Management of mitral regurgitation in heart failure patients

As the failing left ventricle dilates the papillary muscles are displaced, the coaptation of the mitral valve leaflets is decreased, and a central jet of mitral regurgitation appears (fig 11.1). Mitral regurgitation leads to more volume

Figure 11.6. The Alfieri suture for mitral regurgitation. This creates a double channel mitral orifice.
Figure 11.7. One dimensional (M mode) echocardiography showing dramatically improved left ventricular function in an infant six months after partial left ventriculectomy for ischaemic cardiomyopathy in anomalous left coronary artery from the pulmonary artery.
Table 11.4 Mitral valve repair in dilated cardiomyopathy. Left ventricular function and flow before and after annuloplasty




% change*

p Value

End diastolic volume (ml)

335 (107)

307 (103)




End systolic volume (ml)

227 (l0l)

237 (98)




Stroke volume (ml)

58 (l3)

70 (21)

+ 12



Ejection fraction (%)


24 (10)




Mitral inflow (l/mm)

12.4 (5.3)

5.4 (0.5)




Forward cardiac output (l/min)

3.2 (l.o)

4.7 (0.9)




Regurgitant volume (l/min)

9.2 (5.4)

0.8 (0.6)


6 (10.1)


Regurgitant fraction (%)

70 (14)

15 (11)




Values are mean (SD). *Percentage change from preoperative study at 4-6 months postoperatively. NYHA class fell significantly from 3.9 (0.4) to 1.8 (0.5) (p < 0.001).

Reproduced from Bolling etal. J Thorac Cardiovasc Surg 1998;115: 381-8. with permission of the publisher.

Values are mean (SD). *Percentage change from preoperative study at 4-6 months postoperatively. NYHA class fell significantly from 3.9 (0.4) to 1.8 (0.5) (p < 0.001).

Reproduced from Bolling etal. J Thorac Cardiovasc Surg 1998;115: 381-8. with permission of the publisher.

overload of the already dilated left ventricle. Reports of prohibitive operative mortality for mitral valve replacement in dilated cardiomy-opathy patients in the early 1980s suggested that the failing ventricle deteriorates further, if the "blow off" into the left atrium is removed. However, new information shows that mitral valve repair (or replacement) with preservation of the subvalvar apparatus carries low perioperative mortality, good medium term survival, and symptomatic relief through improvement in cardiac index.22

There are now a number of clinical situations where mitral valve repair with or without revascularisation improves outlook for the heart failure patient. These include:

• Ischaemia manifest by angina and variable mitral regurgitation which becomes significantly worse during an acute ischemic episode, causing dyspnoea at rest or left ventricular failure with pulmonary oedema.

• Acute myocardial ischaemia or infarction located inferobasally (right coronary or dominant circumflex distribution) which causes sudden posteromedial papillary muscle dysfunction and mitral regurgitation.

• Acute catastrophic pulmonary oedema caused by papillary muscle rupture (inferobasal in 75% of cases) several days after acute myocardial infarction.

• Chronic progressive dyspnoea (NYHA III or IV) associated with previous myocardial infarction, an enlarged dysfunctional left ventricle, and varying degrees of pulmonary hypertension. This comprises the largest group.

• Patients with idiopathic dilated cardiomyopathy and annular dilatation producing moderate to severe mitral regurgitation through inadequate leaflet coaptation.

The recommended threshold for mitral repair in ischaemic regurgitation is a left ventricular end systolic volume index > 80 ml/ m2 or a calculated regurgitant fraction > 50% of the forward LVEF. Patients with angina, good target vessels, mild to moderate mitral regurgitation, and reversible ischaemia poste-rolaterally on the PET scan can be treated by revascularisation alone. Should valve replacement prove necessary, as much of the subvalvar apparatus as possible should be conserved to maintain left ventricular geometry and function. Division of all chordae tendonae is accompanied by a 47% reduction in LVEmax.

Ischaemic mitral regurgitation is a functional problem of unsuccessful coordination of the entire mitral apparatus rather than simple failure of a single papillary muscle. Two techniques have provided symptomatic improvement in this condition. Firstly, mitral annuloplasty with significant undersizing of the valve ring greatly increases leaflet coaptation.23 Systolic anterior motion (SAM) is avoided because of widening of the aortomitral angle and increased left ventricular size. The undersized valve ring acutely remodels the base of the myopathic heart, helping to re-establish an ellipsoid shape to the left ventricle. Second, and simpler, is the Alfieri stitch. This can be performed either centrally (fig 11.6) or towards the side of the ischaemic papillary muscle.

Bolling has shown the important effect of mitral repair in patients with end stage dilated cardiomyopathy.22 All had severe left ventricular systolic dysfunction with preoperative LVEF ranging from 8-25% (mean 16 (3)%). The average duration of cardiomyopathy was 4 (6) years (range 0-16). All patients underwent remodelling ring annuloplasty with an undersized flexible ring. Half had tricuspid annulo-plasty. Hospital mortality was < 2% while 12 and 24 month survival were 82% and 72%. All patients were restored to NYHA class I or II with mean postoperative LVEF of 26%. Peak exercise Vo2 max rose from a mean of 14.5 to 18.6 ml/kg/min. Echocardiography at two years showed a pronounced reduction in sphericity, regurgitant volume, and regurgitant fraction. LVEF, end diastolic and end systolic volumes were all improved (table 11.4).

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