الفهرس 
Introduction & Aim Of The WorkOnly 14 pages are availabe for public view
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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.