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a Department of CT Surgery, ISMETT, University of Pittsburgh Medical Center, Palermo, Italy
b Office of Research and Biomedical Sciences, ISMETT, University of Pittsburgh Medical Center, Palermo, Italy
c Department of Radiology, ISMETT, University of Pittsburgh Medical Center, Palermo, Italy
Received 4 April 2008; received in revised form 17 July 2008; accepted 28 July 2008.
* Corresponding author. Address: Department of CT Surgery, ISMETT – Mediterranean Institute for Transplantation and Advanced Specialized Therapies, UPMC – University of Pittsburgh Medical Center, Via Tricomi 1, 90127 Palermo, Italy. Tel.: +39 0912192111; fax: +39 0912192354. (Email: gdancona{at}ismett.edu).
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Abstract |
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 Top Abstract 1. Introduction2. Materials and methods3. Results4. Discussion5. Limitations6. ConclusionReferences |
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Key Words: Ischemic • Mitral • Regurgitation • MRI
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1. Introduction |
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TopAbstract1. Introduction2. Materials and methods3. Results4. Discussion5. Limitations6. ConclusionReferences |
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Although a global change in the geometrical relationships among the various components of the unit ventricle-mitral valve apparatus may take place in patients with impaired LV function, these modifications may not always justify the development of IMVR.
In this regard, in our clinical practice we frequently observe a plethora of patients with severely compromised cardiac contractility and dilated ventricular chambers that present with absolutely preserved MV function.
To understand why patients with equally impaired LVEF behave differently in relation to their MV continence, we should extend our analyses beyond the simple geometrical evaluation of the heart and consider, simultaneously, the impact of regional myocardial vitality and perfusion. For this purpose, a comprehensive imaging modality such as cardiac magnetic resonance imaging (MRI) could allow us to depict a clearer image of IMVR in patients with depressed LVEF thus clarifying the purely geometrical and functional modifications that lead to this deleterious occurrence.
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2. Materials and methods |
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TopAbstract1. Introduction2. Materials and methods3. Results4. Discussion5. Limitations6. ConclusionReferences |
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We have summarized our standardized protocol for cardiac MRI in patients with IMVR, and specified the variables of interest to specifically evaluate MV function/morphology, LV function/morphology, and myocardial function/vitality (global and segmental) [1].
In this manuscript, we report our cardiac MRI findings in a series of non-consecutive patients with three vessels coronary artery disease (CAD), depressed LVEF (<40%), and with or without IMVR.
After admission, patients underwent transthoracic echocardiography to confirm cardiac function and evaluate MV function/morphology.
Patients who presented MV or MV apparatus structural abnormalities were excluded from this analysis as well as those that had already undergone any sort of interventional procedure (either invasive cardiology or surgical approach), or had any contraindication to MRI (hemodynamic instability, claustrophobia, presence of in-body paramagnetic material).
After quantitative evaluation of MV regurgitation with echocardiography, two groups were identified: CAD without IMVR (group CAD) and with IMVR (group IMV). Cardiac MRIs recorded variables included: anterior MV leaflet length, MV annular septo-lateral diameter, MV annular inter-commissural diameter, MV annular degree of circularization (septo-lateral diameter/inter-commissural diameter), MV annular area, inter PM distance (PMD), coaptation depth (CD) in 2 and 4 chambers, and tenting area (TA) in 2 and 4 chambers (Fig. 1 ). Whenever appropriate, measurements were taken in systole and diastole. Furthermore, quantitative evaluation of MV regurgitation was performed when present, together with LV end systolic volume (ESV), LV end diastolic volume (EDV), LVEF% (((EDV – ESV)/EDV) x 100), and forward LVEF% (((EDV – ESV – MV regurgitant volume)/EDV) x 100). Perfusion/vitality study was also performed with gadolinium and data recorded following the American Society of Echocardiography scheme of 17 ventricular segments [2].
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To investigate correlation between the different MRI geometrical variables, the presence of MVR, and LVEF%, Pearson correlation test was performed in the overall group.
As LVEF% did not have a normal distribution, logarithmic transformation of LVEF% was used.
Multivariable analysis was performed to identify independent determinants for occurrence of IMVR (logistic regression, stepwise forward procedure) and for log LVEF% (linear regression, stepwise procedure).
The two multivariable analysis models were built including all those variables that at Pearson correlation test had a correlation with IMVR and LVEF% (p < 0.05). All statistical analyses were performed using SPSS (SPSS Inc., Chicago, Ill, United States).
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3. Results |
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TopAbstract1. Introduction2. Materials and methods3. Results4. Discussion5. Limitations6. ConclusionReferences |
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Geometrical measurements were considered before and after indexing for anterior MV leaflet length, as previously indicated [3]. Univariate analysis findings are summarized in Table 1 . As expected, MV regurgitation volume was significantly higher in the IMV group (24.0 ± 12.0 vs 4.5 ± 5.2; p < 0.001) (Table 1). Conventional LVEF% was comparable in the two groups (IMV 34.6 ± 13.0 vs CAD 31.5 ± 13.0; p = ns) as well as forward LVEF% (IMV 24.4 ± 12.1 vs CAD 33.6 ± 12.4; p = ns) (Table 1). Although annular MV area, and annular inter-commissural diameters in systole and diastole were significantly higher in the IMV group, after indexing for anterior MV leaflet length no statistically significant difference was noticed between the two groups (Table 1).
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No independent determinant for occurrence of IMVR was identified (Table 5 ). Left ventricular volumes (end-systolic and diastolic) were the sole independent determinants for log10 LVEF% (Table 6 ).
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4. Discussion |
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TopAbstract1. Introduction2. Materials and methods3. Results4. Discussion5. Limitations6. ConclusionReferences |
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As this condition is associated with excess cardiac morbidity and mortality even in the presence of mild to moderate regurgitation [5], many authors have focused their research on identifying the mechanisms that would lead to the development of IMVR in an attempt to better stratify patients at risk and guide treatment.
Correct understanding of mechanisms leading to IMVR is even more crucial in patients with depressed LVEF%.
We have evaluated with cardiac MRI the impact of LV global and segmental myocardial scarring, LVEF%, as well as various geometric and functional variables of the MV apparatus, on the development of IMVR in patients with LV dysfunction.
Use of cardiac MRI in a similar context has been previously suggested by Sirchai et al. [6].
Our main finding is a higher rate of necrotic areas in the inferior myocardial segments in patients with IMVR. Furthermore, myocardial segmental delayed enhancement had the strongest univariate correlation with occurrence of MV regurgitation.
In our experience, LV dimensions and LVEF% seem to have no direct impact on the development of IMVR and, consequently, equally enlarged ventricles may develop unequal degrees of MV regurgitation.
We believe that, per se, an enlarged ventricle will not automatically lead to an ischemic MV and that the location of the myocardial necrosis will play the main role in the ethiopathogenesis of MV regurgitation. Similar results were reported by Kumanohoso et al. [7] in an evaluation involving patients with prior myocardial infarction (MI) (anterior and inferior) and normal control subjects. The authors evaluated the grade of IMVR by means of quantitative echocardiography and reported that, although global LV dilatation and dysfunction were significantly less pronounced in patients with inferior MI, the percentage of mitral regurgitation jet area and the incidence of significant regurgitation were greater in these patients [7].
This would confirm that IMVR may occur in normally sized ventricles and, in the event of extreme LV dilatation, will occur mainly if the inferior myocardium is necrotic.
We should also emphasize the fact that, in our present analysis, most of the patients had only mild MV regurgitation. In fact, in patients with more advanced mitral regurgitation, the effect of blood volume loading on the left ventricle would become more substantial and, at this advanced stage, it would become more difficult to recognize cause from effect.
The role of MV annular dilatation in the pathogenesis of ischemic MV regurgitation remains controversial. In this regard, many authors have reported that isolated annular dilation does not usually cause important functional mitral regurgitation as leaflet tissue redundancy protects against leaflet abnormal coaptation in isolated annular dilatation [8,9].
However, many others have reported, in different cohorts of patients with IMVR and in animal experimentation, significant increases in either MV septo-lateral or inter-commissural diameters [10–14].
Differently from the majority of the available literature, and as suggested by Jorapur et al. [3], we have used anterior mitral leaflet length to index geometric measurements of the MV apparatus. Anterior leaflet and intertrigonal distance (the distance between the trigones, which corresponds to the fibrous portion of the mitral annulus) are not significantly affected by left ventricular remodeling and have been used as reference measurements for sizing mitral annuloplasty rings.
The importance of using an indexing parameter is reflected in our univariate analysis where MV inter-commissural distance and MV annular area are significantly correlated to occurrence of MV regurgitation only before being indexed by anterior MV leaflet length.
The current leading surgical technique for the treatment of ischemic MV regurgitation is based on the assumption that MV annulus is firmly anchored along the circumference of the anterior leaflet by the tough fibrous skeleton of the heart and, therefore, dilatation of the MV annulus primarily affects the posterior leaflet. As a consequence, all current operative mitral repair strategies contemplate reduction of the MV inlet area by posterior leaflet annuloplasty.
We believe that ischemic MV regurgitation occurs within a more complex scenario that is actually reflected by the high rate of MV regurgitation recurrence after simple posterior annuloplasty [15]. In this context, Gelsomino et al. have recently shown that independent predictors of recurrent MV regurgitation after restrictive annuloplasty include mainly ventricular variables such as end systolic volume, systolic sphericity index, myocardial performance index, and wall motion score index [16].
Altered PMs geometry has been hypothesized as part of the pathogenesis of ischemic MV regurgitation [3,7].
In several MRI studies, Kaji et al. confirmed the importance of the posterior PM displacement (with consequent increase in posterior papillary muscle-septal annulus distance) [11]. Yu et al. reported similar findings concluding that the inter-PMs distance of more than 32 mm and the distance from the anterior mitral annulus to the posterior PM root of more than 64 mm readily distinguished ischemic MV patients from healthy controls and isolated CAD patients [14].
Finally, inter-PMs distance was proposed as an independent predictor for mid-term failure after MV repair for IMVR [17].
In our analysis, inter-PMs distance (absolute and indexed) was homogeneously distributed in patients with and without IMVR and, furthermore, there was not significant correlation between inter-PMs distance and occurrence of MV regurgitation in the overall group. Our findings may be biased by the fact we did not calculate the distance between PMs and MV annulus although we did focus on inter-papillary muscles distance. On the other hand, we found no correlation between the amount of IMVR and the coaptation depth (which would be a surrogate of the distance between PMs and MV annular plane).
In our univariate analysis, non-indexed inter-PMs distance correlated with LVEF%. At multivariable analysis, LV volumes were the sole independent determinants for LVEF%.
This confirms the fact that PMs distance may be a good indicator of LV function and dilatation albeit not necessarily correlated to the degree of IMVR.
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5. Limitations |
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TopAbstract1. Introduction2. Materials and methods3. Results4. Discussion5. Limitations6. ConclusionReferences |
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Finally, as already underlined in the discussion, evaluation of inter-PMs distance was limited to the inter-PMs measurements without taking into consideration the distance from the PMs to the MV annulus. We deliberately decided to concentrate on this parameter as we accepted MV coaptation depth and MV tenting area as good indirect indicators of the distance between PMs and MV.
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6. Conclusion |
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TopAbstract1. Introduction2. Materials and methods3. Results4. Discussion5. Limitations6. ConclusionReferences |
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We are aware that the relatively small number of patients studied in the present analysis may not be sufficient to clearly differentiate the causes in the genesis of IMVR.
At the same time we can suggest that in patients with depressed LVEF%, ischemic MV cannot be explained by global LV and MV geometrical modifications alone. Although PM distance, LV volumes, and LVEF% are correlated, they have no direct independent impact in the development of IMVR. In contrast, inferior myocardial necrosis and increased inter-commissural MV diameters may lead to deformity of MV complex and subsequent IMVR.
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References |
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TopAbstract1. Introduction2. Materials and methods3. Results4. Discussion5. Limitations6. ConclusionReferences |
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