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Eur J Cardiothorac Surg 2006;29:353-354
© 2006 Elsevier Science NL
Cardiothoracic Surgery, University Hospital, 3000-075 Coimbra, Portugal
* Tel.: +351 239 400418; fax: +351 239 829674. (Email: antunes.cct.huc{at}sapo.pt).
In a paper published in this issue of the Journal, Campwala et al. [1] review their patients who were subjected to coronary artery bypass surgery (CABG), looking for incidence, predictors and mechanisms of progression of pre-existing or de novo mitral regurgitation (MR). They found that the development of significant MR following isolated CABG is common (16% of their cases). Progression from mild (2+) to moderate or severe MR was observed in one quarter of the patients. Female gender, history of renal insufficiency, lack of beta-blocker use, MR grade and presence of left bundle branch block were found to be independent predictors of MR progression.
The authors attempted to discuss the pathogenesis of mitral regurgitation and hypothesise that it may occur especially in patients with inadequate revascularization, especially in the area of the posterior descending artery, and in patients with ‘natural progression of LV remodelling’. They believe that MR post-CABG may be prevented by an aggressive revascularization strategy, especially in patients with disease of the posterior descending artery, hibernating myocardium or 2+ mitral regurgitation and other risk factors for development of MR. They recommend ‘strong consideration’ of mitral valve repair concomitantly with CABG in patients with mild (2+) MR, as development of moderate to severe (3 to 4+) MR is very common in these cases.
This is an interesting observational study. To my knowledge, it is the first to analyse risk factors for progression of minimal or mild MR in patients undergoing CABG. It has some limitations, which the authors are the first to recognise, especially the fact that it is a retrospective observational study, including a relatively low number of patients studied and consequently, relatively few patients experiencing deterioration of the MR, and the fact that only patients who had preoperative and postoperative echocardiograms were studied. Nonetheless, I believe that these findings could be important to our comprehension of the problem of ischemic mitral regurgitation (IMR) and its treatment.
Chronic (‘functional’) IMR results from LV remodelling, which is translated by enlargement and dysfunction. In turn, it causes further ventricular and atrial enlargement and annular dilatation, thus creating a vicious circle that may not be reversed by correction of the myocardial ischemia alone. Tethering of the leaflets, especially the posterior, may occur due to abnormal motion of the LV wall. Evidently, IMR is not a disease of the mitral valve but of the LV; it is a dynamic dysfunction, caused by one or more of the above referred mechanisms and must be treated if severe (grade 3/4+). There is a distinction between the dysfunction caused by previous infarction and that caused by active (presumably reversible) ischemia. We should not ignore the dysfunction resulting from viable hibernating but recoverable myocardium [2].
IMR occurs in about 10% of coronary bypass operations and is moderate or severe in 4%. It is usually associated to right coronary or circumflex artery disease (posterior papillary muscle), with restricted posterior leaflet motion. Annular dilatation occurs in 100% of cases and is its sole cause in more than half. Hence, most often repair is easy: just an annuloplasty (ring or suture). Valve replacement is rarely required or justified in chronic cases.
Mitral valve repair is now very widely practiced by most surgical groups and, in the hands of the most experienced, feasible in 85–90% of the cases in most types of pathology, including ischemic. In my own experience, it was possible in 93% of all patients with IMR, defined as MR secondary to ischemia or acute myocardial infarction and no history of rheumatic, degenerative or congenital valve disease, treated concomitantly with coronary revascularization.
In 1997, Perier et al. (personal communication) reported the first large series of mitral valve repair in 187 patients with severe IMR. Early mortality was 4.8% and 5-year survival was 54 ± 14% (60 ± 14% in patients with EF > 45%). Freedom from reoperation was 95 ± 4%. These results proved that not only the procedure is feasible with low mortality and morbidity but also it leads to very favourable medium and long-term results, by comparison with the natural history of the disease.
Under these circumstances, the questions to be answered are: what is the severity of MR? Is ischemia reversible? Is remodelling of the LV reversible? And finally, can the late survival of patients with moderate ischemic mitral regurgitation be influenced by intervention on the valve?
In 1993, Dion [3] had demonstrated that IMR has a negative influence on early and late survival, worse if allowed to persist. Hence, intervention on the mitral valve would be indicated. However, Rydén et al. [4], in 2001, found that the grade of MR is reduced or unchanged after CABG in patients with grade 2 IMR and proposed an operative strategy whereby grade 2 ischemic mitral regurgitation should be treated by CABG alone. On the other hand, in 2003, Paparella et al. [5] found that long-term prognosis for MR patients with poor LV function is worse than that in patients with no MR, but MR was not an independent predictor of long-term mortality. In contrast, Aklog et al. [6] found that CABG alone for moderate ischemic MR leaves many patients with significant residual MR and may not be the optimal therapy for most patients. They concluded that ‘a preoperative diagnosis of moderate MR may warrant concomitant mitral annuloplasty’.
There is now strong evidence of improved survival in patients subjected to mitral valve repair of moderate–severe or severe ischemic regurgitation concomitantly with coronary revascularization, but is there a role for combined CABG and mitral valve surgery before regurgitation is severe?
Although this matter is still the subject of much controversy, it is becoming increasingly clear that the poor prognosis of moderate IMR (grade 2/4, ERO < 20 mm2), the uncertainties regarding the evolution of these regurgitations with ventricular remodelling, and the high risk of late reoperation are incentives to associate valve repair with CABG.
Restrictive annuloplasty, suture or ring, is adequate in most cases. Additional procedures may be required in some patients. New techniques, including asymmetric prosthetic rings specifically designed for this type of pathology, have recently evolved. It is still unknown whether they are superior to simple annuloplasty sutures. On the other hand, long-term (for life?) pharmacological unloading of the LV appears essential to promote reverse remodelling and guarantee stability of the mitral valve repair, as LV dilatation has been correlated with progression of MR. Naturally, these considerations would not apply if valve replacement was necessary. The complications associated with valve prostheses and worse long-term results would recommend a more cautious approach in such cases.
In conclusion, in the last few years there has been a renewed interest in the active treatment of IMR, once considered purely functional and, therefore, susceptible of correction by reversion of the ischemia alone. I, like many others, including Campwala et al. [1], believe that a more aggressive approach to the ischemic mitral valve is warranted.
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