Mitral valve area
MVA · Planimetry in the parasternal short axis at leaflet tips (reference method by echo), with PHT, continuity and PISA as cross-checks
Normal range & thresholds
Normal 4.0–6.0 cm².
‘Very severe’: MVA ≤1.0 cm². Note that the mean gradient is flow- and rate-dependent and is not a severity criterion on its own — the area is.[5,6,7]
| Mild | Moderate | Severe | |
|---|---|---|---|
| MVA | >1.5 cm² | 1.5–2.0 cm² | ≤1.5 cm² |
| Mean gradient | <5 mmHg | 5–10 mmHg | >10 mmHg |
| PHT | <150 ms | ≥150 ms | |
Pathophysiology
Rheumatic mitral stenosis narrows the orifice by commissural fusion, leaflet thickening and chordal shortening, converting the valve into a fixed funnel. Because the obstruction is upstream of the left ventricle, the ventricle is protected and underfilled while the left atrium and the pulmonary circulation absorb the entire pressure load: hence a normal LV, a giant left atrium, atrial fibrillation, pulmonary hypertension and systemic embolism. Gradient depends on flow and on diastolic filling time, so tachycardia and exercise raise it steeply for the same anatomical area — which is why the clinical presentation is exertional and why rate control is genuinely therapeutic.[5]
Raised by
- After percutaneous balloon mitral valvuloplasty or surgical commissurotomy (the intended effect)
- Overestimated by planimetry above the leaflet tips, by an inadequate gain setting, or by the pressure half-time method in the presence of aortic regurgitation, an atrial septal defect, or tachycardia
Lowered by
- Rheumatic heart disease — still the overwhelming cause worldwide,[96] and the reason this parameter matters far more in some populations than in others
- Degenerative mitral annular calcification with calcific extension onto the leaflets — increasingly common in elderly and dialysis patients, and a poor candidate for valvuloplasty
- Congenital (parachute valve, supravalvular ring), radiation, carcinoid, Fabry, mucopolysaccharidoses
- Systemic lupus erythematosus/Libman-Sacks; infective endocarditis with a large vegetation
- Prosthetic or ring stenosis; thrombus or pannus; a left atrial myxoma obstructing the orifice
- Underestimated by planimetry at the wrong level or in a heavily calcified valve
Technique & pitfalls
- Planimetry in the parasternal short axis at the level of the leaflet tips, in early diastole, with gain minimised so that the true orifice is not overwritten — the echo reference method. Scan the whole valve from annulus to tips to find the smallest orifice.
- Do not use the pressure half-time method within 24–72 hours of balloon valvuloplasty — atrial and ventricular compliance change acutely and the derived area is wrong.[5]
- Cross-check with the continuity equation and, in eccentric or calcified valves, with PISA.
- Measure the mean gradient by tracing the whole diastolic envelope — Doppler agrees closely with simultaneous catheterisation when the technique is correct;[44] report the heart rate alongside it, and average 5–10 cycles in atrial fibrillation.
- Score the valve for intervention: the Wilkins score (leaflet mobility, thickening, calcification, subvalvular disease; each 1–4, total ≤8 favours balloon valvuloplasty), plus commissural calcification and MR severity.[45]
- 3D TOE planimetry is the most accurate echocardiographic measurement in a distorted valve.
Pseudo-change & artefact
- Planimetry above the leaflet tips — overestimates the area; the commonest technical error.
- Excess gain filling in the orifice — underestimates.
- PHT invalidated by significant aortic regurgitation, atrial septal defect, tachycardia, first-degree AV block, abnormal LV compliance, advanced age, or the immediate post-valvuloplasty state.[5]
- The continuity equation fails in the presence of significant mitral or aortic regurgitation.
- Gradient measured during tachycardia, anaemia, fever or exercise — markedly overestimates severity.
- Under-sedation and anxiety at the time of study.
- Comparing gradients across studies at different heart rates.
Treatment thresholds
- Severe mitral stenosis (MVA ≤1.5 cm²) with symptoms → intervention, class I. Percutaneous balloon mitral valvuloplasty is first choice for favourable anatomy (Wilkins ≤8, no left atrial thrombus, no more than mild mitral regurgitation, no bicommissural calcification); otherwise surgery.[6,7,45]
- Asymptomatic severe MS → valvuloplasty is reasonable (class IIa) with favourable anatomy plus new-onset atrial fibrillation, systolic pulmonary artery pressure >50 mmHg, a high thromboembolic risk, or planned pregnancy or major non-cardiac surgery.[6,7]
- Discordant symptoms and resting gradient → exercise echocardiography; a mean gradient >15 mmHg or SPAP >60 mmHg on exercise supports intervention.[6,7,28]
- Anticoagulation: rheumatic mitral stenosis with atrial fibrillation requires a vitamin K antagonist, not a DOAC — a rare and important exception in modern practice.[6,40]
- Rate control is genuinely therapeutic: it lengthens diastole and lowers the transmitral gradient at an unchanged valve area.
Next step
- Next: reconcile planimetry, PHT, continuity and gradient; if they disagree, planimetry (ideally 3D TOE) usually wins.
- Then: Wilkins score, commissural calcification, MR severity, and TOE to exclude left atrial appendage thrombus before any valvuloplasty.[45]
- Then: exercise echocardiography where symptoms and resting haemodynamics disagree.[28]
- Then: assess pulmonary pressures, LA size and rhythm; start anticoagulation if there is atrial fibrillation, prior embolism, or left atrial thrombus.[40]
- Then: Heart Team, and secondary prophylaxis against rheumatic fever where relevant.
Drugs
- Rate-limiting drugs — beta-blockers, verapamil, diltiazem, digoxin — lengthen diastole and reduce the gradient. The most effective medical therapy available for this lesion.
- Diuretics relieve pulmonary congestion.
- Vitamin K antagonists for atrial fibrillation, prior embolism or left atrial thrombus; DOACs are not established in rheumatic mitral stenosis.[40]
- Secondary antibiotic prophylaxis against recurrent rheumatic fever.
- No drug enlarges the orifice.
Reversibility
Mechanically reversible, not pharmacologically. Balloon mitral valvuloplasty typically doubles the valve area (from about 1.0 to 2.0 cm²), halves the gradient immediately, and drops pulmonary pressures over weeks to months; restenosis occurs in roughly 30–40% at 10 years and is usually amenable to repeat intervention or surgery in suitable anatomy. Native stenosis progresses at roughly 0.1 cm² per year untreated. Atrial and pulmonary vascular remodelling reverse only partially, which is the argument for intervening before the atrium is destroyed and permanent atrial fibrillation supervenes.[6,45]