11.6.10 Secondary MI due to LV failure

• Traction on the chords prevents systolic mitral occlusion due to LV dilatation and sphericity (outward displacement of the chords);
• Desynchronisation of papillary contraction;
• Annular dilatation;
• Insufficient contraction force to occlude the mitral valve (occlusion force too low compared to traction force);
• Fibrosis and loss of LV compliance.

Figure 11.85: Restrictive MI (type IIIb) in a dilated LV. In systole, the leaflets are trapped within the LV by its dilation. The degree of restriction is defined by the distance from the point of coaptation to the plane of the mitral annulus (tenting distance), the triangular area between the leaflets and the plane of the annulus (tenting area), and the angle of closure of the anterior leaflet measured between the plane of the annulus and the tip of the leaflet [15]. The ratio of LV long to short axis diameter defines the degree of sphericity (normal long to short axis ratio: > 1.5).

 LV dilatation can affect the mitral valve in two different ways [13,15].

• Proportional MI: There is a linear relationship between regurgitant orifice area and LV dilatation (papillary muscle widening, mitral annulus dilatation and flattening). MI decreases in response to pharmacological treatment of ventricular dilatation or the introduction of ventricular assist devices. However, concomitant plasty does not give favourable results [14].
• Disproportionate MI: The MI is larger than would be predicted by the degree of LV dilatation because of local remodelling or out-of-sync papillary muscle contraction (conduction delay). If the QRS is widened, MI tends to worsen with medical treatment of left-sided dilatation. Resynchronisation and MitraClip™ plasty are effective here [21].

MI occurs in 40-60% of cases of left ventricular failure and is a sign of worsening prognosis [11]. Unless severe, the treatment of MI is primarily that of left ventricular failure (see Chapter 12 Treatment of chronic left ventricular failure).

• Converting enzyme inhibitor (CEI) or angiotensin II receptor antagonist (ARA), sacubitril-valsartan combination;
• Beta blocker;
• Anti-aldosterone (spironolactone, epleronone);
• Resynchronisation with a triple-chamber pacemaker: reducing desynchronisation in papillary muscle contraction reduces MI by up to 50% [7].

Correction of MI in dilatative cardiomyopathy is only indicated if the patient remains symptomatic and the MI progresses despite maximal treatment. It only makes sense if there is some likelihood of reversing ventricular remodelling. If the remodelling or pulmonary hypertension is irreversible, suppressing the MI will not change the prognosis, although it will reduce LV volume overload [3,11]. The less advanced the disease, the better the outcome. The clinical results of recent trials summarise the situation [3].

• In centres with extensive experience, mitral valve repair with a restrictive ring has an operative mortality rate of 1.6-5%; patients' functional capacity and quality of life are improved, but the survival rate remains unchanged: 70% at 2 years, 55% at 5 years [10,18].
• The recurrence rate of 20-30% is high because the progression of the primary disease is not interrupted by the operation; certain echocardiographic features are predictive of recurrence [8].
  • Angle of closure of the anterior leaflet with the plane of the mitral annulus > 25°;
  • Angle of closure of the posterior leaflet with the plane of the mitral annulus > 45°;
  • Distance between the coaptation point and the plane of the mitral annulus > 1.1 mm;
  • Tent area between the leaflets and the plane of the mitral annulus > 2.5 cm2;
  • EF < 0.25;
  • LV Vtd > 250 mL, LV Dts > 4.0 to 4.5 cm (difference between European and American recommendations).
• The operative risk of MVR (6-10%) is higher than that of plasty, but the failure rate is much lower; MVR must respect the subvalvular apparatus because the loss of the LV internal skeleton in the context of ventricular failure leads to massive dilatation.
• When the LV is dilated due to aortic insufficiency (telesystolic diameter 6.9 cm), concomitant correction of a moderate MI by plasty does not affect survival and offers no advantage over simple AVR, as the MI resolves in 88% of cases by correction of the AI alone [9].
• The recently fashionable combination of mitral valve surgery with ventricular restraint or resection and plasty of the dyskinetic zone offers no short-term morbidity or mortality benefit, despite the reduction in ventricular dimensions, reduction in MI and increase in EF, and worsens diastolic function [1,22]. Ventricular reduction performed simultaneously with surgical treatment of coronary ischaemia (CABG) or valvular heart disease (mitral valve replacement) does not reduce mortality or morbidity in patients with left heart failure: the operative mortality rate is 4-6% and the 5-year survival rate is 60% in both groups of patients (CABG alone or CABG + LV reduction + mitral valve replacement) [6].
• The current trend in refractory and decompensated left heart failure is towards ventricular assist devices, which solve the problem of MI.

Percutaneous clipping plasty of the end of each leaflet (MitraClip™ plasty) allows non-invasive reduction of MI (see  Endoprosthetic heart valves). When compared to surgical repair, MitraClip™ has a higher technical failure rate (3.2% vs 0.6%, 25-33% residual MI), but significantly lower operative mortality (3.3% vs 16.2%), stroke rate (1.1% vs 4.5%) and bleeding risk (4.2% vs 59%) in high-risk categories [4,16,20]. Current recommendations consider the MitraClip™ appropriate for symptomatic patients with severe primary or secondary MI despite optimal medical therapy, who are considered too high risk for surgery (mortality > 8% for MVR and > 6% for MVP) and who have a life expectancy of at least 1 year [2,12]. Patients with an MI that is disproportionate to the degree of ventricular dilatation are the ones who benefit from clipping [17].

Functional MI in dilatative cardiomyopathy is highly variable depending on haemodynamic conditions. The IPPV acts as a prosthesis for the LV and systemic vasodilatation improves its ejection. Therefore, in GA, regurgitation tends to decrease. When its assessment has a direct therapeutic implication (e.g. unplanned insertion of a support ring), it is of utmost importance to respect two conditions when measuring MI.

• Quantification using techniques that are less dependent on haemodynamics, such as vena contracta diameter, PISA, regurgitant volume calculation or three-dimensional planimetry [5];
• Restoration of baseline conditions: normal SAR (phenylephrine bolus for MAP ≥ 80 mmHg), satisfactory CO (dobutamine infusion), acceptable preload (PCWP ≥ 12 mmHg), ventilator apnoea, no PEEP/CPAP.

 Principle of anaesthesia

Both LV ejection and MI are reduced by systemic vasodilation and positive inotropic stimulation. Patients are usually on maximal therapy.

• Remodelling inhibitors: ACE inhibitors, beta blockers;
• Reduction of LV Vtd with vasodilators: ACE inhibitors, nitroprusside, nitroglycerin;
• Inotropic stimulation: dobutamine, milrinone, epinephrine, levosimendan;
• Pacemaker resynchronisation;
• In acute situations: intra-aortic balloon pump; IABP is particularly effective in reducing MI.

Pre-operative treatment should be maintained until surgery and continued intraoperatively (catecholamines, IABP). If possible, the resynchronisation pacemaker should be left in place, as MI worsens immediately if it is interrupted (use bipolar coagulation) [7]. The preferred choice of inotropes is inodilators (dobutamine, milrinone, levosimendan) and myocardial receptors β1, β2 and α stimulants (adrenaline) because of the changes in the receptor population typical of ventricular failure (decrease in in β1, increase in α ).

• Preload: hypervolemia is the rule due to left heart failure and pulmonary congestion; perfusion and saline intake must therefore be restricted as patients suffer from water and salt retention, and nitroglycerine may be added.
• Afterload: must remain low; reduce SAR with nitroprusside, nitroglycerine, isoflurane.
• Contractility: must be supported by positive inotropic agents, often in high doses (dobutamine, milrinone + epinephrine, levosimendan); IABP is very effective in reducing MI.
• Frequency: maintain 70-80 beats/min as flow rate is highly dependent on frequency given fixed stroke volume.
• Pulmonary arterial pressure: lower PAR by hyperventilation in PHT.
• Positive pressure ventilation: beneficial for LV function and reduction of MI, difficult to wean. 

• Induction with etomidate.
• Maintain with isoflurane and fentanyl; alternative: infusion of midazolam.
• Restrict fluid and saline intake; give preference to vasoconstrictors and positive inotropes for hypotension.
• IPPVI as required, no early extubation after ECC.
• Special monitoring:
  • TEE (changes in MI, LV size and function);
  • Pulmonary artery catheter (PAP, PCWP, anterograde stroke volume, SvO₂); 
  • ScO₂ (peripheral perfusion).
• For more details, see Chapter 12, Anaesthesia for Ventricular Failure.