Mitral valve disease

Mitral stenosis

• Clinical features
  • • Malar flush
    • AF
    • Tapping displaced apex beat
    • Loud S1 and P2
    • Diastolic opening snap
    • Mid-diastolic rumbling murmur over apex (loudest in left lateral position, expiration, with bell)
• Causes
  • • Rheumatic fever (causes >80% of cases worldwide, but much less in the UK)
    • Degenerative
    • Rare forms
      • • Congenital
        • Associated with CTD (SLE, RA)
        • Drug-induced
        • Carcinoid-related
• Signs of severity
  • • AF (found in 45%)
    • Short time between S2 and opening snap
    • Longer murmur
    • Signs of right heart failure
    • Valve area <1.5cm², < 1cm² on echo is critical
• Complications
  • • Atrial Fibrillation
      • • If symptomatic, usually in AF
        • Warfarin usually better than DOAC (see below)
        • Cardioversion unlikely to be successful if severe MS
    • Pulmonary hypertension and right sided heart failure
    • High risk of thromboembolism
    • Secondary TR
    • IE (rare)
    • Mild MS can rapidly progress to severe
• Assessment
  • • If asymptomatic, exercise testing can be useful (better than a stress echo)
    • Mitral annular calcification is also an indicator of CVD severity and is associated with an increased risk of AF, stroke, and death
• Treat with
  • • Betablockers to reduce LA pressure (especially if moderate/severe MS with HF)
    • Can also use diuretics, digoxin, ivabradine and some CCBs if required
    • Avoid ACE-I
    • Warfarin is often best if there is AF
    • Avoid DOAC if valve area <2cm²
• Interventions (usually an option if valve area <1.5cm²)
  • • Balloon valvuloplasty (or PMC, percutaneous mitral commissurotomy).
      • • Contraindicated if LA thrombus, more than mild MR, severe calcification, absence of commissural fusion (as occurs in degenerative MS), severe AV disease, or if the patient also requires a CABG
    • MV repair or replacement (usually replacement)

---

Mitral regurgitation

• Clinical features
  • • Thrusting, displaced apex beat
    • Systolic thrill at apex
    • Soft S1
    • Loud pansystolic murmur over apex, radiates to axilla and loudest in expiration
• Symptoms
  • • Often asymptomatic, but AF can occur
    • Symptoms of associated HF
    • A small subgroup of patients with primary MR have a risk of ventricular arrythmias and SCD (eg in Barlow’s disease)
• Can be classed as
  • • Primary MR
      • • Seen in 55% of MR patients who require treatment)
        • Structural abnormality of the valve (leaflets, chordae papillary muscles, mitral annulus)
    • Secondary MR
      • • Functional MR, due to LV or LA alterations.
        • Can be atrial secondary (preserved EF, normal-ish LV cavity, enlarged LA)
        • Or ventricular secondary (EF <50%, sometimes RMWAs, dilated LV)
• Causes
  • • Most often functional
      • • Secondary to LV dilatation (dilated cardiomyopathy), or LA dilatation with pAF)
        • Severe secondary MR occurs in 10% of HF (especially if reduced EF). Often occurs in the setting of dilated/ischaemic cardiomyopathy
    • Annular calcification
    • Rheumatic fever
    • Valve prolapse (including Barlow’s disease)
    • VSD or ASD
    • Acute MR – acute ischaemia (papillary muscle rupture), chordal rupture, IE
    • Can be related to a collagen disorder, connective tissue disorder, or HOCM
• Clinical signs of severity
  • • Displaced apex
    • S3
    • Signs of pulmonary hypertension
    • EF is usually increased in MR, if low – sign of very severe lesion
• Echo may show
  • • Abnormal valve morphology eg MVP, calcifications
    • Ruptured cords
    • Secondary causes
    • Reduced LV and/or RV function
• Imaging signs of severity
  • • Flail leaflet large coaptation defect, severe tenting, large central jet, large holosystolic convergence zone
    • Vena contracta >7mm, pulmonary vein systolic flow reversal, E-wave dominant, VTI mitral/VTI LVOT >1.4
    • EROA (effective regurgitant orifice area) >40mm^2, Rvol (regurgitant volume) >60mL, RF (regurgitant fraction) >50%
• Refer primary severe MR for intervention if symptoms, or asymptomatic, and any of:
  • • EF <60% or LV dilatation
    • LV ESD >40mm (or LV ESDI >20mm/m² )
    • Criteria are a bit more complex, but AF or secondary TR push in favour of intervention
• Management
  • • Treat HF usual way in secondary MR, before referring for intervention (in 40% MR improves with treatment). Can use SGLT2I if preserved EF
    • Treat AF as usual
    • If primary MR, moderate to severe, and you’re starting them on diuretics – consider referring for TEER
    • If secondary MR consider referring for TEER only if they are on maximal medical therapy for HF or can’t tolerate it.
    • If not high surgical risk, and secondary atrial MR, can sometimes have MR surgery instead of TEER
• Interventions
  • • Transcatheter edge-to-edge repair (TEER)
      • • Performed under GA with TOE guidance, via femoral vein. Patients generally discharged the next day
        • Also used in TR, but trans-septal puncture required for treating MR
        • Good for primary MR especially, but often used in secondary too (especially if mild-moderately dilated LV)
        • Aim to turn severe MR into mild, without causing MS
        • Procedure complications <1%
        • Centrally commissioned – so refer to the nearest centre if they need it
        • Afterwards – single antiplatelet if not anticoagulated (although most have AF, and so will be)
    • Surgical mitral valve repair
    • Valve replacement
      • • Can be transcatheter (novel approach) or open surgery
        • This is only done in a minority
    • Sometimes best to repair or replace the valve in secondary MR if patient is undergoing cardiac surgery for another reason
• Follow up
  • • If severe MR and not for intervention – echo every 6 months
    • If asymptomatic moderate MR and preserved LV function – see annually, echo every 1-2 years