الفهرس | Only 14 pages are availabe for public view |
Abstract The human heart has four valves of which the mitral valve connects the LA and the LV. The normal function of the mitral valve depends on its six anatomic components, which are: the LA wall, the annulus, the leaflets, the chordae tendineae, the papillary muscles, and the LV wall. Any disorder of individual components can disturb the finely coordinated mechanisms of the mitral valve and result in an incompetent valve. It is important to distinguish ischemic mitral regurgitation from mitral regurgitation resulting from other etiologies. IMR is defined as a disease of the LV where mitral insufficiency occurs as a result of myocardial infarction or ischemia. Carpentier introduced a functional classification of mitral regurgitation based on leaflet movement: Type I with normal leaflet movement; Type II with exaggerated leaflet movement; and Type IIIa and IIIb with restricted leaflet movement in diastole and systole, respectively. Mitral regurgitation complicates 40 % of the cases of myocardial infarction and is classified as acute or chronic ischemic mitral regurgitation based on the pathophysiologic mechanism responsible for the regurgitation. After infarction, the papillary muscles are displaced laterally, apically and posteriorly, pulling the leaflet into the left ventricle. Distortion is prominent in the basal anterior leaflet, creating a bend (seagull sign). Papillary muscle dysfunction plays only a minor role compared with apical and inferior papillary muscle displacement caused by ischaemic left ventricular remodeling and dilatation. Because tendinous chords are not extensible, papillary muscle displacement exerts traction on the leaflet, causing tethering, apical leaflet displacement, and impaired coaptation between the leaflets. Together with annular flattening, enlargement, dilatation, and reduced contraction, mitral valve tenting affects leaflet coaptation and causes functional mitral regurgitation in the presence of a structurally normal valve and subvalvular apparatus. A number of surgical techniques have been developed for ischemic mitral regurgitation, but none of these strategies has resulted in clearly improved patient outcomes. Although most surgeons would agree that severe mitral regurgitation should be corrected at the time of CABG and that trivial to mild mitral regurgitation can probably be left alone, the optimal management of moderate ischemic mitral regurgitation remains controversial. Those favoring a conservative approach make several arguments. First, revascularizing ischemic areas will improve regional wall motion and IMR. Second, several studies suggest that performing CABG alone, even if some residual mitral regurgitation persists, does not affect survival. Third, mitral valve surgery adds significantly to the operative risk of CABG. Fourth, patients with IMR tend to have small left atria, which makes mitral valve exposure and repair difficult. However, many surgeons have advocated more liberal use of mitral repair in patients with moderate IMR at the time of CABG. They present several key arguments: The preoperative echocardiogram represents a brief snapshot of the severity of mitral regurgitation at the time of diagnosis. The fact that many patients with “moderate” mitral regurgitation present with significant symptoms of congestive heart failure or enlarged left atria suggests that they probably have frequent episodes of more severe mitral regurgitation.CABG alone will not correct moderate IMR in many patients. Significant residual mitral regurgitation can result in symptoms and decreased survival. Mitral annuloplasty is technically feasible, and it alone will almost always correct moderate ischemic mitral regurgitation, which makes mitral valve replacement never necessary. Mitral valve repair can now be performed at the time of CABG with an operative mortality rate as low as 3% to 4%. When significant residual mitral regurgitation remains, it exposes the patient to the potential need for reoperative mitral valve surgery in the presence of patent grafts, which carries significant operative risk. We evaluated short term outcome of ischemic moderate mitral regurgitation (IMR) after myocardial revascularization alone versus revascularization combined with mitral valve repair. group (I) was comprised of 20 IHD patients with IMR who underwent CABG for revascularization alone and was compared with group (II) comprised of another 20 IHD patients with IMR who underwent revascularization together with MV repair. The preoperative profile of both patient groups was similar with no statistically significant differences as regards to age, sex, and risk factors for IHD, clinical status, and preoperative investigations. The majority of our patients in both groups were in a NYHA class of II-III (NYHA class III in 55% in group I and 60% in group II). It was found in both groups that 45% of the patients in group I and 55% of the patients in group II had a previous posteroinferior infarction. On clinical evaluation of our patients, we found that 45% of the patients in group I and 50% in group II had a murmur on cardiac auscultation. In our study, it was found that there was no correlation between the preoperative left atrial dimension and the presence of moderate IMR. The operative and postoperative results of our two studied groups were similar. There were no statistically significant differences as regards the total bypass and ischaemic times, weaning off bypass, the dosage or length of time patients were on inotropic support, the need for IABP counterpulsation, the period of mechanical ventilation, the total blood loss, the perioperative morbidity or mortality, and the total period of ICU or hospital stay. In our operative results, TEE downgraded the mean of the jet area from 5 ± 0.2 in group I and 5.5 ± 0.5 in group II by echo preoperatively to 4.5 ± 0.4 in group I and 5 ± 0.4 in group II. Comparing the TEE results of the two study groups, pre and postoperative showed no statistical significance between group I who did revascularization alone and group II who did both revascularization and undersized ring. The ICU course (duration of mechanical ventilation, inotropes/hour, ICU stay) of both groups showed no statistical difference. There was no statistically significant difference in the improvement of the ejection fraction between the 2 groups. Furthermore, in group I patients who had revascularization alone, the grade of mitral regurge dropped in 17 patients to absent or grade 1-2 while in group II, 19 patients dropped to absent or grade 1-2. There was no statistical significance between the two study groups. There is discrepancy in the literature as to agreement with these results. In the follow-up period, we assessed the patients ED, ES, LA and EF. There were no statistical differences between the 2 studied groups concerning their echo finding. Using Spearman’s rank correlation coefficient, we tried to find whether any correlation existed between these variables, and the grade of IMR postoperatively. A positive correlation was found between preoperative LVEDD and LVESD on one side and the degree of postoperative EF on the other side. A negative correlation was demonstrated between the preoperative EF%, grafting of PDA and the grade of postoperative IMR. |