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J Thorac Cardiovasc Surg 2002;123:911-918
© 2002 The American Association for Thoracic Surgery
Surgery for Acquired Cardiovascular Disease (ACD) |
From The International Heart Institute of Montana Foundation at St Patrick Hospitala and The University of Montana,b Missoula, Mont.
Received for publication May 29, 2001. Revisions requested July 27, 2001; revisions received Sept 19, 2001. Accepted for publication Oct 16, 2001. Address for reprints: Carlos M. G. Duran, MD, PhD, The International Heart Institute of Montana, 554 West Broadway, Missoula, MT 59802 (E-mail: duran{at}saintpatrick.org).
| Abstract |
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| Introduction |
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| Materials and methods |
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Surgical protocol
Anesthesia was induced with intravenous ketamine (1.0 mg/kg) and propofol (4.0 mg/kg) and maintained with isoflurane (1.5%-2.5%). Artificial ventilation was achieved with a volume-regulated respirator (North American Drager, Telford, Pa) supplemented with oxygen at 2 L/min. The heart was exposed by means of a standard left thoracotomy through the fourth intercostal space. The left femoral (16F) and left internal thoracic (10F) arteries were cannulated. A venous cannula was inserted into the right atrium (32F). The aorta and arch vessel were crossclamped, and cold crystalloid cardioplegic solution was infused into the root. One-millimeter ultrasonic crystals were implanted and secured with 5-0 polypropylene sutures (Figure 1).
The anterior leaflet is identified with the letter "A," the posterior leaflet is identified with the letter "P," and those paired structures to the left or right of the surgeon are identified with the numerals 1 or 2.
15 Through a left atriotomy, 6 crystals were placed on the mitral anulus: left and right trigones defining the intertrigonal distance (T1-T2); the midpoint of the anterior and posterior anulus defining the anteroposterior mitral diameter (AM-PM); and the left and right lateral extremities of the insertion of the posterior leaflet, defining the mitral transverse diameter (P1-P2). Through a transverse aortotomy, a crystal was placed at the lowest point of each of the right (R), left (L), and noncoronary (NC) sinuses of Valsalva corresponding to the aortic base of the aortic root. The crystals were oriented so that they pointed toward the lumen. The crystal's electrodes were exteriorized through the aortic wall at each point of insertion to reduce their possible interference with valve movements. The same surgeon placed all crystals to avoid interoperator variability. A high-fidelity catheter-tipped pressure transducer (model 510; Millar Instruments, Houston, Tex) was placed in the proximal ascending aorta and through the apex in the LV cavity. A flow probe was placed on the ascending aorta (Transonic Flowmeter T206; Transonic Systems Inc, Ithaca, NY).
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Definition of the phases of the cardiac cycle
In both groups of animals, the geometric changes were time related to each phase of the cardiac cycle defined from the aortic and LV pressure tracings.
16,17 End-diastole or the beginning of systole and of the isovolumic phase was defined as the point of positive inflexion of the LV pressure tracing (dP/dt > 0). The end of isovolumic contraction was defined as the beginning of ejection at the crossing point of LV and aortic pressure tracings (gradient of aortic/LV pressure = 0). The dicrotic notch in the aortic pressure curve defined the end of ejection. The end of isovolumic relaxation was defined as the lowest point of LV pressure tracing after ejection (dP/dt = 0).
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Definition of the anatomic regions
The aortic annular base was studied at each time point of the cardiac cycle by determining its area calculated from the 3 basal crystals and the changes in the 3 basal lengths between crystals (NC-R, R-L, and L-NC). The mitral anulus was studied by determining its area, 5 circumferential lengths (T1-T2, T2-P2, P2-PM, PM-P1, and P1-T1), and 2 diameters (anteroposterior AM-PM and transverse P1-P2).
Data acquisition and calculation of annular deformations
Crystal displacements were measured with the Sonometrics Digital Ultrasonic Measurement System TRX Series 16 and 1-mm transmitter-receiver crystals. A postprocessing program (SonoSOFT Version 3.1.4, Sonometrics Corp) was used to examine each individual length tracing between crystals and for 3-dimensional reconstruction of the crystal coordinates. All crystal distances, pressures, flows, and electrocardiographs were synchronized and recorded at the same time line on the same screen with the Sonometrics system.
Length data were obtained directly from the measured distances between the pair of crystals, and Lagrangian strain
18 was used to define the deformation from maximum to minimum values. The aortic root basal area was defined from the 3 corresponding crystals and calculated by using the Heron formula.
19 The mitral anulus area was calculated from the 5 corresponding crystals that were broken into 3 triangles and calculated with the Heron formula. The aortic root diameter was calculated with the circumscribe formula.
Each length and area was defined by 2 percentages: (1) the total percentage of change with reference to minimum and maximum value and (2) the percentage change for each phase of the cardiac cycle relative to the total changes over the entire cardiac cycle.
Measurements and statistical analysis
Aortic and mitral anulus dynamic data were calculated separately. 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 means ± 1 SEM. Univariate generalized linear model statistical methods were used to test for significant differences between each aortic base length expansion. Area and length changes of the aortic and mitral anulus within each group were tested for significance by using the Student t test for paired observation. The time-related changes of the aortic base L-NC length and the mitral intertrigonal distance (T1-T2) during each phase of the cardiac cycle were compared by using standard linear regression analysis (the Pearson correlation). The slope-regression parameter was examined by using analysis of variance. All statistical analyses were done with the SPSS 0.9 program.
| Results |
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Aortic anulus base motion during the cardiac cycle
From end-diastole to the first third of ejection, the basal area of the aortic root expanded by +29.8% ± 3.3%, with +50.7% ± 4.5% of the expansion occurring before ejection (Figure 2 and Table 1).
The aortic root basal diameter increased by +10.6% ± 0.3% from end-diastole (20.7 ± 0.4 mm) to the first third of ejection (22.9 ± 0.3 mm). The expansion of the aortic annular base was initiated during late diastole and increased dramatically during the isovolumic contraction until the first third of ejection, when it reached maximum expansion. Although the 3 basal lengths expanded during systole, their expansions were significantly different (generalized linear model, P < .001): R-L (+19.2% ± 2.0%) expanded more than L-NC (+12.9% ± 2.0%) and more than NC-R (+8.4% ± 0.8%). Therefore it was the myocardial septal portion of the aortic root base (R-L basal length) that expanded most during the cardiac cycle, whereas the aortomitral junction (L-NC basal length) increased by +12.9% ± 2.0%.
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| Discussion |
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Previous studies described the aortic valve complex (including the aortic root) as a dynamic structure, expanding before and during ejection as a mechanism to reduce shear stress on the leaflets and to maximize LV function.
1-6 Furthermore, Van Renterghem and colleagues
3 described a heterogeneous motion of the aortic annular base with the expansion of the aortomitral junction (L-NC basal length) while the remaining segments adjoining the myocardium were contracting. Very noisy signals, as well as data available for less than half of the animals, might explain the difference with our study, which confirmed the systolic expansion of the aortomitral junction but also showed the simultaneous expansion of the 2 other segments in significantly different proportions (P < .001).
Mitral anulus motion has been also extensively described by using radiopaque markers, as well as 3-dimensional sonomicrometry.
7,9,10,14,20 According to previous studies, maximum mitral anulus area is observed during early diastole, with most of the annular size reduction occurring during the presystolic period. Proportion differences with other studies might be explained by the hemodynamic conditions, which are known to substantially affect the mitral anulus contraction.
7 The anteroposterior anulus reduction found in our study (23%) was more than double the 8% to 10% reported by Glasson and colleagues.
9 In addition to a possible variability in marker location, the fact that Glasson and colleagues' animals were studied under ß-blockade might explain this difference. More recently, interest has been focused on the heterogeneous mitral anulus motion, with an unexpected systolic expansion of the anterior portion.
9,10 Glasson and coworkers
9 considered that the lengthening of the anterior mitral anulus was possibly related to a passive elongation of the fibrous tissue by the active contraction of the surrounding part of the anulus or LV myocardial fibers.
Although our data confirmed the systolic expansion of the anterior mitral anulus, we hypothesize a different mechanism. Anatomically, both valves are situated in the common orifice at the base of the left ventricle and are separated by the aortic curtain anchored to the 2 fibrous trigones. Superiorly, the aortic curtain is part of the aortic root anulus, and inferiorly, it is in continuity with the anterior leaflet of the mitral valve.
21,22 In an attempt to analyze the functional relationships between the 2 valves, it was decided to study the time-related events in the aortic and mitral anuli. Ascending aortic and LV pressures were required to precisely define the different phases of the cardiac cycle and the percentage of the cyclic changes occurring in each experimental animal.
Analysis of the combined data from the aortic and mitral annular movements clearly showed their complementary synchronicity. The mitral anulus contracted by -16% from mid-diastole to the second half of ejection. Seventy percent of this contraction occurred before the isovolumic phase related to the posterior mitral anulus contraction, whereas the expansion (11.5% ± 2.3%) of the anterior part of the anulus or intertrigonal distance was delayed from late diastole until the first third of ejection. In opposition to mitral orifice contraction, the aortic anulus expanded by about 30% from late diastole to the first third of ejection, with 50% of its expansion occurring during the isovolumic phase (r = 0.85). These changes are surprising given the fibrous nature of the intertrigonal area. However, the explanation became apparent when we analyzed the movements of the crystal placed at the base of the aortic curtain midway between the 2 trigonal crystals (AM). The angle formed by this point (AM) as its apex and both trigones as sides (T1 and T2) showed that it decreased during systole by -9%, which illustrated the posterior bulging of intertrigonal portion (AM) toward the mitral orifice. These findings corroborated previous descriptions of systolic annular folding related to the posterior displacement of the anterior mitral anulus toward the left atrium.
9,11,12
All these data show that the aortic and mitral valves are part of a single structure. Both valves share a common area (the aortic curtain) but also function in synchrony, facilitating their function during the cardiac cycle. During early diastole, the mitral orifice becomes larger because of the very significant expansion of its anteroposterior and transverse diameters. The anteroposterior enlargement is primarily caused by the expansion of the posterior anulus but also by the displacement of the intertrigonal area toward the aortic orifice (reducing its overall length; Figure 5
, a). During systole, the aortic orifice expands, including a displacement of the intertrigonal space toward the posterior mitral anulus, facilitating ejection (Figure 5
, b). The synchronized movements of the mitral and aortic anuli are a complex mechanism designed to facilitate the filling and emptying of the left ventricle.
These findings should have important clinical implications. Mitral or aortic valve replacement with a rigid prosthesis must significantly interfere with the normal movements of the other valve. If the valve is repaired, insertion of a rigid annuloplasty ring that immobilizes not only the posterior mitral anulus but also the aortic curtain must interfere with aortic valve dynamics. It is hoped that these data will stimulate new thinking on the surgical approach to left-side valvular surgery.
Limitations of the study
The main limitation of this study is the comparison of the aortic and mitral anulus dynamics with 2 different groups of animals under different hemodynamic conditions at the time of data recording. Although the mean heart rates were different, cardiac output and systemic pressures were similar. The validity of this comparison lies in the fact that the measurements obtained were not related to absolute time (milliseconds) but to the percentage of change in distances and areas related to each phase of the cardiac cycle in each animal. Because the parameters (aortic and LV pressure) used to define the different phases of the cardiac cycle were identical in both groups, we compared the time-related changes of the aortic and mitral anuli within each phase of the cardiac cycle. Also, the acute and invasive nature of our model, particularly the deleterious effect of cardiopulmonary bypass and ischemia, might have resulted in an abnormal valve behavior. Furthermore, it can also be argued that the high heart rate present at the time of data acquisition (probably caused by catecholamine release) might alter the aortic or mitral annular motion recorded during the shorter cardiac cycles. No autonomic blockade was used to avoid LV function depression and therefore depressed systolic mitral annular motion. The constant patterns found in all animals and the fact that all geometric changes were related to the cardiac phases support the validity of our findings. The possible source of error caused by the presence of crystals and attached electrodes is inherent to all marker techniques. Although the aortic root electrodes were passed through the aortic wall at each location and therefore outside the aortic lumen, the mitral anulus electrodes traversed the left atrium. Furthermore, variability in the precise location of the crystals must be considered, although, being conscious of this problem, all operations were performed by the same individual. Also, it must be pointed out that our findings in the sheep cannot be totally applicable to human subjects.
| Appendix: Discussion |
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Do your conclusions have an implication in understanding the aortic root; that is, does a stentless prosthesis or a rigid ring have the same effect on those dynamics as, for instance, a flexible or rigid ring on the mitral valve?
Dr Lansac. Thank you for this question. I think it is a very good point. The fact is that the increase in length of the intertrigonal distance is not huge, but approximately 2 mm. It is not very accurate to talk about absolute values because they changed between animals.
The fact that the intertrigonal distance is moving with the aortic valve suggests that if you have a flexible device on the aortic side, it will not interfere with the mitral valve. The expansion of the intertrigonal distance was really clearly related to the expansion of the aortic root to maximize ejection. The expansion of the aortic root that we previously studied showed that the aortic volume was expanding more than 30%, and that each area of the aortic root was expanding by 60% at end-diastole. Therefore, it is a combined mechanism to either maximize LV filling or to maximize ejection.
| Acknowledgments |
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| Footnotes |
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| References |
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