What is the Role of Surgery in the Treatment of Ischaemic Mitral Regurgitation?21 March 2017
By: Sitara Khan
Ischaemic mitral regurgitation (MR) refers to regurgitation that results not because of a structural abnormality through the mitral valve, but rather due to a distortion of the subvalvular apparatus by enlargement and remodelling of the left ventricle, due to ischaemic heart disease. It is important to note that although the pathology arises as a consequence of previous myocardial infarction, it does not necessarily imply ongoing active ischaemia. Furthermore, it is not to be confused with the MR that results in the acute setting of a myocardial infarction that has resulted in rupture of a papillary muscle. The nomenclature can be confusing, as the terms “secondary” and “functional” MR are also used. The prevalence of ischaemic MR in the post-acute phase following MI has been varyingly reported as 8-74%1. One of the more robust studies, which included echocardiographic data on nearly 800 patients, reported an incidence of approximately 50%, with severe MR occurring in 12%2.
Remodelling of the infarcted left ventricle results in mitral regurgitation by i) reducing the closing forces of the valve due to LV dysfunction (hypokinetic areas and dyssynchrony) and ii) tethering of the leaflets due to apical and lateral displacement of the papillary muscle, and annular dilation. Importantly, it is a dynamic condition, the severity of which can vary with loading conditions.
Why is it Important?
In the chronic phase post-MI, ischaemic MR is associated with excess mortality independently of baseline characteristics and degree of LV dysfunction. Grigioni et al3 observed a 5-year survival of 30±5% in 200 patients with ischaemic MR >16 days post-MI, compared to 50±6% in 109 matched controls. The adjusted relative risk of mortality in the presence of ischaemic MR was 1.88. The mortality risk is related directly to the degree of MR, as defined by effective regurgitant orifice and regurgitant volume. Therefore, detecting and quantifying ischaemic MR provides important information for risk stratification and clinical decision making in the chronic post-MI phase.
Repair or Replacement for Patients with Severe MR?
In patients with organic MR – in which the regurgitation is due to a structural abnormality of the valve leaflets or chordae (e.g. mitral valve prolapse) – repair of the valve is superior to replacement. However, the optimal surgical technique in ischaemic MR is not well-defined. A randomised controlled trial assigned 251 patients with severe ischemic mitral regurgitation to undergo either mitral-valve repair or chordal-sparing replacement4. The primary end-point was the imaging parameter of LV end-systolic volume index (LVESVI) at 12 months. (A primary end-point of survival would have required the enrolment of thousands of patients). The two groups had similar LVESVI, LV ejection fraction, death rate, functional status and adverse cardiac / cerebrovascular events at 12 months. However, the rate of recurrence of moderate or severe MR was higher in the repair group than in the replacement group (32.6% vs. 2.3%, P<0.001). The authors concluded that there was no significant difference in LV reverse remodelling or survival at 12 months between patients who underwent mitral-valve repair and those who underwent mitral-valve replacement. Replacement provided a more durable correction of mitral regurgitation, but there was no significant between-group difference in clinical outcomes. However, the two-year outcomes of this study show that in fact there were more frequent heart failure – related adverse events and cardiovascular admissions in the repair group5.
Does Valve Surgery Improve Outcome in Patients with Moderate MR Undergoing Coronary Artery Bypass Grafting (CABG)?
The first randomised trial to study this involved 102 patients, and found an improvement in LV reverse remodelling (assessed using end-diastolic and end-systolic dimensions) and heart failure symptoms in the CABG plus MV repair group compared to the group that underwent CABG alone6. More recently, a larger randomised study involving 301 patients found no significant difference in reverse LV remodelling (assessed by measuring LVESVI) or survival at 2 years7. Concomitant mitral valve repair was associated with a reduced prevalence of moderate or severe mitral regurgitation, but this did not improve survival or reduce overall adverse events or readmissions. Indeed, patients in the MV repair group had an increased rate of neurological events, which were attributed to the longer time on cardiopulmonary bypass, and risk of embolisation. The MV repair group patients also had a higher rate of supraventricular arrhythmias, probably again due to the the more invasive nature of the surgery required (left atrial incision required for exposure of the valve).
What do the guidelines say?
It should be noted that the European Society of Cardiology (ESC) Guidelines on the Management of Valvular Disease were released in 2012, prior to the publication of several randomised trials mentioned above8. Optimal medical treatment is essential, and patients enrolled in the trials described above were receiving this. Therapies such as ACE-inhibitors and beta blockers, by promoting reverse LV remodelling, should reduce the tethering force that promotes regurgitation. Cardiac resynchronisation therapy is also recommended in appropriate patients, and by restoring papillary muscle synchrony, may increase closing forces, and thus improve regurgitation.
In patients with severe ischaemic MR who are undergoing CABG, and have an LV ejection fraction >30%, the level of recommendation for valve surgery is class I, with valve repair being preferable. This recommendation falls to IIa if the patient has moderate (as opposed to severe) MR. There is also a IIa recommendation for patients with severe MR but an ejection fraction <30%, who have a revascularisation option and evidence of viability. If patients have severe MR but no revascularisation option, then surgery is a class IIb recommendation if they are symptomatic on optimal medical and device therapy, and have a low co-morbid status.
Ischaemic MR results from distortion of the subvalvular apparatus from ventricular remodelling in coronary artery disease. It is common, occurring in up to half of patients post- myocardial infarction. Its presence confers a poor prognosis, increasing the relative risk of death at 5 years by nearly two-fold. There are relatively few randomised trials that have studied the effects of valve surgery on patients with ischaemic MR, but almost all of them have been published since the 2012 ESC guidelines on valvular disease. The current ESC guidelines recommend valve repair over replacement, with a class I recommendation in severe MR and EF > 30%, and class IIa recommendations in patients with moderate MR / EF <30%.
1 Agricola E et al. Ischemic mitral regurgitation: mechanisms and echocardiographic classification. Eur J Echocardiogr. 2008 Mar;9(2):207-21.
2 Bursi F et al. Heart failure and death after myocardial infarction in the community: the emerging role of mitral regurgitation. Circulation. 2005, vol. 111 (pg. 295-301).
3 Grigioni et al. Ischemic mitral regurgitation: long-term outcome and prognostic implications with quantitative Doppler assessment Circulation. 2001;103:1759-1764
4 Acker et al. Mitral-valve repair versus replacement for severe ischemic mitral regurgitation. N Engl J Med 2014; 370:23-32.
5 Goldstein D. Two-Year Outcomes of Surgical Treatment of Severe Ischemic Mitral Regurgitation. N Engl J Med 2016; 374:344-353.
6 Fattouch K. POINT: Efficacy of adding mitral valve restrictive annuloplasty to coronary artery bypass grafting in patients with moderate ischemic mitral valve regurgitation: a randomized trial.
J Thorac Cardiovasc Surg. 2009 Aug;138(2):278-85.
8 Vahanian et al. Guidelines on the management of valvular heart disease (version 2012).
Joint Task Force on the Management of Valvular Heart Disease of the European Society of Cardiology (ESC).; European Association for Cardio-Thoracic Surgery (EACTS)., Eur Heart J. 2012 ct;33(19):2451-96.
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