus, aortic fibrous annulus, and aortic muscular annulus were calculated throughout the cardiac cycle from three dimensional marker coordinates as was mitral annular area and aortic annular area. Aorto-mitral angle was determined as the angle between the centroid of the aortic annulus markers, the saddle horn, and the centroid of the mitral annulus markers. Aortic annulus and mitral annulus flexion was expressed as the difference between maxi-

mum and minimum values of the aortic and mitral annulus angles during the cardiac cycle. Results. Mitral and aortic annular areas changed in roughly a reciprocal fashion during late diastole and early systole with an overall 32 ⴞ 8% change in aortic annular area and a 13 ⴞ 13% change in mitral annular area. Aortic fibrous annulus changed much less than aortic muscular annulus (6 ⴞ 2% vs 18 ⴞ 4%; p ⴝ 0.0003) as did mitral fibrous annulus relative to mitral muscular annulus (4 ⴞ 1% vs 8 ⴞ 2%; p ⴝ 0.004). Aortic annulus and mitral annulus flexion was 8 ⴞ 2° and increased to 11 ⴞ 2° (p ⴝ 0.009) with inotropic stimulation. Conclusions. Dynamic aortic and mitral annular area changes were not mediated through the anatomic fibrous continuity. Aorto-mitral flexion, which increased with enhanced contractility, may facilitate left ventricle ejection. The effect of valvular surgical interventions on aorto-mitral flexion needs further investigation. (Ann Thorac Surg 2003;76:1944 –50) © 2003 by The Society of Thoracic Surgeons

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been utilized as an anchor to reduce mitral annular size and correct acute ischemic mitral regurgitation [12]. Recently, Lansac and colleagues [9] demonstrated complimentary synchronicity of aortic and mitral valve annular dynamics throughout the cardiac cycle mediated by aorto-mitral continuity, thus proposing functional significance of the anatomic link between the two valves and refuting the static physiology of the fibrous annulus of both valves. However, interpretation of these results was hampered, because aortic and mitral dynamics were studied in two separate groups of animals under different hemodynamic conditions. To date, simultaneous assessments of mitral and aortic annular motion in vivo has not been reported. Such knowledge may aid in the design of more physiologic valvular prostheses and development of reparative techniques that do not impede the function of either valve. With this goal in mind, we investigated simultaneous mitral and aortic annular dynamics using radiopaque marker technology in normal adult sheep.

he mitral and aortic valves share a common ventricular orifice and their proper function is integral in maintaining normal cardiac performance. Much has been learned about aortic [1–3] and mitral [4 – 6] dynamic valvular physiology, yet the valves have been studied in isolation, which essentially ignores their anatomic and physiologic relationships. Although the left ventricular outflow tract and the mitral annulus have been previously investigated in clinical [7] and experimental [8] studies, only recent attention has been drawn to the synchronous performance of the two valves [9]. As the valves are anatomically coupled through fibrous aortomitral continuity, a physiologic interdependence may intuitively be expected. This common region, corresponding to the mitral inter-trigonal distance, represents an important anatomical marker used for classification of congenital heart anomalies [10] and sizing of mitral annular prostheses [11]. The fibrous continuity has also Presented at the Poster Session of the Thirty-ninth Annual Meeting of The Society of Thoracic Surgeons, San Diego, CA, Jan 31–Feb 2, 2003. Address reprint requests to Dr Miller, Department of Cardiothoracic Surgery, Falk Cardiovascular Research Center, Stanford University School of Medicine, Stanford, CA 94305-5247; e-mail: [email protected] stanford.edu.

Material and Methods Surgical Preparation Seven healthy adult sheep were used (weight, 72 ⫾ 4 kg). This surgical preparation has been previously described

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Fig 1. Schematic representation of the mitral and aortic annular marker arrays used in the study. (AML ⫽ anterior mitral leaflet; L ⫽ left aortic cusp; LFT ⫽ left fibrous trigone; NC ⫽ noncoronary aortic cusp; PML ⫽ posterior mitral leaflet; R ⫽ right aortic cusp; RFT ⫽ right fibrous trigone.)

[5]. Briefly, the animals were pre-medicated with ketamine (25 mg/kg intramuscularly) and anesthesia induced with sodium thiopental (6.8 mg/kg intravenously), and were maintained with inhalational isofluorane (1% to 2.2%). Four tantalum radiopaque markers (inner diameter, 0.8 mm; outer diameter, 1.3 mm; length, 1.5 to 3.0 mm) were inserted through a left thoracotomy beneath the left ventricle (LV) epicardial surface along equally spaced longitudinal meridians with an additional marker being placed at the LV apex. After establishing cardiopulmonary bypass and with the heart arrested, 10 markers were sewn through a left atriotomy onto the mitral annulus. One marker was placed on the anterior and posterior mitral commissure, one on each fibrous trigone, and one at the center of the fibrous (annular saddle horn) and posterior annulus. One marker was placed between the mid-posterior annulus and each commissure, and one between each fibrous trigone and each commissure. The complete annular marker array is shown in Figure 1. Subsequently a transverse aortotomy was made 5 mm above the sinotubular ridge, and three markers were sutured at the nadir of the belly of each aortic cusp (left, right, and noncoronary) to define the aortic annulus. The left and noncoronary aortic annular markers corresponded closely to the left and right mitral fibrous trigone markers, respectively. After completion of marker placement, the atriotomy and aortotomy were closed and the cross clamp was removed. After resuscitation, the animal was weaned from bypass. A micromanometer pressure transducer (PA4.5-X6 [Konigsberg Instruments, Inc, Pasadena, CA] was placed in the LV chamber through the apex, and the apical marker was sutured in place.

After 8 ⫾ 1 days (mean, ⫾1 standard deviation) each sheep was taken to the experimental cardiac catheterization laboratory. Animals were sedated with ketamine (1 to 4 mg/kg/h intravenous infusion) and diazepam (5 mg intravenous bolus as needed), intubated, and mechanically ventilated (veterinary anesthesia ventilator 2000 [Halowell EMO, Pittsfield, MA]). Esmolol (20 to 50 ␮g/ kg/min) and atropine sulfate (0.01 mg/kg/min) intravenous infusions were utilized to minimize reflex sympathetic and parasympathetic responses. Simultaneous biplane videofluoroscopy and hemodynamic data recordings were initially acquired for all 7 animals under stable baseline conditions in normal sinus rhythm. Subsequently, data were obtained before and after (1) inotropic augmentation (calcium chloride 1 g intravenous bolus), (2) a 30% increase in systolic pressure with neosynephrine, and (3) a decrease in LV afterload with sodium nitroprusside. Because of technical difficulties the data during hemodynamic interventions were obtained in only 6 of 7 animals. A 5-minute stabilization interval was allowed between each data acquisition sequence. All animals received humane care in compliance with the “Principles of Laboratory Animal Care” formulated by the National Society for Medical Research and the “Guide for Care and Use of Laboratory Animals” prepared by the National Academy of Sciences and published by the National Institutes of Health (National Institutes of Health Publication 85-23, revised 1985). This study was approved by the Stanford Medical Center Laboratory Research Animal Review Committee and conducted according to Stanford University policy.

Data Acquisition and Analysis Data acquisition [5], digitization [13], and threedimensional reconstruction [14] was performed as previously described. Two to three consecutive steady state beats during baseline, and each of the three hemodynamic interventions were designated as baseline, calcium, neosynephrine, and nitroprusside data for each animal, respectively. End systole was defined as the frame containing peak negative LV rate of pressure fall (⫺dp/dt); end diastole was defined as the videofluoroscopic frame containing the peak of the electrocardiogram R-wave. Instantaneous LV volume was computed from the epicardial LV markers using a space-filling multiple tetrahedral volume method [15]. Mitral annular area was determined by first dividing the annulus into “pie slices” based on the annular centroid and the 10 annular markers, which were then summed to yield total annular area. Aortic annular area was derived in a similar triangular fashion using the three aortic annular markers. Total mitral annular perimeter was expressed as the sum of the 10 individual annular segment lengths with the fibrous mitral annulus represented by four segments spanning the distance between the fibrous trigones and the muscular annulus denoted by the remaining six segments. The fibrous portion of the aortic annulus was represented by the distance between the left and non-

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Experimental Protocol

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CARDIOVASCULAR Fig 2. Group mean mitral annular area (solid squares), aortic annular area (open squares), and left ventricular pressure (LVP solid line) throughout the cardiac cycle for 7 animals at baseline. A 650 ms time window centered at end diastole (ED) (dashed vertical line at t ⫽ 0) is illustrated for all variables. Error bars indicate one standard error of the mean. (LVP ⫽ left ventricular pressure.)

coronary aortic markers, and the sum of the remaining two segments was considered to be the muscular aortic annulus. Aorto-mitral annular flexion throughout the cardiac cycle was assessed by calculating the angle formed by the centroid of the aortic annular markers, the annular saddle horn marker, and the centroid of the mitral annular markers. Thus the “hinge” of the angle was placed at the center of aorto-mitral continuity, which constitutes the anatomic coupling junction between the two valves.

Statistical Analysis All data are reported as mean ⫾1 standard deviation unless otherwise stated. Hemodynamic and markerderived data from consecutive steady-state beats from each heart were time-aligned at end diastole. Marker data were calculated over 20 frames before and after end diastole, thus allowing evaluation over a time period of 650 ms. The mean and standard deviation for each variable at each sampling instant were computed during each condition. Data were compared using the Student’s t test for independent and dependent observations.

Results The average hemodynamics for all seven animals at baseline included a heart rate of 116 ⫾ 8 minute⫺1, LV dp/dt of 1,380 ⫾ 252 mmHg per second, peak LV pressure of 99 ⫾ 9 mmHg, end diastolic LV volume of 139 ⫾ 44 mL, and end diastolic LV pressure of 23 ⫾ 5 mmHg. Group mean mitral annular and aortic annular areas throughout the cardiac cycle are shown in Figure 2. Total annular circumference and length of the muscular and fibrous portion of the aortic and mitral annulus during the cardiac cycle are illustrated in Figure 3. Mitral annular

Fig 3. Group mean total annular circumference (top), fibrous annulus length (middle), and muscular annulus length (bottom) for mitral annulus (solid squares), and aortic annulus (open squares) throughout the cardiac cycle for 7 animals at baseline. Left ventricular pressure (LVP) tracing (solid line) is shown in each panel. A 650 ms time window centered at end diastole (ED) (dashed vertical line at t ⫽ 0) is illustrated for all variables. Error bars indicate 1 standard error of the mean.

and atrial annular areas changed in roughly a reciprocal fashion during late diastole and early systole (Fig 2) with maximum mitral annular area observed in late diastole and peak aortic annular area seen just prior to LV ejection. Change in atrial annular area from maximum to minimum during the cardiac cycle was 32 ⫾ 8%, whereas mitral annular area changed by 13 ⫾ 13%. Aortic fibrous annulus changed much less than aortic muscular annulas (6 ⫾ 2% vs 18 ⫾ 4%; p ⫽ 0.0003) as did relative to mitral fibrous annulus (4 ⫾ 1% vs 8 ⫾ 2%, respectively; p ⫽ 0.004). The dynamic change in total mitral and aortic annular circumference closely reflected the change in the muscular portion of each annulus, respectively; and the fibrous portion of each annulus appeared to contribute little to its dynamic physiology (Fig 3). As the two valves are directly linked through fibrous aorto-mitral continuity, the aorto-mitral angle throughout the cardiac cycle was calculated (Fig 4). At baseline, the average change in this angle from maximum to minimum during the cardiac cycle was 7 ⫾ 2°, which was an 8 ⫾ 2% reduction from maximum value. This angle was smallest in late systole and early diastole and subsequently increased during diastolic LV filling. At end diastole, the angle reached 64 ⫾ 18% of its maximum value, which was

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Fig 4. Group mean aorto-mitral angle (solid squares), left ventricular pressure (LVP) (solid line), and left ventricular (LV) volume (dashed line) throughout the cardiac cycle for 7 animals at baseline. A 650 ms time window centered at end diastole (ED) (dashed vertical line at t ⫽ 0) is illustrated for all variables.

subsequently observed at 100 ⫾ 59 ms after end diastole (corresponding to end-isovolumic contraction). During ejection there was a rapid decrease in the aorto-mitral angle. To evaluate further aorto-mitral physiological linkage, annular dynamic motion was measured under varying hemodynamic conditions created by infusion of calcium chloride, sodium nitroprusside, or neosynephrine. Hemodynamic variables before and after each pharmacological intervention (n ⫽ 6) are listed in Table 1 group mean mitral and aortic annular areas throughout the cardiac cycle under these hemodynamic conditions are shown in Figure 5, and changes in aorto-mitral angle are illustrated in Figure 6 (Table 2). The reciprocal change during late diastole and early systole in mitral and aortic annular areas was maintained during the hemodynamic manipulations (Fig 5). Annular area contraction during the cardiac cycle was only affected by inotropic stimulation with calcium; alterations in afterload did not affect annular area reduction of either valve (Table 2). Simi-

Fig 5. Group mean mitral annular area (squares) and aortic annular area (circles) throughout the cardiac cycle before calcium (Ca) infusion (closed symbols) and after Ca infusion (open symbols) (top), sodium nitroprusside (Snp) infusion (middle), or neosynephrine (Neo) infusion (bottom). A 650 ms time window centered at end diastole (ED) (dashed vertical line at t ⫽ 0) is illustrated for all variables.

larly, the change in aorto-mitral angle throughout the cardiac cycle was influenced only by calcium infusion. This response to inotropic stimulation indirectly indicates that annular dynamics are mediated by the muscular portion of each annulus. To confirm the relative adynamic behavior of the fibrous aorto-mitral continuity, the length of the fibrous portion of the mitral annulus was calculated during each hemodynamic intervention.

Table 1. Hemodynamics

⫺1

HR (min ) LV dp/dtmax (mm Hg/sec) LVPmax (mm Hg) EDV (mL) ESV (mL) LVEDP (mm Hg) LVESP (mm Hg) a

Precalcium

Calcium

Pre-sodium Nitroprusside

Sodium Nitroprusside

Preneosynephrine

Neosynephrine

114 ⫾ 12 1,539 ⫾ 185 104 ⫾ 11 140 ⫾ 47 110 ⫾ 38 24 ⫾ 7 64 ⫾ 15

108 ⫾ 16 2,750 ⫾ 360a 116 ⫾ 10 132 ⫾ 44a 93 ⫾ 32a 23 ⫾ 7 57 ⫾ 8

101 ⫾ 18 1,590 ⫾ 277 102 ⫾ 9 139 ⫾ 48 110 ⫾ 41 24 ⫾ 6 62 ⫾ 11

119 ⫾ 17 1,470 ⫾ 221 83 ⫾ 10a 131 ⫾ 40 100 ⫾ 32 18 ⫾ 6a 60 ⫾ 7

116 ⫾ 12 1,814 ⫾ 135 104 ⫾ 9 138 ⫾ 46 106 ⫾ 36 23 ⫾ 7 63 ⫾ 13

119 ⫾ 16 1,891 ⫾ 163 124 ⫾ 8a 140 ⫾ 48 111 ⫾ 39 28 ⫾ 6a 73 ⫾ 7

p ⬍ 0.05 vs pre- by Students t test for dependent observation.

EDV ⫽ left ventricle end-diastolic volume; ESV ⫽ left ventricle end-systolic volume; HR ⫽ heart rate; maximum positive rate of change of left ventricle pressure; LVPmax ⫽ maximum left ventricle pressure; pressure; LVESP ⫽ left ventricle end-systolic pressure.

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LV ⫽ left ventricle; LV dp/dtmax ⫽ LVEDP ⫽ left ventricle end-diastolic

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Comment

CARDIOVASCULAR Fig 6. Group mean aorto-mitral angle throughout the cardiac cycle before calcium (Ca) infusion (solid squares) and after Ca infusion (open squares) (top), sodium nitroprusside (Snp) infusion (middle), and neosynephrine (Neo) infusion (bottom). A 650 ms time window centered at the end-diastole (ED) (dashed vertical line at t ⫽ 0) is illustrated for all variables.

The change in length of the inter-trigonal distance throughout the cardiac cycle did not differ before or after calcium (5 ⫾ 1% vs 6 ⫾ 3%; p ⫽ 0.5), nitroprusside (5 ⫾ 1 vs 7 ⫾ 2; p ⫽ 0.1), or neosynephrine (5 ⫾ 2 vs 5 ⫾ 1%; p ⫽ 0.7) infusion.

With the evolution of newer annular and valvular prosthetic devices for mitral and aortic valve repair and replacement, better understanding of the interaction between aortic and mitral valvular dynamics is important. The aortic and mitral valves share a common annular portion, known clinically as aorto-mitral continuity or the aortic-mitral curtain, and are anatomically coupled. The physiology of each annulus until recently [9], however, has only been studied in isolation. We simultaneously measured mitral and aortic annular dynamics in sheep and found that the annular areas of the two valves changed in roughly a reciprocal fashion during late diastole and early systole; the dynamic behavior of each annulus was mainly due to changes in each respective muscular portion. The fibrous continuity between the valves was relatively adynamic, even during inotropic stimulation. The angle between the two annuli flattened during diastole and decreased rapidly during LV ejection. Aortic and mitral annular area and angular position change during the cardiac cycle were influenced by inotropic stimulation, whereas alterations in afterload had little effect. The extent of mitral annular area reduction during the cardiac cycle observed in this study supports previously published ovine data [5, 9, 16], and the 32 ⫾ 8% change in aortic annular area corresponds closely to the 30 ⫾ 3% figure reported recently in sheep by Lansac and coworkers [1]. The change in annular circumference of both valves paralleled closely the dynamics of the muscular portion of each annulus, whereas the fibrous continuity was relatively static. These findings agree with our previous observations of segmental heterogeneity of the ovine mitral annulus [17], but these findings are discordant with the data reported by Lansac and colleagues [9] who found that the mitral intertrigonal distance changed by 11.5 ⫾ 2.3% during the cardiac cycle, whereas the corresponding fibrous portion of the aortic annulus changed by 12.9 ⫾ 2.0%. In our study, the fibrous segment of the aortic and mitral annulus changed by only 6

Table 2. Mitral and Aortic Annular Geometry

2

MAAmax (cm ) MAAmin (cm2) MAAcont (%) AAAmax (cm2) AAAmin (cm2) AAAcont (%) AA-MA anglemax (°) AA-MA anglemin (°) AA-MAflex (°) a

Precalcium

Calcium

9.2 ⫾ 1.6 8.0 ⫾ 1.4 14.4 ⫾ 2.2 2.1 ⫾ 0.4 1.5 ⫾ 0.3 34 ⫾ 6 97 ⫾ 8 88 ⫾ 8 8.3 ⫾ 1.4

8.8 ⫾ 1.5 7.4 ⫾ 1.2a 18.1 ⫾ 3.1a 2.1 ⫾ 0.5 1.4 ⫾ 0.3a 44 ⫾ 10a 96 ⫾ 8 85 ⫾ 10a 11.8 ⫾ 2.3a

Pre-sodium Nitroprusside

Sodium Nitroprusside

Preneosynephrine

Neosynephrine

9.2 ⫾ 1.7 8.0 ⫾ 1.6 15.5 ⫾ 2.6 2.0 ⫾ 0.4 1.5 ⫾ 0.4 36 ⫾ 6 98 ⫾ 9 88 ⫾ 7 9.3 ⫾ 2.2

8.8 ⫾ 1.3 7.5 ⫾ 1.1 18.1 ⫾ 5.5 2.0 ⫾ 0.4 1.4 ⫾ 0.3a 41 ⫾ 6 96 ⫾ 8a 86 ⫾ 8a 9.7 ⫾ 2.2

9.0 ⫾ 9.2 7.7 ⫾ 1.3 17.1 ⫾ 2.0 2.0 ⫾ 0.5 1.5 ⫾ 0.4 37 ⫾ 4 97 ⫾ 8 88 ⫾ 8 9.3 ⫾ 1.0

9.2 ⫾ 1.6a 7.8 ⫾ 1.3 17.7 ⫾ 3.1 2.1 ⫾ 0.5a 1.5 ⫾ 0.3 38 ⫾ 6 96 ⫾ 9 89 ⫾ 9 7.8 ⫾ 2.2

a

p ⬍ 0.05 vs pre- by Student’s t test for dependent observations.

AAA ⫽ aortic annular area; AA-MA angle ⫽ angle between aortic and mitral annulus; cont ⫽ percent area reduction from maximum to minimum; flex ⫽ angular excursion from maximum to minimum; MAA ⫽ mitral annular area; max ⫽ maximum; min ⫽ minimum.

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TIMEK ET AL AORTO-MITRAL ANNULAR DYNAMICS

⫾ 2% and 4 ⫾ 1%, respectively. This discordance may be due to experimental design; Lansac and colleagues [9], studied two separate groups of open-chest, relatively hypotensive animals under different hemodynamic conditions. Furthermore, our measurements of mitral intertrigonal distance were based on five rather than three markers, perhaps yielding more precision. Our data indicate that fibrous continuity does not act as a piston between the two valves to facilitate filling in diastole and ejection in systole, as suggested by Lansac and coworkers [9]; instead, valvular area change appears to be mediated by dynamic motion of the muscular portion of each respective annulus. Mitral annular area reduction occurs predominantly prior to ventricular systole [5] and is strongly influenced by atrial contraction [18], whereas aortic annular expansion may be related to volume redistribution during isovolumic contraction [19]. Although aorto-mitral fibrous continuity may change little during the cardiac cycle, it represents an anatomic coupling between the two valves, and it is an important clinical landmark [10]. Mitral annular rings are sized according to the inter-trigonal distance by some due to the presumed structural stability of the fibrous anterior mitral annulus, but recent animal [17] and human [20] data suggest that this region actually can dilate in disease states, thus challenging surgical dogma. Whether dilation of the mitral inter-trigonal distance would lead to aortic annular dilatation remains unknown, but the constant anatomic relationship between these structures [11] suggest that this is possible. More recently, fibrous continuity has been used as an anchor in an experimental mitral reparative technique (septal-lateral mitral annular reduction) to correct acute ischemic mitral regurgitation [12]. Such annular cinching did not perturb normal mitral annular dynamics [21], and the current findings of little motion of the fibrous continuity lend support to this approach. Dynamic interaction between the mitral annulus and the left ventricular outflow tract was first explored by Komoda and colleagues [7] in normal human subjects using magnetic resonance imaging. These investigators found the left ventricular outflow tract to be at approximately a 120° angle to the posterior mitral annular plane at end diastole with subsequent decrease in this angle during systole. The near 90° aorto-mitral angle reported in our study is in agreement with normal human subjects [22], although smaller than that reported by Komoda and colleagues [7]. Notwithstanding the differences between humans and sheep, we used the mitral annular centroid in our calculations, whereas Komoda and colleagues [7] only used the posterior portion of the annulus. When Komoda and colleagues’ [7] magnetic resonance imaging reconstructions are examined and the entire mitral annular plane is considered, the left ventricular outflow tract mitral annular angle approaches a right angle, as we had observed. An aorto-mitral angle value of 133 ⫾ 10° in healthy human subjects has been reported [23], but these measurements were obtained from two-dimensional views of contrast ventriculograms, thereby ignoring the three-dimensional geometry of each valve. We found

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that the aorto-mitral angle increased progressively during diastole with increasing LV volume reaching a plateau in late diastole, followed by a sharp increase during isovolumic contraction. Dynamic annular flexion may aid LV filling and ejection by maintaining proper orientation of the two valve planes. Furthermore, proper orifice position may be important for orientation of flow patterns within the LV chamber as an almost complete redirection of blood flow occurs between LV inflow and LV outflow [24]. It is also possible that a portion of the change in aorto-mitral angle is attributable to flexion toward the atrium of the anterior mitral annulus [25]. However, a substantial amount of anterior annular flexion occurs during isovolumic contraction [25, 26] when the aorto-mitral angle increases at its fastest rate. Furthermore, inotropic stimulation significantly increased aorto-mitral angular excursion even though mitral annular flexion is independent of the inotropic state [17]. During calcium infusion, the minimum angle between the two annuli decreased significantly, thereby increasing angular excursion and bringing the two valves closer during systole. We speculate that this enhanced flexion may assist in LV ejection allowing the closed mitral valve to “sweep” LV volume toward the LV outflow tract. With LV afterload reduction during sodium nitroprusside infusion, both maximum and minimum angle values were lower, but total angular excursion did not change. Thus, ventricular peak systolic pressure may affect the baseline aorto-mitral angle value, whereas the inotropic state determines its excursion during systole. However, increased LV pressure during neosynephrine infusion did not alter baseline minimum or maximum angle values, although it is possible that even higher values of LV pressure might have done so. The changes in aortomitral angle observed in this experiment were small, but a difference of only 8° was reported between normal and post-infarct human hearts [23], which suggests that small changes may have physiologic significance. These data provide evidence that the aortic and mitral valves have common dynamic physiology, although their annular area change during the cardiac cycle do not appear to be mediated through anatomic coupling across fibrous aorto-mitral continuity. Whether fixation of either annulus with a rigid prosthetic device would alter the aortomitral angle and have any adverse effect on valvular function is unknown; further studies are needed to investigate the effect of valvular surgical interventions on aorto-mitral flexion and simultaneous valvular dynamic physiology. The above data must be interpreted in light of several study limitations of our experiment. Although a constant anatomic relationship between the aortic and mitral valves has been reported in both humans and sheep [11] caution must be used when extrapolating these findings to humans as a true aortic fibrous “annulus” may be difficult to identify in human hearts [27] and myocardial contribution to aortic annular motion may be greater in sheep [28]. Myocardial marker studies require suturing miniature tantalum markers to the cardiac structures of interest, and the presence and collective mass of the

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markers may alter normal annular motion. However, the markers utilized in this study were very small (4 to 8 mg) and would not be expected to affect the normal dynamics of either annulus. The changes in aorto-mitral angle throughout the cardiac cycle observed in our study were quite small, and their physiologic significance may be questioned; however, previous studies have shown that very small (1 to 2 mm) three-dimensional geometric alterations may have profound effects on valvular physiology and competence in sheep [16]. Furthermore, calculations of aortic annular dynamics were based on only three annular markers, thus the validity of these measurements may not be as great as those of mitral annular dynamics in which 10 markers were used. Hence the discrepancy between mitral and aortic annular area change throughout the cardiac cycle may be smaller than we observed.

We appreciate the superb technical assistance provided by Mary K. Zasio, BA, Carol W. Mead, BA, and Maggie Brophy, AS. Supported by grants HL-29589 and HL-67025 from the National Heart, Lung, and Blood Institute. Drs Timek, Lai, Green, Rodriguez, and Tibayan are Carl and Leah McConnell Cardiovascular Surgical Research Fellows. Dr Timek is a recipient of the Thoracic Surgery Foundation Research Fellowship Award. Drs Timek, Tibayan, and Green were supported by NHLBI INRSA grants HL-10452, HL-67563, and HL-09569, respectively. Dr Lai was supported by a fellowship from the American Heart Association, Western States Affiliate. Dr Rodriguez was supported by the American College of Surgeons Resident Research Scholarship.

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12. 13. 14.

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17. 18. 19. 20.

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Aorto-mitral annular dynamics Tomasz A. Timek, G. Randall Green, Frederick A. Tibayan, David T. Lai, Filiberto Rodriguez, David Liang, George T. Daughters, Neil B. Ingels, Jr and D. Craig Miller Ann Thorac Surg 2003;76:1944-1950 Updated Information & Services

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