11.13.3 Aortic stenosis and mitral insufficiency

 This combination is the most common (20% of polyvalvulopathies) [2]. In the presence of MI, the LV functions with two outlets for ejection: the aortic valve (anterograde) and the mitral valve (retrograde). By slowing anterograde ejection, aortic stenosis increases the regurgitant fraction and potentiates MI. Dilatation of the LA reduces the preload required to maintain systolic volume across the stenosis. Enlarged by the volume overload, the LV must eject against a high afterload while working over a large radius of curvature, which is mechanically very unfavourable. By facilitating LV ejection, MI leads to an underestimation of this ventricular dysfunction; the EF is very optimistic compared to the functional reality of the LV. On echocardiography, the LV is larger than in pure aortic stenosis. The combination of AS + MI is usually due to ARF, but is also seen in calcific degeneration in the elderly, in which case the MI is secondary to calcification of the mitral leaflets and annulus. MI may also be purely functional, associated with pressure overload and LV dysfunction (50% of cases), in which case the leaflets are normal and the insufficiency is usually moderate.

The presence of a significant MI in a patient undergoing aortic valve replacement raises the problem of simultaneous correction of the two pathologies, which means an increase in operative mortality: on average 2.7% for single AVR and 6.5% for double replacement [5]. It is important to define the mechanism and severity of MI as accurately as possible in order to make an optimal surgical decision [1,3,4].

• Severe MI: a regurgitant orifice > 0.4 cm² and a vena contracta > 0.7 cm in structural MI (> 0.3 cm² and > 0.4 cm in ischaemic MI) are the most relevant indices. Colour jet size, PISA and regurgitation fraction are too dependent on haemodynamic conditions (increased LV afterload due to aortic stenosis). The presence of a severe MI is generally accepted as an indication for simultaneous replacement (MVR) or plasty (MVP), as it triples the mortality of AVR and the risk of cardiogenic shock during perioperative haemodynamic changes. On the other hand, there is virtually no likelihood of subsequent regression [6].
• Moderate to severe MI (regurgitant orifice 0.2-0.4 cm² and vena contracta 0.3-0.6 cm): This doubles the operative mortality of AVR. If it is structural, there is a tendency to treat it at the same time if the operative risk is low or moderate (probable mortality of the combined operation < 5%) [4].
• Functional MI: With reduction of intraventricular pressure, it regresses after AVR in half of the cases, but does not improve in the long term in the other half [7].
• Factors favouring regression of MI after AVR: functional MI due to LV dysfunction, high preoperative aortic transvalvular pressure gradient.
• Factors associated with non-regression of MI after AVR: degenerative or rheumatic MI, mitral annular calcification, LA dilatation, chronic AF, pulmonary hypertension.

In patients at low or intermediate surgical risk with moderate-to-severe MI with a low probability of regression after AVR (structural MI), the surgical risk of double replacement is justified. If the surgical risk is high or the probability of regression of the MI is high (functional MI), single AVR is preferred [3].

The ideal conditions for each of the two pathologies appear to be contradictory; in fact, SAR should be high due to aortic stenosis to ensure coronary perfusion and low to limit MI. In reality, the increase in afterload is much more related to the aortic stenosis, which is fixed, than to SAR which is distal to the aortic valve. SAR can therefore be maintained with a vasopressor according to myocardial perfusion requirements without significantly affecting MI.

 

Hemodynamics in aortic stenosis and mitral insufficiency

Aortic stenosis is the most dangerous component. High preload Normal to low rate Contractility preserved (inotropic support required) SAR preserved (diastolic blood pressure) Low PAR

 

 

© CHASSOT PG, BETTEX D, August 2011, last update November 2019