Fig. 13.1
Left ventricular remodeling. Contrast-enhanced cardiac Magnetic Resonance. (a) Left panel: LV chamber appears dilated and distorted. (b) Right panel: late gadolinium enhancement images showing extensive antero-apical ventricular remodeling in 2-chamber view surrounded by transmural fibrosis
Although the knowledge of the mechanisms underlying ischemic mitral regurgitation has improved over half a century, many aspects remain controversial, leaving the therapeutic strategies perplexing in their diversity and not fully effective. Indeed, chronic ischemic MR is a “complex and dynamic disease”, involving coronary arteries, mitral annulus, subvalvular apparatus and ventricle, in which the large number of geometric and hemodynamic variables and the complex interaction between each other carries the risk of a suboptimal result when treated.
From Ischemic LV Remodeling to Mitral Regurgitation: In Search of the Target Lesion
LV remodeling is a complex, dynamic and time-dependent process, which may occur in different clinical conditions, including MI, leading to chamber dilatation, altered configuration and increased wall stress [6]. It begins within the first few hours after an MI and results from fibrotic repair of the necrotic area with scar formation, elongation, and thinning of the infarcted zone. LV volumes increase, a response that is sometimes considered adaptive, associated with stroke volume augmentation in an effort to maintain a normal cardiac output as the ejection fraction declines. However, beyond this early stage, the remodeling process is driven predominantly by eccentric hypertrophy of the non-infarcted remote regions, resulting in increased wall stress, chamber enlargement and geometric distortion [7]. These changes, along with a decline in performance of hypertrophied myocyte, increased neurohormonal activation, collagen synthesis, fibrosis and remodeling of the extracellular matrix within the non-infarcted zone, result in a progressive decline in ventricular performance [8]. At the same time, the papillary muscle (PM) displacement, which may occur as a consequence of the LV dilatation, results in leaflet tethering of the mitral valve at closure with lack of a proper coaptation, in turn leading to secondary MR (Fig. 13.2). In addition, ventricular dilatation results in annular enlargement, which further increases valve incompetence. Indeed, after the first description by Burch et al. [9] in 1963 supporting the central role of PM dysfunction as the basic mechanism of ischemic MR, a large number of experimental and clinical studies have reported contrary results. Large-animal models have shown that both left ventricular dilation and posterior PM infarction were necessary for the development of MR [10]. A retrospective study by Okayama et al. [11] in patients with single-vessel coronary disease using cardiac magnetic resonance (CMR) to quantify PM infarction and MR found an association between the presence of delayed enhancement (DE) in PM and MR, specifically in patients with large infarctions and bilateral PM enhancement. Other studies, however, have underlined a weaker role for PMs in ischemic MR. Dog models of ischemic MR showed that when PM was selectively infarcted, it did not produce MR, whereas larger infarctions encompassing the PM and adjacent myocardium did produce MR [12]. In the same study by Okayama et al. [11], patients with single vessel right coronary artery disease as well as PM infarction had less MR than patients who had no PM infarction.
Fig. 13.2
Ischemic mitral regurgitation. Apical 4- (a) and 2-chamber (b) view showing ischemic MR
One of the latest studies seems to have elegantly reconciled this old debate to better clarify the role of papillary muscles compared to that of the adjacent remodeled LV wall. In a large prospective cohort of 153 patients with first ST-segment elevation MI without intrinsic mitral valve disease, Chinitz et al. [13] evaluated the incidence and severity of ischemic MR as well as coronary and ventricular anatomy using a multimodality imaging (echocardiography to quantify MR, angiography to identify the culprit coronary lesions, and a high resolution DE-CMR sequence to define the extent of PM infarction – partial vs. complete – and ventricular infarction). The results showed that neither complete nor partial PM infarction necessarily led to the development of MR. However, the amount of infarcted myocardium was significantly associated with the development of ischemic MR, even after a multivariate analysis, confirming the role of the underlying ventricular infarction and adverse remodeling as the primary culprit for the development and progression of chronic ischemic MR. Furthermore, once established, ischemic MR, can itself worsen the remodeling process, altering LV loading conditions, increasing diastolic wall stress (which can worsen eccentric hypertrophy with further LV dilatation and dysfunction) and end-systolic wall stress in patients with chronic MR because of induced LV remodeling, with decreased contractility and increased end-systolic volume, driving a vicious circle in which MR begets more MR [14]. Having said that, it is still unclear if the volume overload created by MR adds a greater pathologic burden to an already adverse condition or, simply, the worse prognosis is related to a poorer LV function and functional MR is merely an indicator of this bad condition.
Ischemic Mitral Regurgitation According Different Phenotypes of LV Remodeling
Usually, ischemic MR occurs in nearly 50–60 % of patients with previous inferior MI due to a bulging of the inferior and posterior LV basal and midventricular segments underlying the PMs [3, 15, 16]. However, clinical studies, including one of the most recent from Levine and co-workers, outlined the importance of anteroapical MI causing MR despite the absence of inferobasal wall motion abnormalities [17]. In this case, mitral regurgitation grade correlated most strongly with tethering length due to the displacement of the papillary muscles.
Recently, our group addressed the differences between anterior and posterior remodeling in patients with previous MI undergoing surgical ventricular reconstruction (SVR) [18]. From a morphological point of view, post-infarction remodeling occurred at different LV levels in the two study groups (A, anterior versus P, posterior). The LV apex is primarily involved after an anterior MI (Fig. 13.3, left panel), as we previously reported [19]. As a consequence, the conicity index (obtained from the apical to short axis ratio) was significantly greater in the anterior remodeling group (A) compared to posterior (P). Conversely, a previous inferior MI determined a regional remodeling of the basal and mid segments of the inferopostero-lateral wall (Fig. 13.3, right panel), with a significant increase in LV transverse diameters and consequently in the sphericity index (obtained from the short to long axis ratio). LV basal involvement in posterior dilatation causes lateral displacement of the posteromedial PM leading to a significant increase in the interpapillary distance in Group P compared to Group A. As a consequence, patients in group P presented with a higher incidence of severe MR (55 % vs 25 %, respectively, p = 0.01), which determined higher LV mass, larger left atrium dimensions, higher pulmonary artery pressure and higher rate of right ventricular dysfunction. After analyzing the data according to the presence or not of moderate to severe MR in the two different patterns of LV remodeling, we observed that in posterior remodeling the main geometrical change associated with severe MR was an increase in the interpapillary distance, without significant difference in the tenting area. On the contrary in anterior remodeling, MR occurs mainly in the setting of global LV dilatation, with tethering of both mitral valve leaflets due to apical displacement of PMs; hence, increased mitral tenting area was the major determinant of severe MR, without a concomitant significant increase in interpapillary distance. Furthermore, when Cox Regression analysis was applied separately to the two study groups, severe preoperative MR remained a significant independent predictor of long-term mortality in Group A but not in Group P. We speculated that, behind the above mentioned geometrical assumptions, in patients with previous anterior MI, MR occurs mainly in the setting of global LV dilatation and severe dysfunction, reflecting a more advanced stage of disease.
Fig. 13.3
(a) Left panel: the LV apex is primarily involved after an anterior MI. As a consequence, the conicity index (CI, obtained from the apical – c – to short axis ratio – b) is significantly greater in the anterior remodeling compared to posterior remodeling group. (b) Right panel: a previous inferior MI induces a regional remodeling of the basal and mid segments of the inferopostero-lateral wall, with a significant increase in LV transverse diameters and consequently in the sphericity index (SI, obtained from the short – b -to long axis ratio – a)
This is also consistent with the fact that, in the group A, patients with severe MR showed worsened right ventricular function compared to patients with mild MR. This phenomenon was not observed in the group P even though in both groups, patients with severe MR showed a similar increase in systolic pulmonary artery pressure.
Surgical Operative techniques
The Rationale to Perform Surgical Ventricular Reconstruction to Reverse LV Remodeling
Surgical Ventricular Reconstruction (SVR) of the LV chamber has been introduced as an optional therapeutic strategy aiming to reduce LV volumes through the exclusion of the scar tissue from the LV cavity, thereby reducing the ventricle size to a more physiological volume, reshaping the distorted chamber and improving cardiac function through a reduction of LV wall stress in accordance with the principle of Laplace’s law. Since LV wall stress is directly proportional to LV internal radius and pressure, and inversely proportional to wall thickness, any intervention to optimize this relationship would be beneficial either in terms of improving wall compliance and reducing filling pressure, or as wall stress is a crucial determinant of afterload, in terms of enhancing contractile performance of the LV by increasing the extent and velocity of systolic fiber shortening [20]. Furthermore, SVR of failing ventricles is usually combined with myocardial revascularization with the aim of treating the underlying coronary artery disease, although in recent years the percentage of patients with ischemic LV dysfunction without significant coronary disease has increased due previous percutaneous coronary interventions (PCI). Lastly, SVR offers either the possibility to repair the mitral valve through the LV opening or the potential of improving mitral functioning by improving the LV [21, 22].
SVR Technique
The operation is performed under cardiac arrest, with antegrade cold crystalloid cardioplegia. A complete myocardial revascularization is performed first, when indicated, with particular attention to revascularize the proximal left anterior descending segment, to preserve the upper part of the septum. For this purpose, a left internal mammary artery is almost always placed on the left anterior descending artery. Revascularization is completed, when indicated, through sequential saphenous vein coronary bypass grafting on other diseased coronary arteries.
After completion of coronary grafting, the ventricle is opened with an incision parallel to the left anterior descending artery, starting at the middle scarred region and ending at the apex. The cavity is carefully inspected and any thrombus is removed if present. The surgeon identifies the transitional zone between scarred and non-scarred tissue, driven by cardiac magnetic resonance with late gadolinium enhancement (LGE), when previously performed, or alternatively by echocardiographic analysis. After that, a pre-shaped mannequin is inserted into the LV chamber and inflated with saline (Fig. 13.4, upper panel on the left). The mannequin is useful to optimize the size and shape of the new LV, particularly when the ventricle is not very enlarged (to reduce the risk of a too small residual cavity), or when the transitional zone between scarred and non-scarred tissue is not clearly demarcated, as occurs in akinetic remodeling. Furthermore, the mannequin is useful in giving the surgeon the correct position of the apex and in maintaining the long axis of the ventricle in a physiologic range (7.5/8.5), reducing thereby the risk of sphericalization of the new ventricle. The size of the device is defined by multiplying the body surface area of the patient by 50 ml. The exclusion of dyskinetic or akinetic LV free wall is performed through an endoventricular circular suture passed in the tissue of the transitional zone (Fig. 13.4, upper panel on the right). The conical shape of the mannequin guides the orientation of the plane of the endoventricular circular suture at the transitional zone, obliquely towards the aortic flow tract, mainly in rebuilding the new apex. The reconstruction of the apex may be difficult when the apical and inferior regions are severely dilated and scarred; in this case, a plication of the distal inferior wall is performed before patch suturing, thus placing the apex in a more superior position leaving a small portion of scar. The mannequin is removed before the closure of the ventricle and the opening is closed with a direct suture (simple stiches) if it is less than 3 cm large or with an elliptical, synthetic patch if greater than 3 cm to avoid distortion of the cavity (Fig. 13.4, lower panel on the left). In the first case, a second stratum with the excluded tissue is sutured on the first suture to avoid bleeding. If the closure is performed by using a patch (usually a Dacron patch), a few millimeters of border is left when sewing the patch in an everting way (Fig. 13.4, lower panel on the right). This technique assures a good hemostasis and makes it easier to put some additional stiches, if needed. The position of the patch is crucial in determining the residual shape of the new ventricle. To this aim, the surgeon pays attention to positioning the patch with an oblique orientation, toward the aortic outflow tract. In this way we avoid obtaining a box-like shape of the ventricle that may occur when the orientation of the patch is almost parallel to the mitral valve. More recently, the growing number of PCI has changed the pattern of LV remodeling in that the classical, dyskinetic aneurysm has almost disappeared and there is an increased incidence of a more diffuse akinetic remodeling. In the latter case, the use of the mannequin is crucial in determining the final result. The LV cavity is restored using the mannequin as a cast and the wall is closed with a running suture over the mannequin without a suture on the transitional zone. The final shape is more elliptical because the surgeon starts the suture in a higher position close to the aortic valve.
Fig. 13.4
SVR procedure for anterior remodeling (schematic). Upper panel: The mannequin is inside the ventricle (on the left); the circular suture follows the curvature of the mannequin to re-shape the ventricle in an elliptical way (on the right). Lower panel: The patch is used to close the ventricular opening
Mitral Valve Repair
When indicated, the mitral valve is repaired through the ventricular opening with a double arm stitch running from one trigone to the other one, embedding the two arms in the posterior anulus of the mitral valve (Fig. 13.5). To avoid tears of the posterior left of the mitral valve (as has previously occurred), the suture is reinforced with a Teflon strip. After that, the suture is tied to undersize the mitral orifice. A Hegar sizer no. 26 is used to size the mitral annulus. Alternatively, a restrictive mitral annuloplasty with a ring implantation may be performed in selected patients, when the LV opening is not big enough to have a good exposition of the mitral valve.
Fig. 13.5
Mitral valve repair. Mitral valve is repaired through the ventricular opening with a double arm stitch running from one trigone to the other one
Tailored Approaches
The surgical procedure as described above is usually performed to reverse LV remodeling after an anterior MI. However, the procedure may be tailored to approach different patterns of post-infarction LV remodeling, varying from the classic posterior aneurysm with a bulging of the inferior wall and a well-defined neck (Fig. 13.6), to a global LV dilatation with regional wall dysfunction at the inferior and posterior region, according to the site of coronary occlusion (Fig. 13.7). Surgery for the posterior aneurysm generally involves a patch to close the neck of the aneurysm. Otherwise, the treatment of global dilatation of the infero-posterior wall is more complex and varies according to the relationship between the site of the scar and the dilatation (with or without involvement of the posterior septum) with respect to the papillary muscles. After an inferior MI, there are two possibilities: a – the dilatation is mainly between the two papillary muscles (Fig. 13.8) or b – the dilatation is between the posteromedial papillary muscle and the septum, which is deeply involved (Fig. 13.9). We use two techniques for LV dilatation after an inferior MI. The first involves opening the scarred wall at the level of the scar or at the level of the collapsed area, parallel to the posterior descending artery (Fig. 13.10, on the left panel). A continuous 2/0 Prolene suture is performed to obtain the re-approximation of the two papillary muscles and the exclusion of the entire dilated zone. The suture is started at the beginning of the dilatation (sometimes just at the level of the mitral annulus) and continues toward the apex. According to the second technique, the wall is opened and the continuous suture is brought behind the posteromedial papillary muscle, bringing the posterior wall against the septum.
