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Asian Cardiovasc Thorac Ann 2006;14:394-398
© 2006 Asia Publishing EXchange Ltd


ORIGINAL CONTRIBUTIONS

Kinking of the Atrioventricular Plane During the Cardiac Cycle

Wolfgang A Goetz, PhD, Emmanuel Lansac, MD, Hou-Sen Lim, MS, Scott A Stevens, PhD, Patricia A Weber, DrPH, Carlos MG Duran, PhD

The International Heart Institute of Montana Foundation, St. Patrick Hospital and Health Sciences Center, The University of Montana Missoula, USA

For reprint information contact: Carlos Duran, MD Tel: 1 406 329 5668 Fax: 1 406 329 5880 Email: Cduran{at}saintpatrick.org, The International Heart Institute of Montana, 554 West Broadway, Missoula, MT 59802, USA.


    ABSTRACT
 TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Systolic descent of the atrioventricular plane toward the relatively stationary left ventricular apex is well described. As the atrioventricular plane includes two separate valvular units, systolic atrioventricular plane displacement should not be homogenous. In 6 sheep, sonomicrometric crystals were implanted at the base of the right coronary sinus, anterolateral and posteromedial fibrous trigones, posterior mitral annulus, left ventricular apex, and the tips of the anterior and posterior mitral leaflets. The aortomitral angle was calculated and related to simultaneous left ventricular and aortic pressures and mitral valve movement. The aortomitral angle was largest at end diastole (150.73° ± 15.48°). During isovolumic contraction, it narrowed rapidly to 144.90° ± 16.64°, followed by a slower narrowing during ejection until it reached its smallest angle at end systole (139.66° ± 16.78°). During isovolumic relaxation, the aortomitral angle increased to 143.66° ± 16.02° at the beginning of diastole. During the first third of diastole, it narrowed again to 141° ± 16.24° before re-expanding to maximum at end diastole. During systole, the atrioventricular plane descended non-homogeneously toward the apex, with kinking at the hinge between the aortic and mitral annulus plane. This deformation of the atrioventricular plane has relevance in valve surgery.


    INTRODUCTION
 TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
When the heart muscle contracts, it displaces the atrioventricular (AV) plane. Consequently, during systole, the AV plane moves toward the almost stationary left ventricular (LV) epicardial apex.16 It has been reported that the aortomitral angle depends on LV performance.7 Narrowing of the aortomitral angle can be observed after implantation of a mitral valve prosthesis and after mitral valve repair with a rigid annuloplasty ring.8,9 As the AV plane includes 2 separate valvular units, systolic AV plane displacement should not be homogenous. The purpose of this study was to use sonomicrometry to determine the changes in the aortomitral angle occurring during each phase of the cardiac cycle. We also studied the opening and closing of the mitral valve because it has been used to define the different phases of the cardiac cycle.


    PATIENTS AND METHODS
 TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
The study was carried out on 6 adult Targhee sheep (58 ± 18 kg; Sherick Farm, Missoula, MT, USA). All animals received humane care in accordance with the Principles of Laboratory Animal Care, formulated by the Animal Welfare Act in the Guide for Care and Use of Laboratory Animals prepared by the Institute of Laboratory Animal Resources and published by the National Institutes of Health (NIH publication #85-23, revised 1996). The use of these animals and the protocol for this research was also reviewed and approved by the Institutional Animal Care and Use Committee of the University of Montana.

The sheep were premedicated with ketamine 1 mg·kg–1 and propofol 4 mg·kg–1.Artificial ventilation was achieved using a volume-regulated respirator (North American Drager, Telford, PA, USA). The electrocardiogram was monitored continuously with 5 leads. Anesthesia was maintained with intermittent intravenous propofol and isoflurane at 0.5% to 2.5%, as needed. The heart was exposed with a standard left thoracotomy through the 4th intercostal space and a T-shaped incision of the pericardium. In preparation for cardiopulmonary bypass (CPB), a bolus injection of heparin 300 U·kg–1 was infused with a target activated clotting time of 480 sec or more. The ascending aorta was cannulated with a 16F arterial cannula. A 32F dual-stage single venous cannula (Medtronic, Inc., Minneapolis, MN, USA) was inserted into the right atrium. After starting CPB, an LV vent was inserted through the LV apex. The ascending aorta was crossclamped, followed by infusion of cold blood cardioplegia into the aortic root. Five 5-mm ultrasonic crystals (Sonometrics Corp., London, Ontario, Canada) were implanted and secured with 5/0 polypropylene sutures at the midpoint of the posterior mitral annulus (PMA), the anterior and posterior fibrous trigones (AFT and PFT), the lowest point of the right coronary sinus (RCS), and the apex of the heart. In addition, 1 mm crystals were placed at the midpoint of the free margin of the anterior and posterior mitral leaflets (AML and PML; Figure 1Go).


Figure 1
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Figure 1. Crystal locations. A = left ventricular apex, AFT = anterior fibrous trigone, AML = tip of the anterior mitral leaflet, PFT = posterior fibrous trigone, PMA = midpoint of the posterior mitral annulus, PML = tip of the posterior mitral leaflet, RCS = right coronary sinus.

 
The electrodes of the crystals on the PMA, AML, PML, AFT, and PFT were exteriorized through the left atriotomy. The electrode at the base of the RCS was exteriorized though the aortotomy. The apex electrode was exteriorized through the apex. A high-fidelity catheter-tipped pressure transducer (Model 510; Millar Instruments, Houston, TX, USA) was placed within the lumen of the proximal ascending aorta and in the LV cavity through the apex. After weaning from CPB, the venous and arterial cannulas were removed, and heparin was neutralized with protamine. The pericardium was closed with 3/0 polypropylene suture. Epicardial echocardiography was performed to detect mitral insufficiency and ensure that the movement of the mitral valve was not compromised by the crystals or their attached electrodes. Recordings were taken after the animal was hemodynamically stable (at least 30 min after weaning from CPB) to ensure normal loading conditions.

Geometric changes were time-related to each phase of the cardiac cycle defined from the aortic and LV pressure curves and mitral leaflet motion. End of diastole was defined as the point of increasing LV pressure tracing (dP/dt > 0). End of isovolumic contraction was defined as the beginning of ejection at the crossing point of the LV and aortic pressure curves (gradient LV/aortic pressures = 0). The dicrotic notch in the aortic pressure curve defined end ejection. End of isovolumic relaxation, or the initial phase of diastole, was defined by the mitral valve opening and determined by the initial separation of the crystals located in the free edges of the leaflets (AML-PML).10

The mitral annulus plane was defined as the plane that included both fibrous trigones (AFT and PFT) and the middle of the PMA. The aortic annulus plane was defined as the plane incorporating both fibrous trigones (AFT and PFT) and the lowest point of the RCS (Figure 1Go). Both planes defined the base of the heart, with the hinge at the axis between AFT and PFT. The aortomitral angle was defined as the angle formed by the aortic and mitral annulus planes. It was calculated from a line traced between the RCS and the midpoint of AFT and PFT and another line traced between the PMA and the midpoint of AFT and PFT. The apex of the angle was found at the axis between the AFT and PFT (Figures 1Go and 2Go).


Figure 2
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Figure 2. Aortomitral angle {theta}. AFT = anterior fibrous trigone, PFT = posterior fibrous trigone, PMA = midpoint of the posterior mitral annulus, RCS = right coronary sinus.

 
Distances between crystals were measured with Sonometrics Digital Ultrasonic Measurement System TRX Series using 13 transmitter/receiver crystals. A post-processing program (Sonometrics Corporation, London, Ontario, Canada) was used to examine each individual distance between crystals and for 3-dimensional reconstruction of the crystal coordinates. The data sampling rate was 200 Hz. Millar pressure transducer control units (TCB 600) and MIKRO-TIP pressure transducers (Millar Instruments Inc., Houston, TX, USA) were used to obtain the LV and aortic pressures. Pulmonary and left atrial pressures were taken directly through a 20 gauge needle and a conventional pressure transducer. All distances and pressures were displayed and recorded simultaneously on the same screen by the Sonometrics system to ensure that all data were synchronized and recorded on the same timeline. An effort was made to record the measurements under stable hemodynamic conditions of heart rate and loads, with a closed pericardium.

Distances were explored in a coordinate-independent analysis, using only distance measurements.11 After close examination of the data, 3 consecutive heartbeats that contained the least amount of noise were chosen for analysis. The summary statistics are reported as mean ± standard deviation. Hemodynamic and geometric data were compared using the two-tailed t test with a significance level of p < 0.05 (corrected by stepdown Bonferroni for multiple pair-wise comparisons). Statistical analyses were carried out with SAS 8.2 PROC MULTTEST software (SAS Institute, Cary, NC, USA).


    RESULTS
 TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
All 6 sheep survived implantation of the sonomicrometric crystals (Figure 1Go). Necropsy after sacrifice showed the crystals were in the correct positions. Hemodynamic parameters at the time of data acquisition included heart rate 108.7 ± 14.3 beats·min–1, central venous pressure 10.2 ± 1.6 mm Hg, systolic pulmonary artery pressure 24.8 ± 5.4 mm Hg, mean pulmonary artery pressure 17.0 ± 3.0 mm Hg, diastolic pulmonary artery pressure 12.7 ± 3.4 mm Hg, left atrial pressure 9.3 ± 1.2 mm Hg, LV systolic pressure 95.5 ± 10.9 mm Hg, and LV end-diastolic pressure 14.8 ± 5.2 mm Hg. Sinus rhythm was present in all sheep after weaning from CPB (Table 1Go). No mitral regurgitation or restriction of mitral valve movement could be detected using epicardial echocardiography.


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Table 1. Time Pattern of the Cardiac Cycle
 
Explored distances between the LV apex and crystals at the aortic and mitral annuli were largest at diastole. During systole, all longitudinal distances shortened significantly, and the AV plane descended non-homogeneously toward the apex. Shortening of the distance from the LV apex to the PMA was the largest of all longitudinal distances explored ( p < 0.05; Table 2Go).


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Table 2. Change of Geometry During the Cardiac Cycle
 
During the entire cardiac cycle, the aortomitral angle changed by 11.06° ± 6.86°. It was largest at the end of diastole (150.73° ± 15.48°; Figures 2Go and 3Go; Table 3Go). During isovolumic relaxation, the aortomitral angle narrowed rapidly by –5.82° ± 3.72° ( p < 0.05) to 144.90° ± 16.64°, followed by a slower narrowing during ejection by –5.24° ± 3.50° ( p < 0.05) until it reached the smallest angle at the end of systole (139.66° ± 16.78°). During isovolumic relaxation, the aortomitral angle increased by 3.99° ± 3.11° to 143.66° ± 16.02° at the beginning of diastole. During the first third of diastole, it narrowed again by –2.37° ± 0.7° to 141° ± 16.24° before re-expanding by 9.44° ± 4.69° ( p < 0.05) to a maximum at the end of diastole.


Figure 3
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Figure 3. Phases of the cardiac cycle with changes in the aortomitral angle. 1 = beginning of isovolumic relaxation, 2 = beginning of ejection, 3 = end of ejection, 4 = end of isovolumic relaxation. A = A-wave of the mitral valve, AA = ascending aorta, AML = tip of the anterior mitral leaflet, E = E-wave of the mitral valve, LV = left ventricular, PML = tip of the posterior mitral leaflet.

 

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Table 3. The Aortomitral Angle at 5 Time Points
 

    DISCUSSION
 TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Mitral annulus motion during the cardiac cycle has been studied extensively. The mitral annulus has been found to have a saddle shape and it undergoes complex deformation during the cardiac cycle.2,1214 The change of angle between the mitral annulus and the LV outflow tract during the cardiac cycle in humans was described by Komoda and colleagues.15 Timek and colleagues16 recently reported that the aortomitral angle changed by 7° ± 2° during the cardiac cycle, increasing significantly during inotropic stimulation. The aortomitral angle excursion was slightly larger in our experimental setting. We can confirm their observation that the aortomitral angle is largest at the end of diastole and narrows rapidly during isovolumic relaxation. The use of sonomicrometry and its high time resolution allowed us to describe the excursion of the aortomitral angle more precisely during the different phases of the cardiac cycle. Timek and colleagues16 implanted markers only on the aortic and mitral annuli. Placing a marker at the apex of the heart allowed us to relate the excursion of the aortomitral angle to LV geometric changes. During systole, the AV plane moves toward the almost stationary epicardial LV apex.16

This displacement of the AV plane toward the apex is an important component of the pump function of the heart.17 It is an expression of the systolic performance of the LV and reflects myocardial contractility.7 The AV plane consists of the aortic annulus plane and the mitral annulus plane forming an angle at the hinge of the aortomitral junction between the two fibrous trigones.9,13 During the cardiac cycle, the aortomitral angle performs a consistent pattern of narrowing and widening with the smallest angle at the end of systole and the widest angle at the end of diastole. Our data confirm that LV shortening is maximal between the apex and the PMA, resulting in tilting of the mitral annulus plane toward the PMA.1,4,13 The aortic root is also pulled toward the LV apex, but to a lesser extent than the PMA. The PMA follows LV shortening, whereas the aortic annulus and the fibrous trigones (i.e., the aortomitral junction) are tightly connected to the aortic root. As a result, the descent of the aortic annulus and the fibrous trigones must counteract the recoiling elastic force of the ascending aorta, reducing the extent of motion allowed. The PMA has no such restriction and is free to move.

The LV inflow pattern depends on the aortomitral angle. Omoto and colleagues8 demonstrated that LV inflow is directed along the posterolateral wall to the LV apex in late diastole, and LV outflow is directed along the septum to the LV outflow tract. When the aortomitral angle is narrowed, the diastolic flow patterns are reversed anteriorly-posteriorly from normal. Left ventricular inflow is directed toward the septum and, therefore, into the LV outflow tract, while LV outflow is displaced posterolaterally into the LV inflow region. Consequently, the risk of systolic anterior motion increases because of the reversed diastolic flow pattern.9 Narrowing of the aortomitral angle after implantation of a rigid annuloplasty ring in the mitral position will move the AML closer to the septum and also increase the risk of systolic anterior motion. We hypothesize that after implantation of a rigid prosthesis in the mitral annulus, the aortomitral junction motion will follow the descent of the PMA, changing the hinge of the AV plane towards the septum. This will narrow the angle of the LV outflow tract towards the septum with reduction of the LV outflow tract orifice, creating some degree of LV outflow tract obstruction. Moving the hinge of the AV plane towards the septum will also move the AML closer to the septum, altogether increasing the risk of systolic anterior motion. It can be concluded from these findings that the LV flow pattern depends on the aortomitral angle, and changes in the aortomitral angle have consequences on the systolic and diastolic LV blood flow pattern. We hypothesize that our observed changes in the aortomitral angle during the cardiac cycle direct optimal LV inflow to save kinetic energy and control AML motion.

In this experimental model, it was impossible to address the rotational motions of the left ventricle, which are essential for understanding LV function. Sonomicrometry allows precise recording of distances with a high resolution, but it is impossible to distinguish between active contraction and passive changes of distances. The sonomicrometric crystals and their electrodes might have interfered with the normal movements of the different structures. Also, the locations of the crystals might vary between animals. To reduce this possibility, all surgeries were performed by the same surgeon and mitral valve leaflet motion was confirmed by echocardiography. All data were acquired in an acute, anesthetized, open-chest animal after CPB and cardioplegia, with the pericardial cavity surgically closed in all animals. Despite this nonphysiologic condition, the observed changes were very consistent among all animals. However, findings in sheep are not necessarily applicable to the human.

Nevertheless, it was concluded that during systole, the AV plane propels non-homogeneously toward the LV apex. This systolic deformation of the AV plane causes the aortomitral angle to narrow by 11.06° ± 6.86° during the cardiac cycle. This insight into LV function advocates the use of a flexible prosthesis in valve surgery to preserve AV plane deformation during the cardiac cycle.


    ACKNOWLEDGMENTS
 
WA Goetz was supported by a grant from Deutsche Forschungsgemeinschaft, Kennedyallee 40, 53175 Bonn, Germany, and the Max Kade Foundation, Inc., New York, NY, USA. Hou-Sen Lim was supported by grant ARC 13/96 from the Singapore Ministry of Education and Nanyang Technological University.

We appreciate the technical assistance of Leslie Trail, Lorinda Smith, and Holly Meskimen in the animal laboratory, and the editorial assistance of Jill Roberts.


    REFERENCES
 TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

  1. Hoglund C, Alam M, Thorstrand C. Atrioventricular valve plane displacement in healthy persons. An echocardiographic study. Acta Med Scand 1988;224:557–62.[Medline]

  2. Komoda T, Hetzer R, Uyama C, Siniawski H, Maeta H, Rosendahl UP, et al. Mitral annular function assessed by 3D imaging for mitral valve surgery. J Heart Valve Dis 1994;3:483–90.[Medline]

  3. Gorman JH 3rd, Gupta KB, Streicher JT, Gorman RC, Jackson BM, Ratcliffe MB, et al. Dynamic three-dimensional imaging of the mitral valve and left ventricle by rapid sonomicrometry array localization. J Thorac Cardiovasc Surg 1996;112:712–26.[Abstract/Free Full Text]

  4. Assmann PE, Slager CJ, Dreysse ST, van der Borden SG, Oomen JA, Roelandt JR. Two-dimensional echocardiographic analysis of the dynamic geometry of the left ventricle: the basis for an improved model of wall motion. J Am Soc Echocardiogr 1988;1:393–405.[Medline]

  5. Lundback S. Cardiac pumping and function of the ventricular septum. Acta Physiol Scand Suppl 1986;550:1–101.[Medline]

  6. Alam M, Rosenhamer G. Atrioventricular plane displacement and left ventricular function. J Am Soc Echocardiogr 1992;5:427–33.[Medline]

  7. Harmon KE, Sheehan FH, Hosokawa H. Effect of acute myocardial infarction on the angle between the mitral and aortic valve plane. Am J Cardiol 1999;84:342–4, A8.[Medline]

  8. Omoto R, Matsumura M, Asano H, Kyo S, Takamoto S, Yokote Y, et al. Doppler ultrasound examination of prosthetic function and ventricular blood flow after mitral valve replacement. Herz 1986;11:346–50.[Medline]

  9. Mihaileanu S, Marino JP, Chauvaud S, Perier P, Forman J, Vissoat J, et al. Left ventricular outflow obstruction after mitral valve repair (Carpentier’s technique). Proposed mechanisms of disease. Circulation 1988;78(3 Pt 2):I78–84.

  10. Despopoulos A, Silbernagl S. Cardiovascular System. Color Atlas of Physiology. 5th Edition. Thieme, New York 2003:186–221.

  11. Dagum P, Timek TA, Green GR, Lai D, Daughters GT, Liang DH, et al. Coordinate-free analysis of mitral valve dynamics in normal and ischemic hearts. Circulation 2000;102(19 Suppl 3):III62–9.

  12. Lansac E, Lim KH, Shomura Y, Goetz WA, Lim HS, Rice NT, et al. Dynamic balance of the aortomitral junction. J Thorac Cardiovasc Surg 2002;123:911–8.[Abstract/Free Full Text]

  13. Komoda T, Hetzer R, Oellinger J, Sinlawski H, Hofmeister J, Hubler M, et al. Mitral annular flexibility. J Card Surg 1997;12:102–9.[Medline]

  14. Glasson JR, Komeda MK, Daughters GT, Niczyporuk MA, Bolger AF, Ingels NB, et al. Three-dimensional regional dynamics of the normal mitral annulus during left ventricular ejection. J Thorac Cardiovasc Surg 1996;111:574–85.[Abstract/Free Full Text]

  15. Komoda T, Hetzer R, Oellinger J, Siniawski H, Hofmeister J, Hubler M, et al. The relationship between the mitral annulus and left ventricular outflow tract. ASAIO J 1997;43:932–6.[Medline]

  16. Timek TA, Green GR, Tibayan FA, Lai DT, Rodriguez F, Liang D, et al. Aorto-mitral annular dynamics. Ann Thorac Surg 2003;76:1944–50.[Abstract/Free Full Text]

  17. Alam M, Hoglund C, Thorstrand C, Philip A. Atrioventricular plane displacement in severe congestive heart failure following dilated cardiomyopathy or myocardial infarction. J Intern Med 1990;228:569–75.[Medline]




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