Eur J Cardiothorac Surg 2008;34:755-759. doi:10.1016/j.ejcts.2008.04.052
Copyright © 2008, European Association for Cardio-thoracic Surgery. Published by Elsevier. All rights reserved.
Differences in mitral valve-left ventricle dimensions between a beating heart and during saline injection test
Michihito Nonaka,
Akira Marui,
Masahira Fukuoka,
Takeshi Shimamoto,
Shinji Masuyama,
Tadashi Ikeda,
Masashi Komeda*
Department of Cardiovascular Surgery, Graduate School of Medicine, Kyoto University, 54 Shogoin-Kawara, Sakyo, Kyoto 606-8507, Japan
Received 13 October 2007;
received in revised form 12 April 2008;
accepted 21 April 2008.
* Corresponding author. Tel.: +81 75 751 3784; fax: +81 75 751 4960. (Email: komelab{at}kuhp.kyoto-u.ac.jp).
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Abstract
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Objective: Saline injection test performed during mitral valvuloplasty is popular; however, discrepancies are sometimes noticed between the ‘naked eye’ findings of regurgitation during the saline injection test and the echocardiographic findings after surgery. These discrepancies may arise due to the geometric differences in the mitral valve-left ventricular complex between the saline-injected left ventricle (LV) and the beating LV. Therefore, to elucidate these differences, we compared the three-dimensional geometries between these two conditions. Methods: Sonomicrometry crystal markers were implanted in seven mongrel dogs at the mitral annulus, edge of the mitral leaflets between scallops, tips of papillary muscles, and LV apex under cardiopulmonary bypass. Geometric data of the LV were acquired during the saline injection test and in the beating heart. Results: The commissural width was greater and the annular height was lesser during the saline injection test than in the beating heart (20.5 ± 5.1 mm vs 17.2 ± 2.2 mm, p
< 0.01 and 5.5 ± 1.8 mm vs 7.3 ± 2.2 mm, p
< 0.05, respectively), indicating that the saddle-shaped mitral annulus was flattened during the test. Additionally, the middle scallop width and the distance between the papillary tips were greater during the test (14.0 ± 4.2 mm vs 11.3 ± 3.6 mm, p
< 0.05 and 22.9 ± 5.9 mm vs 11.6 ± 5.0 mm, p
< 0.01, respectively), implying that the middle scallop was stretched by the traction of the chordae. The distance between the papillary tips and the mitral annular plane remained constant in both the conditions (19.3 ± 2.6 mm vs 18.6 ± 6.2 mm, not significant). Conclusions: The saline injection test could aid in determining the length of the reconstructed chordae. However, the test may provide inaccurate data of the mitral-LV dimensions due to the flattened annulus and overstretched leaflets.
Key Words: Saline injection test (regurgitation test) • Mitral valvuloplasty • Mitral leaflets • Mitral annulus • Saddle shape
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1. Introduction
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Mitral valvuloplasty (MVP) is one of the standard surgeries performed for the treatment of mitral regurgitation (MR) [1–4]. During MVP, the saline injection test (SIT) is commonly employed to confirm the coaptation of the mitral valve and determine the characteristics of regurgitation before and after MVP, if any. However, discrepancies are sometimes noticed between the naked eye findings of regurgitation during SIT and the echocardiographic findings after operation [5]. The discrepancies may arise due to the geometric differences in the mitral valve-left ventricular (LV) complex between the saline-injected LV and the beating LV. If these differences are elucidated, postoperative coaptation of the mitral valve can be accurately predicted even under cardioplegic arrest during MVP. Thus, in the present study by using normal mongrel dogs, we compared the three-dimensional (3D) shapes of the mitral valve components between the beating heart and during SIT under cardioplegic arrest.
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2. Materials and methods
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2.1 Animals
In this study, we used seven normal mongrel dogs that were supplied by Oriental BioService, Inc. (Kyoto, Japan). The average weight of the dogs was 18.3 ± 0.9 kg. All the dogs received humane care in compliance with the Principles of Laboratory Animal Care formulated by the National Society for Medical Research and the Guide for the Care and Use of Laboratory Animals prepared by the National Academy of Sciences and published by the NIH (DHEW [NIH] publication 85-23, revised 1985). The study was approved by the Kyoto University Research Animal Review Committee and conducted in accordance with the policies of the Kyoto University.
2.2 Surgical preparation
Surgical preparation was carried out according to methods that have been described previously [6,7]. Briefly, the seven mongrel dogs were administered premedication, and anesthesia was induced; subsequently, they were intubated. An arterial line was placed in the femoral artery for monitoring the systemic blood pressure (BP). A Swan-Ganz catheter was inserted through the right internal jugular vein for monitoring the pulmonary arterial pressure (PA). A central venous line was placed in the femoral vein. Preoperative measurements of hemodynamic parameters such as heart rate (HR), BP, PA, pulmonary capillary wedge pressure (PCWP), and cardiac output (CO) were acquired.
The dogs were placed in the right lateral decubitus position. Left thoracotomy was performed through the left fifth intercostal space. The pericardium was incised along the left phrenic nerve, and the left common carotid artery was exposed. The right atrium and the left common carotid artery were cannulated after heparinization (300 IU/kg), and an aortic root cannula was inserted through the ascending aorta. After the establishment of a cardiopulmonary bypass (CPB), the aorta was cross-clamped, and the heart was arrested by injecting a crystalloid cardioplegic solution that contained potassium.
2.3 Implantation of sonomicrometry crystal markers
Prior to SIT, sonomicrometry crystal markers (diameter = 2.3 mm, length = 2.3 mm; Sonometrics Corporation, Ontario, Canada) were inserted beneath the left ventricular epicardial surface at the LV apex and the root of each papillary muscle (PM) (Fig. 1
, lateral view) [8–10]. Under the CPB, sonomicrometry crystal markers (outer diameter = 1.0 mm, length = 1.0 mm) were sutured onto the tip of each PM. Further, in order to delineate the circumference of the mitral annulus (MA), identical crystal markers were sutured onto 6 points of the MA, including points on the anterior and posterior commissures. In addition, four crystal markers were sutured at the edge of each mitral leaflet between the scallops (Fig. 1, upper view) [11]. After the markers were implanted, a micromanometer pressure transducer (Millar Instruments, Inc., Houston, TX) was placed in the LV chamber through the LV apex.
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Fig. 1. Implantation points of sonomicrometry crystal markers (APM = anterior papillary muscle, PPM = posterior papillary muscle, ACOM = anterior commissure, PCOM = posterior commissure).
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2.4 Measurement of the distances between each crystal marker
During SIT, in order to avoid geometric distortion by left atrial (LA) traction, the LV chamber was filled with saline injected through a 20 Fr catheter fixed at the LV apex without traction of the heart. The distances between each crystal marker were automatically recorded.
After SIT, the dogs were rewarmed, the left atriotomy was sutured using a 5-0 monofilament suture, the aorta was declamped, and the animals were weaned from the CPB. After the hemodynamic parameters had stabilized, the distances between each crystal marker were measured at the peak LV pressure in the beating heart, that is, immediately before the T wave on the electrocardiogram. The hemodynamic parameters and the marker-derived data from three consecutive steady beats were averaged for each of the seven animals.
2.5 Mitral annular geometry
The mitral annular plane was defined as the least-squares plane fitted to the six points of the MA [12]. In order to calculate the annular height (AH), we first obtained the orthogonal displacement of each annular marker from the annular plane, and the distance between the two maximally displaced markers above and below this plane was then used as the mitral AH.
2.6 Statistical analysis
All values are expressed as mean ± standard deviation. The results of the comparison of the dimensions between the two groups (the saline-injected heart and the beating heart) were statistically analyzed using the Wilcoxon signed rank test. All statistical analyses were performed using the StatView® software (SAS Institute, Inc., Cary, NC).
The authors had full access to the data and assume full responsibility for their integrity. All authors have read and agreed to the manuscript as written.
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3. Results
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The CPB time was 52 ± 17 min with an aortic cross-clamp time of 38 ± 9 min. The LV pressure during SIT was 41.5 ± 8.1 mmHg. The peak LV pressure in the beating heart was 96.2 ± 13.2 mmHg, and the LV end-diastolic pressure was 9.9 ± 4.8 mmHg. The distances (mm) between each crystal marker are shown in Table 1
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3.1 Left ventricle
In the short-axis dimension, the distance between the bases of the anterior and posterior PMs (solid lines in Fig. 2) was significantly greater during SIT than in the beating heart (35.5 ± 11.0 mm vs 24.1 ± 9.1 mm, p
< 0.01). In the longitudinal dimension, the distance between the apex and the mid-anterior/posterior MA (dotted lines in Fig. 2
) during SIT was similar to that in the beating heart.
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Fig. 2. The geometry of the left ventricle. During SIT, the LV expanded in the short-axis dimension and became more spherical (solid line = variable, dotted line = constant, SIT = saline injection test, APM = anterior papillary muscle, PPM = posterior papillary muscle).
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3.2 Papillary muscles
The distance between the tips of each PM during SIT (solid line in Fig. 3
) was significantly greater than that in the beating heart (22.9 ± 5.9 mm vs 11.6 ± 5.0 mm, p
< 0.01). The lengths of the anterior and posterior PMs (dotted lines in Fig. 3) remained constant.
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Fig. 3. The geometry of the papillary muscles. During SIT, the distance between the tips of each papillary muscle increased to almost twice the distance in the beating heart (solid line = variable, dotted line = constant, SIT = saline injection test, APM = anterior papillary muscle, PPM = posterior papillary muscle).
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3.3 Mitral annulus
The distance between the anterior and posterior commissures (commissural width, CW; Fig. 4
) was significantly greater during SIT than in the beating heart (20.5 ± 5.1 mm vs 17.2 ± 2.2 mm, p
< 0.01). The AH (Fig. 4) during SIT was significantly lesser than that in the beating heart (5.5 ± 1.8 mm vs 7.3 ± 2.2 mm, p
= 0.031). The distance between the mid-anterior MA and mid-posterior MA points (annular depth) during SIT was similar to that in the beating heart (dotted lines in Fig. 4). The total circumference of the MA (defined as the sum of each segment along the MA) exhibited no difference between the two groups.
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Fig. 4. The geometry of the mitral annulus. In SIT, the mitral annulus was more flattened than in the beating heart; the commissural width was greater and the annular height was lesser (solid line = variable, dotted line = constant, SIT = saline injection test, CW = commissural width, AH = annular height, ACOM = anterior commissure, PCOM = posterior commissure).
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3.4 Mitral leaflets
The width of the middle portion of the anterior mitral leaflet (AML) and that of the middle scallop of the posterior mitral leaflet (PML) were significantly greater during SIT than in the beating heart (14.0 ± 4.2 mm vs 11.3 ± 3.6 mm, p
= 0.012 for the AML; 15.7 ± 4.6 mm vs 10.8 ± 3.4 mm, p
< 0.01 for the PML; solid lines in Fig. 5
). The distance from the mid-anterior/posterior MA to the edges of the mitral leaflets did not change (bold dotted lines in Fig. 5). The widths of the para-commissural scallops also remained constant (narrow dotted lines in Fig. 5).
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Fig. 5. The geometry of the mitral leaflets. During SIT, the mitral leaflet was stretched in the commissural direction and the bulge was less. The middle scallop was more stretched due to the traction of the chordae (solid line = variable, dotted line = constant, SIT = saline injection test).
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3.5 Mitral sub-apparatus
The distance from the PM tip to the MA plane was defined as the orthogonal (perpendicular) displacement between the PM tip and the MA plane (as described above). This distance was constant in both the groups (anterior PM tip-MA plane: 19.3 ± 2.6 mm vs 18.6 ± 6.2 mm, not significant [NS]; posterior PM tip-MA plane: 21.1 ± 4.3 mm vs 21.8 ± 4.7 mm, NS; dotted lines in Fig. 6
).
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Fig. 6. The distance between the PM tip and the MA plane. The distance between the PM tip and the MA plane remained constant in the saline-injected heart and the beating heart (dotted line = constant, SIT = saline injection test, MA = mitral annulus, APM = anterior papillary muscle, PPM = posterior papillary muscle).
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4. Discussion
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It is recognized that the shape of the mitral valve during SIT may differ from its shape in the beating heart [1]. However, the mitral components that differ and the differences between the findings during SIT and those in the beating heart are yet unclear. Understanding the geometric discrepancies in the dimensions of the mitral valve-LV components between a saline-injected heart (during SIT) and in the beating heart might contribute to a more accurately performed MVP. To the best of our knowledge, this is the first report that compares the 3D geometries of the mitral valve-LV components during SIT with those in the naturally beating heart.
4.1 Main findings
The following were the differences between the 3D characteristics of the mitral valve LV components observed during SIT and those obtained in the beating heart: (1) the saddle-shaped MA was more flattened during SIT, (2) the middle portion of the AML and the middle scallop of the PML were more laterally stretched and less bulged (i.e. they were flattened) during SIT, (3) the distance between the tips of the anterior and posterior PMs was considerably greater during SIT, and (4) the LV chamber was more spherical during SIT. However, the distance from the tip of each PM to the MA during SIT was nearly identical to that in the beating heart. Thus, SIT may provide useful geometric information for the assessment of the chordal length. The abovementioned differences may explain the discrepancies between the dimensions of the mitral valve LV components observed during SIT and those obtained in the beating heart.
4.2 Bulge of the mitral leaflet
In the current study, the middle scallop of the mitral leaflets during SIT was probably stretched in the commissural direction by the flattened mitral annulus and the traction of the marginal chordae and had less bulge [13]. On the other hand, the mitral leaflets in the beating heart are more bulging, and the coaptation area of the leaflets might be larger than that during SIT. Further, the change in the shape of the PML during SIT is greater than that of the AML. Therefore, in MVP, if the bulge of the reconstructed mitral leaflets is up to an appropriate degree during SIT, their bulge would increase in the beating heart; this may induce valve prolapse, inadequate coaptation, or redundancy of the scallops, particularly of the PML [11,14–16]. Thus, the shape of the leaflets during SIT should be such that they have a lesser bulge than that required after MVP. Moreover, the placement of an annuloplasty ring causes the leaflets to bulge further; hence, it is important to carefully consider the changes in the bulging of the mitral leaflets.
4.3 Determination of the length of artificial chordae
In the present study, the distance from the PM tip to the MA plane did not change either during SIT or in the beating heart. This implies that the lengths of the reconstructed artificial chordae could be accurately determined during SIT under cardioplegic arrest during MVP [17–19]. We have shown that the distance from the PM tips to the MA was constant throughout the beating cardiac cycle because of the linked movement of the mitral valve LV complex [20]. It is interesting to note that this distance was identical during SIT and in the beating heart.
4.4 LV pressure in SIT
In SIT, saline was injected in a manner such that the mitral valve naturally closed with appropriate LV expansion. In order to determine the appropriate LV pressure by saline injection during SIT, we evaluated the following three LV pressure ranges as a preliminary study: less than 30 mmHg, between 30 and 60 mmHg, and more than 60 mmHg. An LV pressure of less than 30 mmHg did not close the mitral valve. An LV pressure of more than 60 mmHg excessively expanded the LV, flattened the MA, and stretched the mitral leaflets [21]. Therefore, we employed an LV pressure ranging between 30 and 60 mmHg during SIT. As a result, the LV pressure during SIT was 41.5 ± 8.1 mmHg. This was considerably lower than that in the beating heart.
4.5 Limitations
The present study had several limitations. First, we did not evaluate the geometry of the mitral valve-LV components by using an annuloplasty ring. In clinical settings, an annuloplasty ring is usually applied during MVP. However, the purpose of the present study was to compare the geometric discrepancies in the mitral valve-LV complex without using the annuloplasty ring between saline-injected heart (during SIT) and the beating heart. Nevertheless, we realize the importance of comparing the geometric differences while using an annuloplasty ring. We would like to investigate this in a future study.
Second, we used normal hearts in this study. A degenerative change and a functional alteration in the mitral valve are the major causes of MR. However, because it is difficult to establish an experimental degenerative MR model and to wean from CPB in a canine model of ischemic functional MR, we primarily used the normal model.
Third, saline was not injected through the mitral valve as performed in the clinical settings in order to avoid excessive distortion of the heart. This fact might be responsible for the results of the present study.
4.6 Conclusions
Since the distance from the PM tip to the MA plane was nearly identical during SIT and in the beating heart, SIT could aid in determining the lengths of the reconstructed chordae. However, SIT may provide inaccurate data of the mitral valve-LV dimensions during MVP due to the flattened MA and overstretched leaflets.
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Acknowledgments
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We would like to express our gratitude to Toshiya Sato (Department of Biostatistics, Graduate School of Public Health, Kyoto University) for statistical collaboration in this study.
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Footnotes
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Presented at the American Heart Association Scientific Meeting in Chicago, USA November 12–15 2006.
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Abstract
1. Introduction
