Chapter 10 – Mitral Valve Surgery

Abstract

The normal adult MV area is 4–6 cm2. Unlike other heart valves, the MV consists of two asymmetric leaflets. The aortic (anterior) leaflet makes up 65% of the valve area but its base forms only 35% of the circumference. The mural (posterior) leaflet usually consists of three main scallops, although there may be up to five. The leaflets are joined at the anterolateral and posteromedial ends of the commissure. The aortic MV leaflet shares the same fibrous attachment as the non-coronary cusp of the AV.

Chapter 10 Mitral Valve Surgery

Jonathan H. Mackay and Francis C. Wells

The normal adult MV area is 4–6 cm². Unlike other heart valves, the MV consists of two asymmetric leaflets. The aortic (anterior) leaflet makes up 65% of the valve area but its base forms only 35% of the circumference. The mural (posterior) leaflet usually consists of three main scallops, although there may be up to five. The leaflets are joined at the anterolateral and posteromedial ends of the commissure. The aortic MV leaflet shares the same fibrous attachment as the non-coronary cusp of the AV.

The complete valve apparatus consists of the leaflets, which arise from the A-V junction and the chordae tendinae. The chordae connect the leaflets to the papillary muscles, muscular projections from the non-compacted layer of the LV (Figure 10.1). There are two principal fibrous condensations that form the trigones; posterosuperior and antero-inferior. They are placed approximately equidistant within the sector of the valve between the two lateral ends of the commissure. This fibrous condensation extends for up to a third of the circumference of the orifice. It is commonly misstated that there is a complete annulus of circumferential fibrous tissue.

Figure 10.1 Mitral leaflet opening during diastole, and coaptation (central overlap) and apposition (relative height of leaflets) during systole. CT, chordae tendinae; PM, papillary muscle.

During diastole, MV leaflet opening should permit unimpeded flow from LA to LV. During systole, coaptation of the MV leaflets protects the pulmonary circulation from high LV pressures. The tensor apparatus, consisting of the chordae tendinae and papillary muscles, makes significant contributions to the LV function and ejection fraction.

MV surgery is still most often undertaken through a sternotomy though right thoracotomy may be used particularly for redo MV surgery. Minimal access surgery, which entails peripheral cannulation and a right mini-thoracotomy, is becoming more widespread. Its benefits await substantiation by a prospective randomized study (see Chapter 12).

Mitral Stenosis

MS in adults is defined as a valve area of less than 2 cm² and is classified as severe or critical when the valve area is less than 1 cm². The vast majority of cases are secondary to rheumatic fever, although a history of an earlier acute febrile illness is often absent. Leaflet thickening and commissural fusion occurs secondary to the inflammatory process. Other valve diseases, particularly involving aortic and tricuspid valves, are common. Pure MS is less common than mixed stenosis and regurgitation, as a result of the fixed orifice.

Clinical Features

Exertional dyspnoea is the commonest presentation and the onset is usually insidious. Other presentations include haemoptysis, new-onset AF or peripheral embolic events.

Pathophysiology

Fixed obstruction to blood flow between the LA and the LV creates a pressure gradient across the MV. The left atrial pressure (LAP) increases to maintain the CO.

Pressure gradient = [ Flow Rate/( K × valve area ) ]²

where K is the hydraulic constant. An elevated LAP and the presence of a low LVEDP results in an increased MV gradient (Figure 10.2). The consequences of an elevated LAP include:

LA hypertrophy and, later, dilatation
AF
Reduced pulmonary compliance
PHT and eventually RV ‘stress’ and TR

AF reduces the LV filling particularly when associated with fast ventricular rates. PHT is initially reversible but becomes irreversible following sustained chronic elevation of PVR.

Figure 10.2 Pressure waves for MS

The LV pressure–volume loop in MS is small and shifted to the left due to a reduction in LV pressure and volume loading (Figure 10.3).

Figure 10.3 LV pressure–volume loop in MS

The LV systolic function may be depressed due to myocardial fibrosis and chronic underloading. Figure 10.4 illustrates the effect of reducing the valve orifice area on the relationship between transmitral flow rate and pressure gradient. Decreasing the MV area has a dramatic effect on the flow rate required to generate the diastolic pressure gradient at which pulmonary oedema develops.

Figure 10.4 Rate of transmitral diastolic blood flow versus mean diastolic MV gradient for normal (4–6 cm²) and stenotic MVs (0.5–2 cm²)

Investigations

2D echocardiography: Leaflets thickened, possibly calcified, doming and reduced opening.
PWD gradient (pressure half-time; PH-T): MV inflow is quantified with PWD or CWD (Figure 10.5). The rate of fall of blood flow velocity of the E (early diastolic filling) wave is attenuated in MS. The PH-T method uses the slope of E-wave deceleration to calculate the MV area. Calculation of the latter by the PH-T method is unreliable in the presence of an incompetent AV. AR contributes to LV diastolic filling, causing transmitral blood flow velocity to decline more rapidly. The net result is an underestimation of the severity of MS.
CFD: The proximal isovelocity surface area (PISA) method can be used to estimate the MV orifice area.

MV orifice area (cm²) = 220/Pressure half-time (ms)

Figure 10.5 Estimation of the MV orifice area using diastolic transmitral blood flow velocity to calculate the PH-T. The latter is defined as the time required for the magnitude of the instantaneous transmitral pressure gradient to fall by half. From the modified Bernouilli equation P = 4 x v² (where P = pressure and v = velocity) it can be deduced that for pressure to halve, velocity must fall by 30%. In the example above, the PH-T is 220 ms, which gives an MV area of 220/220 = 1.0 cm².

Anaesthetic Goals

A high LAP is required to overcome the resistance to LV filling. Excessive preload may cause LA distension and AF. Control of HR is paramount. Tachycardia does not allow sufficient time for LV filling and results in a reduced LVEDV. Bradycardia is poorly tolerated due to the relatively fixed SV. Loss of sinus rhythm can decrease the CO by 20%. Consider synchronized DC shock in acute onset AF – if no LA thrombus is present.

The SVR needs to be maintained particularly in patients with tight stenosis and an active sympathetic nervous system. LV contractility is rarely a problem in pure MS where greater emphasis should be placed on protecting the RV from increases in PVR and PHT (Box 10.1).