Valvular heart disease

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Chapter 4 Valvular heart disease

Aortic stenosis

AS can occur at the valvular, subvalvular or supravalvular level. Valvular AS most commonly occurs with degeneration of a normal three-cusp aortic valve architecture. Bicuspid valves degenerate far earlier than tricuspid valves and are the second most common cause of AS in the adult, with rheumatic heart disease being the third. Subvalvular AS is caused by a fibrous or fibromuscular membrane which encircles the LVOT causing outflow tract obstruction. These patients typically present in adulthood with recurrence of a previously resected subvalvular membrane. Subvalvular stenosis can also be caused by asymmetric septal hypertrophy, abnormal MV or papillary muscle insertion, or posterior displacement of the infundibular septum. Supravalvular AS is uncommon, producing narrowing usually at the sino-tubular junction. It occurs in patients with Williams syndrome (60%), and there are familial forms and sporadic idiopathic cases.

AS has a long asymptomatic period after which clinical symptoms such as angina, exertional dyspnoea and effort syncope may result. Since symptoms develop late in the pathophysiology of AS, clinical deterioration soon follows if valve replacement is not undertaken. Obstruction to the LVOT leads to elevated LV pressures and compensatory LVH which initially maintains cardiac output and reduces LV wall stress, but ultimately decreases LV compliance and increases end-diastolic pressure. Increased myocardial oxygen demand causes myocardial ischaemia and later LV failure.

CMR is a robust method of calculating the severity of AS and correlates well with continuous wave Doppler echocardiography. However, it is far superior to echocardiography in identifying the cardiovascular functional and morphological sequelae of AS, such as post-stenotic dilatation of the ascending aorta, degree of LVH, and myocardial viability (Figures 4.1 and 4.2). These are important factors in the assessment of patients prior to valve replacement surgery, which often includes CABG and aortic root replacement. CMR also provides an excellent modality for serial surveillance of parameters such as LV function, volumes and mass in patients under follow-up and post operatively. This is done using the pre-contrast part of the protocol outlined in Chapter 1. Cines can demonstrate thickening and bulging of the aortic cusps and turbulent flow in the aorta. Imaging in an oblique sagittal plane parallel to the valve may demonstrate restricted opening and closure of the valve, and is frequently satisfactory for direct planimetry of the valve orifice and evaluation of bicuspid valve morphology. Direct planimetry can be performed using cine imaging or velocity mapping sequences (Figure 4.3).

Velocity mapping is primarily used, however, to calculate the pressure gradient across the AV using the modified Bernoulli equation;

image

where ΔP (mmHg) is the pressure drop across the stenosis, and Vmax is the peak velocity (m/s) determined by velocity mapping 1 to 1.5 cm above and parallel to the valve plane (Figure 4.3d). The typical Venc setting for the LVOT is 2 m/s, and 2.5 to 4 m/s for the aorta. An initial Venc of 2.5 m/s is often used and adjusted upwards if there is velocity aliasing (Figure 1.3). The velocity of blood flow through the AV is greater than that through the MV.

Velocity mapping, SSFP cines and FSE imaging are combined to determine the level of obstruction in AS. It is important to use information from all these sequences since a thin subaortic shelf is not reliably excluded even with high-resolution FSE CMR techniques. The initial planes and sequence required are the LVOT cines with subsequent imaging targeted by the pattern of turbulence demonstrated on these views.

Severity of AS is graded as: mild >1.5 cm2, moderate 1.0–1.5 cm2, severe <1.0 cm2, and critical <0.8 cm2. In severe AS, the peak transvalvular gradient is usually >50 mmHg.

Specific CMR reporting features for AS include:

Aortic regurgitation

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