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Ann Thorac Surg 2006;82:2102-2109
© 2006 The Society of Thoracic Surgeons

Original Articles: Cardiovascular

Preoperative and Late Postoperative Mitral Regurgitation in Ventricular Reconstruction: Role of Local Left Ventricular Deformation

Giuseppe Barletta, MD, FESCa,*, Anna Toso, MDa, Riccarda Del Bene, MD, PhDa, Marisa Di Donato, MDa, Michel Sabatier, MDb, Vincent Dor, MDb

a Department of the Heart and Vessels, A.O.U. Careggi, Florence, Italy
b Monaco Cardio Thoracic Center, Montecarlo, Monaco

Accepted for publication July 6, 2006.

* Address correspondence to Dr Barletta, Department of the Heart and Vessels, A.O.U. Careggi, Via Mariti 2, Florence 50127, Italy. (Email: g.barletta{at}dac.unifi.it).


   Abstract
Top
 Abstract
Introduction
 Material and Methods
 Results
 Comment
 References
 
BACKGROUND: We sought to analyze the characteristics of local left ventricular deformation related to functional mitral regurgitation (MR) in post–anterior myocardial infarction scar, and to evaluate how local remodeling contributes to late development of MR after surgical ventricular reconstruction by endoventricular circular patch plasty repair.

METHODS: Two hundred twenty-one consecutive patients (aged 60 ± 9 years; 193 males) with previous transmural anterior infarction underwent heart catheterization both before and 1 year after endoventricular circular patch plasty repair. Preoperative global left ventricular shape determinents (eccentricity and circularity indexes), regional curvature and wall motion (centerline), and both preoperative and 1-year postoperative hemodynamic parameters (volumes, ejection fraction, capillary wedge and pulmonary artery pressures) were calculated.

RESULTS: Forty-eight patients had (MR patients), and 173 did not have (NoMR patients) angiographic MR grade 2 or more preoperatively; at follow-up, 30 NoMR patients had MR (late MR [LMR]). Before surgery, MR patients had larger left ventricular volumes, higher capillary wedge and mean pulmonary artery pressures, and lower ejection fraction and cardiac index. The LMR patients had similarly high capillary wedge and pulmonary artery pressures as MR patients; otherwise, they did not differ from NoMR patients. Mitral regurgitation patients had wider lateral wall akinesia and greater inferior wall asynergy; the inferobasal region was hypokinetic in LMR patients. In MR patients, inferior wall systolic curvature was less negative; the inferobasal region had a more positive curvature in LMR patients.

CONCLUSIONS: Local deformation of the inferior wall with loss of systolic inward bending is associated with functional MR, while asynergy and systolic deformation of the inferobasal region and high capillary wedge pressure are prognostic signs of MR development late after endoventricular circular patch plasty repair.


   Introduction
Top
 Abstract
 Introduction
Material and Methods
 Results
 Comment
 References
 
Functional mitral regurgitation (MR) is due to the incomplete closure of the leaflets of a structurally normal mitral valve as a consequence of left ventricular (LV) dysfunction [1, 2] and remodeling. The link between LV remodeling and functional MR has long been investigated, and extensive evidence has shown that functional MR results from LV distortion, which displaces the papillary muscles and tethers the mitral valve coaptation line toward the apex, restricting mitral leaflet closure [1, 3–7]. The pathophysiology of functional MR is even more complex, however, and comprises mitral annulus deformation and perturbed dynamics [8] and impaired LV systolic function. In fact, the annulus contributes to functional MR with dilatation and, more importantly, with reduced presystolic and systolic area shrinkage, while the leaflet closing force mechanism [9] focuses on an imbalance between the transmitral pressure force developed by the left ventricle in systole and the forces hampering mitral leaflet closure, that is increased tethering forces and increased left atrium pressure.

Functional MR is an ominous step toward heart failure [10], and in previous myocardial infarction (MI) is associated with increased mortality [11, 12]. The complexity of LV remodeling in the chronic phase of MI and the difficulties in separating dysfunction and dilation in patients has been acknowledged [13], calling more and more attention on the importance of local distortions in LV shape, as opposed to nonspecific increases in volume or decreases in EF as having a central role in disrupting mitral valve coaptation [14]. In other words, the importance of local remodeling as opposed to global remodeling has emerged as a key issue in our understanding, with theoretic and practical implications.

Surgical ventricular reconstruction in patients with ischemic heart failure is currently being viewed as an opportunity to reduce LV volume, "restore" ventricular geometry, and reverse ischemic MR [15]; however, a paradox has already been evidenced that, in a substantial number of patients without MR preoperatively, MR develops 1 year later [16–18]. The geometric correlates of late MR (LMR) in surgical ventricular reconstruction candidates have already been published [16], but the role of regional deformation was not analyzed, and the late development of MR remains poorly understood. That LMR may be related to local LV deformation is an appealing hypothesis able to open new options in the preoperative assessment of the non-infarcted segments in patients candidates to surgical ventricular reconstruction to optimize the outcome [15].

In the present study, we extended to a large population of consecutive patients with previous anterior post-MI scar, who were candidates to surgical ventricular reconstruction because of heart failure symptoms, the analysis of the geometric correlates of LMR and looked for the possible role played by regional deformation in LMR; further, we sought to identify the predictors, if any, of late development of MR after endoventricular circular patch plasty repair (the Dor procedure). To this purpose, we retrospectively selected a group of patients with previous anterior post-MI scar undergoing endoventricular circular patch plasty repair, and analyzed their preoperative hemodynamic data.


   Material and Methods
Top
 Abstract
 Introduction
 Material and Methods
Results
 Comment
 References
 
Two hundred and twenty-one consecutive patients (mean age, 60 ± 9 years; 193 males) were retrospectively selected among 307 patients with previous anterior MI scheduled for endoventricular circular patch plasty repair, who underwent complete diagnostic hemodynamic study at the Cardiothoracique Center of Monaco from June 1987 to June 1995. The study protocol was approved by the Ethics Committee of the Cardiothoracique Center of Monaco, and the patients agreed by signing an informed consent to adhere to the follow-up schedule. Patients with previous inferior myocardial infarction, clinical or instrumental evidence of valvular, pericardial, congenital or infiltrative heart disease, structural mitral valve lesions, such as mitral prolapse or rheumatic disease, acute myocardial infarction, atrial fibrillation or flutter were excluded. Forty-eight patients had angiographic MR grade 2 or more requiring mitral valve replacement in 13 (MR group). Of the 173 patients without angiographic MR, 30 had MR at the 1-year follow-up hemodynamic study (LMR group): it was mild in 13, moderate in 14, and moderate to severe in 3. The group of patients without MR at any stage comprised 143 patients (NoMR group). In-hospital postoperative medical management was similar among the three groups; chronic medical therapy was left to the discretion of the attending physician.

Patients were studied before surgery and 1 year after surgical ventricular reconstruction by endoventricular circular patch plasty repair [19]; no clinical events had occurred to any patient between discharge and the follow-up reevaluation. Each angiographic study comprised right and left heart catheterization, coronary angiography and ventricular angiography in two consecutive single-plane projections (30 degrees right and 60 degrees left anterior oblique projections). Preoperative endocardial outlines of LV angiograms were traced and digitized using a uniform 0.1-mm sampling (digitizer MYPAD-A3, K-510 mK2).

The normal range of LV function and shape determinants was defined with reference to a previously published group of 32 control patients (20 males, aged 54 ± 10 years), who had no coronary artery disease, history of MI, thoracic surgery, or electrocardiographic abnormalities [20, 21].

Wall motion was analyzed in terms of centerline fractional shortening, and LV volumes calculated according to Chapman, as previously described [21]. The shortening fraction of 90 chords, from the aortic corner (chord 1) to the mitral plane (chord 90), was obtained by dividing the systolic shortening of each chord by the end-diastolic LV perimeter to compensate for differences in size [22], and graphically reported in terms of Z value, that is the standard deviations of mean normal shortening fraction. Akinesia was identified by Z value of fractional shortening of two or more consecutive chords of –2 or less.

The extent of anterior, inferior (right anterior oblique [RAO] projection) and lateral (left anterior oblique [LAO] projection) akinesia was computed. The Duke Jeopardy Score[23, 24]was calculated. The coronary tree was divided into six segments: the left anterior descending coronary artery (LAD), diagonal branches of the LAD, septal perforating branches, the circumflex coronary artery, obtuse marginal branches, and the posterior descending coronary artery. All segments distal to a 70% or greater stenosis were considered to be at risk and assigned 2 points, the maximum possible score being 12.

Global LV shape was evaluated by calculating the eccentricity index [25] and the circular shape index [26] of end-diastolic and end-systolic LV contours in the RAO projection. The eccentricity index, according to an ellipsoidal model, takes into account the major and the minor axes of the left ventricle and ranges between 1 (ellipse) and zero (circle), while the circular index represents the ratio of the original shape to that of a circle, ranging between 1 (circle) and zero (straight line).

Regional LV shape was quantitatively evaluated by measuring the regional curvature (namely, the reciprocal of the radius of the circle that best fits a segment of the arc centred at any point), that was calculated by means of a windowed Fourier series approximation of contours, in which the number of harmonics and the filter-window are chosen locally to minimize the reconstruction errors and maximize the smoothness of the curve [27]. Differently from the original method proposed by Mancini and colleagues [28], this approach analyzes open contours and allows measuring adequately curvatures of the basal LV regions. Curvature analysis in RAO projection started from the anterior aortic corner (point 1) and proceeded clockwise in 90 equidistant points to the mitral plane (point 90); the Z value of curvature was calculated. All shape analyses were carried out by two experienced observers (B.G. and T.A.) who were unaware of the clinical data.

Statistical Analysis
Data are reported as mean ± SD. Comparisons between groups were performed by one-way analysis of variance followed by Bonferroni t test. Comparisons between preoperative and one-year data were performed by two-way repeated measure analysis of variance. Distribution among groups was analyzed by contingency coefficient or Fisher’s exact test. Survival analysis was performed by means of Kaplan-Meier procedure, and comparison among subgroups was performed by log-rank test. The performance of wall motion abnormalities in identifying LMR in all patients without MR before surgery was analyzed by receiver-operating characteristic (ROC) procedure. A probability (p) level less than 0.05 was considered significant.


   Results
Top
 Abstract
 Introduction
 Material and Methods
 Results
Comment
 References
 
The clinical preoperative data are reported in Table 1. The MR patients had a higher prevalence of heart failure, while angina was significantly less frequent in the MR and LMR patients.


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  		Table 1. Preoperative Clinical Characteristics by Groups
 
Preoperatively (Table 2), MR patients had larger LV volumes with higher capillary wedge and mean pulmonary pressures. Worse hemodynamics was indicated by lower ejection fraction and lower cardiac index. LMR patients had similarly higher capillary wedge pressure and mean pulmonary pressure as MR patients, but did not differ from NoMR patients as to the other hemodynamic variables.


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  		Table 2. Preoperative and 1-Year Hemodynamic Data
 
The extent of coronary disease was similar in the groups as indicated by the jeopardy score; details of the coronary lesions are reported in Table 3.


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  		Table 3. Coronary Lesion Distribution (%) in Patients Without MR, With MR, and With Late MR
 
Patients with MR had a wider extent of anterior, inferior and lateral wall akinesia (Table 2); moreover, they had a greater asynergy of the inferior wall (Fig 1). Patients with late MR did not exhibit any difference as to motion of the anterior and lateral walls compared with NoMR patients; they had a lower extent of inferior akinesia, but their inferobasal region was hypokinetic (Z value of fractional shortening ≤ –1; Fig 1). The ROC analysis showed that the areas under the ROC curves relative to the inferobasal region ranged from 0.714 to 0.710 in predicting LMR development: namely, more than 70% of patients with hypokinesia of the central chords of the inferobasal region had late mitral regurgitation.


Figure 1
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  		Fig 1. Preoperative wall motion analysis (centerline method). The plot shows the Z values (mean ± SE) of fractional shortening along the left ventricular (LV) perimeter, from the aortic corner to the mitral plane. The symbol * marks the LV zones of statistical differences in wall motion between mitral regurgitation (MR) patients (solid circles) and no MR (NoMR) patients (open circles). The symbol § marks the LV zones of statistical differences in wall motion between late MR (LMR) patients (squares) and NoMR patients.

 
Global LV diastolic shape indexes did not indicate a more spherical LV shape in MR patients, who, however, had significantly reduced eccentricity and increased circularity in systole with reduced systodiastolic changes in circularity (Table 4) in respect to NoMR patients. Comparing systodiastolic values of regional curvature, MR patients did not modify inferior wall shape, whereas NoMR patients showed a significantly inward bulging of the inferior wall in systole (as shown by more negative curvature; Fig 2).


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  		Table 4. Measurements of Global Left Ventricular Shape
 

Figure 2
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  		Fig 2. Regional curvature analysis. Graphs are reported on three parallel planes: on each plane, systolic (grey circles) and diastolic (black circles) curvature values (mean ± SE) are plotted along the left ventricular (LV) perimeter, from the aortic corner to the mitral plane, for no mitral regurgitation (NoMR) patients in the front plane, for MR patients in the intermediate plane, and for late MR (LMR) patients in the back plane. Arrows ({downarrow}) indicate the area where systolic shape changes are different in NoMR patients in comparison with MR patients (two-way analysis of variance for repeated measures). The negative curvature of the inferior wall of NoMR patients significantly increased, whereas it was unchanged in MR patients.

 
In comparing systolic curvatures among the three groups (Fig 3), LMR patients had a loss of inward bulging of the basal LV regions, as indicated by more positive curvature, mainly of the inferobasal region in respect to patients without MR.


Figure 3
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  		Fig 3. Systolic curvature values (mean ± SE) of no mitral regurgitation (NoMR) patients (black circles), MR patients (dark grey circles), and late MR (LMR) patients (light grey circles), graphically reported along the left ventricular (LV) perimeter from the aortic corner to the mitral plane. The symbols * and {circ} indicate the zones with statistically different curvature values, with respect to NoMR patients, of MR and LMR patients, respectively.

 
Revascularization was always as extensive as possible, without differences among the groups as to number of venous grafts (NoMR, 2.11 ± 0.99; MR, 1.91 ± 0.95; LMR, 1.77 ± 0.77) and left or right internal mammary artery grafts (NoMR, 1.08 ± 0.49; MR, 0.91 ± 0.50; LMR, 1.10 ± 0.40). The grafted territories were similar among groups and are detailed in Table 5.


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  		Table 5. Revascularization Pattern
 
At 1 year (Table 2), the beneficial effects of ventricular reconstruction were evident in all patients, but the increase in EF was lower and mean pulmonary pressure was greater in LMR patients: the reduction in LV volumes was less, and the increase in capillary wedge pressure was greater, most probably as a result of the late development of MR.

Survival at 1 year showed increased mortality for MR patients (20.8 % versus 7% in NoMR and 3.3% in LMR patients, Fisher exact test = 7.985, p = 0.014). The Kaplan-Meier curve up to 120 months (Fig 4) showed that survival was less in the MR group (log-rank [Mantel-Cox] {chi}2 = 8.588, p = 0.018), but no difference exists between LMR and NoMR. It is worth noting that no difference in survival among the groups was evident when deaths after the first month were considered (log-rank [Mantel-Cox] {chi}2 = 0.612, p = not significant).


Figure 4
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  		Fig 4. Kaplan-Meier curves in patients without mitral regurgitation (NoMR = solid line), with preoperative mitral regurgitation (MR = dotted line), and with late mitral regurgitation (LMR = dashed line). Numbers represent patients at risk for each group. Survival was better for NoMR and LMR patients than for MR patients, but after the first month (operative mortality), the survival curves were similar.

 

   Comment
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
References
 
Mitral regurgitation in ischemic heart disease affects 19% of patients after MI [10, 29]. In our selected population of chronic post-MI myocardial scar patients, the incidence of angiographic grade 2 or more MR at the time of the preoperative evaluation was somewhat higher, reaching 21.7%, although in keeping with the referral for surgery, which was based on the severity of heart failure symptoms more than angina.

Greater akinesia of the lateral wall, asynergy, and local deformation (loss of negative curvature) of the inferior wall characterized patients with preoperative MR, pointing at tethering of papillary muscles and tenting of mitral leaflets as the pathophysiologic mechanism of MR. While the greater asynergy of the anterolateral wall reflects the magnitude of the ischemic damage, asynergy of the inferior wall was unlikely related to an ischemic substratum, because the entity of right coronary disease was the same in MR patients as compared with NoMR patients.

The loss of negative systolic curvature of the inferior region has emerged as a key element of MR in post-MI anterior aneurysm patients (see Fig 5), in keeping with the notion that preserved inward bending of the inferior wall before surgery is an important predictor of functional recovery after ventricular restoration [30, 31]. The loss of inward bulging (less negative curvature) of the inferior region influenced systolic eccentricity and circularity, which decreased and increased, respectively, without sphericalization [30] of the left ventricle at global LV shape analysis. The increase in sphericity index at end-systole has been suggested as the only predictor of the increase in MR after coronary bypass and ring annuloplasty [32].


Figure 5
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  		Fig 5. Mechanism of negative systolic curvature. On the top row: mean diastolic (grey dots) and systolic (black dots) ventricular contours of mitral regurgitation (MR) patients (A) and no MR patients (B) were reconstructed by Fourier shape analysis (24 harmonics) by using the average spectrum of each group in comparison. The shape difference between the two groups is well apparent. On the bottom row: a scheme illustrating how the presence of a negative systolic curvature of the inferior wall (B—short arrows) preserves mitral leaflet coaptation, while its absence (ie, positive curvature; A—upward vertical arrow) tethers the papillary muscle (PM) and tents mitral leaflets promoting MR. (AO = aorta.)

 
The importance of end-systolic inferior wall curvature and its relation to functional MR in anterior aneurysms may gain an even more intriguing meaning within the framework of the myocardial band concept introduced by Torrent-Guasp and colleagues [33]. In keeping with the myocardial band theory, the inferior wall and the inferior papillary muscle should represent the site where descending fibers of the apical loop have just changed their orientation becoming ascendant (Fig 6). Therefore, the inferior wall has predominantly longitudinal fibers, as stated by Streeter [34], whose contraction, according to the myocardial band theory is end systolic or early diastolic and responsible for the lengthening of LV cavity which precedes and permits diastolic filling. It is conceivable that in a setting like this, end-systolic curvature of the inferior wall is a key determinant of mitral valve closure: if the inferior wall has a normal negative curvature (ie, convex toward LV cavity shape), contraction does not preclude mitral leaflet coaptation; if curvature is less or not at all negative (ie, flat or concave shape), mitral leaflet tenting ensues.


Figure 6
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  		Fig 6. The myocardial band according to Torrent-Guasp and colleagues [33] is shown, modified to show the projection of the left ventricular basal loop onto the angiographic right anterior oblique (RAO) view, and to indicate its continuity with the anterolateral region and the posterior papillary muscle. (Ao = aorta; apm = anterior papillary muscle; AS = ascending segment; DS = descending segment; lf = left trigonus; LFW = left free wall; PA = pulmonary artery; ppm = posterior papillary muscle; rf = right trigonus; RFW = right free wall.)

 
The appreciation of a putative cause-effect relation between MR and inferior wall deformation and flattening supports innovative surgical approaches to MR based on local reverse remodeling of the inferior wall, able to affect the pathophysiologic mechanism of MR [35] better than ring annuloplasty alone, which reduces tethering only at the annular and not at the ventricular end, and whose limitations have recently been outlined [32].

A not insignificant percentage of patients undergoing endoventricular circular patch plasty repair at the Monaco Cardio Thoracic Center who did not have preoperative MR eventually had LMR over the follow-up [16]. Kihara and colleagues [18] recently reported similar data, whereas Yuge and colleagues [17] found even higher values in a much smaller population. Late MR did not represent an important feature of clinical deterioration in the present study, as it was mild or moderate in the majority of cases. Kaplan-Meier analysis of survival is in keeping with this view and showed no difference in mortality at a very long term follow-up (at least 7 years), although its development might determine a worse late outcome.

The hemodynamic burden imposed by MR generated similar changes in LV geometry both in case of preoperative MR and when MR developed after endoventricular circular patch plasty repair. We sought to identify the variables that could differentiate among patients without preoperative MR those who will and those who will not have late MR. Two key factors had statistical significance: asynergy and deformation of the inferobasal region of the left ventricle, and high values of capillary wedge pressure in the absence of any specific reason for that. The myocardial band theory may help explain the functional importance of preoperative shape and asynergy of the inferobasal region in the development of MR after ventricular restoration surgery. The LV inferolateral region belongs to the basal circumferential loop of the myocardial band; however, it should be the site where the basal loop continues into the descending loop (Fig 5). Such a continuity may explain the functional and morphologic impairment of a region remote from the ischemic damage. The link between asynergy and deformation of the inferobasal region and late MR can be identified in the interference between the circumferentially arranged myocardial fibers of ventricular origin that insert into the posterior muscular component of the mitral annulus and the systolic contraction of the annulus itself.

The complexity of the interplay is even bigger because impaired annulus contraction not only is dependent on, but also causes abnormal function of the basal LV regions. In this scenario, preexisting high capillary wedge pressure may contribute to MR development by hampering the closure kinetics of the mitral leaflets owing to a reduced driving pressure (where driving pressure equals LV systolic pressure minus left atrial systolic pressure) [9]; thus, it also may interfere with left atrium function and consequently with the presystolic annulus shrinkage [36]. Far from being just speculations, we believe that the preoperative identification of key elements able to trigger the possible development of functional MR in patients scheduled for surgical ventricular reconstruction could guide both the surgical and postoperative therapeutic strategy.

Limitations of the Study
The era of three-dimensional analysis has started and new insights into LV remodeling and mitral annulus shape and function will refine our understanding of the mechanisms of functional MR. Nonetheless, three-dimensional analysis is still on its way and is far from being validated, standardized, and widely applied in the clinical arena; therefore, sound old methods need not be disregarded yet [37].

Curvature analysis is free of geometric assumptions, provides some regional shape information, and can compare shape with a population-derived normal value. However, curvature is sensitive to noise in border tracing, and interpretation of this parameter is less than intuitive, since regional shape abnormalities affect curvature not in the region itself but at its boundaries. Furthermore, the method assumes an anatomic correspondence between each point on the patient’s and the normal reference’s LV silhouettes.

Conclusions
The present angiographic study identifies local deformation and reduced wall motion of the inferobasal region of the left ventricle and increased capillary wedge pressure as preoperative predictors of late occurrence of mitral regurgitation after surgical ventricular reconstruction. Despite the concern that late development of MR after the Dor procedure has raised, our survival results indicate that MR does not impact negatively on survival. The data presented in this study refer to a historic series of patients operated upon between 1989 and 1995. Since then, our surgical approach has slightly changed: mitral valve repair is now the first choice and is performed more frequently, and the mortality rate, which was high with mitral replacement, has significantly decreased (to less than 10% since 1998). The new surgical tool represented by the balloon sizer technique may further reduce the eventual development of mitral regurgitation after endoventricular plasty patch repair.


   References
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 References
 

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Jerry Braun
Ann. Thorac. Surg. 2006 82: 2110. [Extract] [Full Text] [PDF]



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Ann. Thorac. Surg., December 1, 2006; 82(6): 2110 - 2110.
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