Mitral stenosis refers to narrowing of the mitral valve aperture, and thus providing a restriction on flow between the left atrium and ventricle.
By far the most common cause is rheumatic fever. The inflammatory process leads to thickening of the leaflets (and chordae tendineae) and can lead to the valve leaflets dusing together. This is not a common pathology in the developed world anymore but remains a common problem in developing world.
Other causes include:
Multisystem inflammatory disorders e.g sarcoidosis, SLE, RA
Degenerative calcification (rarely leads to significant MS)
Infective endocarditis (with large vegetations)
The development of stenosis is often very slow, and compensated for for many years. The inflammatory changes lead to impaired valve leaflet movement and can result in increased fusion of the valve leaflets, producing a reduced valve area. The narrowed valve area produces an increased resistance to flow between the left atrium and ventricle. Initially there is atrial dilation, which reduces pressure elevation. As the MS and resistance progresses however, there is remodelling of the atrium with changes such as myocardial hypertrophy and fibrosis, as well as geometric changes. The increased pressure to overcome the resistance to flow is transmitted back to the pulmonary circulation (leading to pulmonary hypertension) and subsequently the right side of the heart. With significant disease, there can be impairment of ventricular filling, with reduction in end-diastolic volumes, and subsequent reduction in cardiac output.
The remodelling of the LA means that atrial fibrillation is a common consequence of MS. Clot formation within the LA is also common, with the physiological changes, as well as the presence of AF, being contributory.
The latent period before symptom onset can be very long, varying from 15 to 40 years after an episode of rheumatic fever. Symptoms will develop as the compensatory changes begin to fail, and pulmonary hypertension and right heart failure begin to develop. Symptoms can include:
Reduction in activity levels
More frequent lower respiratory tract infections
The onset of atrial fibrillation of pregnancy may be the trigger of a rapid decompensation in patients with significant disease.
Signs Clinical examination may include:
Signs of right heart failure - elevated JVP, Hepatosplenomegaly, peripheral oedema
Low pitched mid-late diastolic murmur - heard best at apex with bell of stethoscope
Loud first heart sound
ECG May commonly be atrial fibrillation P mitrale (an enlarged p wave) is a possible finding if the are in sinus. There may be ECG changes of right ventricular hypertrophy.
CXR Pulmonary oedema may be present. Left atrial enlargement may be visible Calcification of the mitral valve may also be seen.
Echocardiography An essential investigation in the diagnosis and assessment of MS. Echocardiographic findings form a key part of assessing the severity of MS. The main criteria are:
Mitral valve area
Mitral valve area (cm^2)
Normal - 4-6
Mild - 1.6-2
Moderate - 1.0-1.5
Severe - <1
Pressure gradient (mmHg)
Mild - <5
Severe - >10
Symptoms will usually not develop until the valve area is under 2cm^2.
Atrial fibrillation This is common, and ventricular tachycardia from this leads to suboptimal haemodynamics. It reduces diastolic time (needed for ventricular filling) and increases atrial pressure. As higher rates can therefore impair cardiac function, rate control is generally used (usually through beta blockade). Rhythm control has clear superiority, but the atrial remodelling usually makes this difficult to achieve. Anticoagulation is indicated in patients with AF. It may also be indicated in patients with MS without AF if they have had an embolic event, of evidence of atrial clot.
Dyspnoea This will usually be treated with diuretic therapy. Long acting nitrates are another option to improve symptoms. As noted above, beta blockers can improve cardiac performance if there was fast ventricular response to AF and this can subsequently improve exercise tolerance.
Surgical intervention is often indicated in patients with severe symptomatic MS. Development of pulmonary hypertension is also another fairly strong indication to intervene.
The procedure of choice is usually percutaneous commissurotomy. This is an endovascular procedure that involves passing a balloon across the valve and dilating it, splitting the fused edges. This does commonly result in some MR, but this is no worse than moderate in about 80% of cases. An increase in valve area to >1.5cm^2 can usually be achieved.
Contraindications to this approach include:
Heavily calcified valve
Additional planned surgical intervention.
Coexisting MR (any more than mild)
In these circumstances, open heart surgery and mitral valve replacement will usually be the approach. Valve replacement rather than repair is preferred as the outcomes are generally better in this pathology. At surgery there may be consideration for AF ablation (if they have AF) or excision of left atrial appendage if there have been problems with thrombosis. Mitral valve replacements are usually mechanical in nature and require anticoagulation.
Patients with MS may present for noncardiac surgery or for definitive valve treatment.
Preoperative Assessment will involving assessing the severity of any MR, its functional impact and any complications. If patients are asymptomatic, then surgery is generally tolerated well. However, if there is functional limitation from the MS, then consideration of management of the valve lesion should be considered prior to elective surgery.
Patients with anticoagulation for AF will need this discontinuing perioperatively. Conversion to heparin is commonly done, although if the indication is purely AF, a short perioperative period without anticoagulation is relatively low risk.
Investigations should be ordered as required. Many of these are discussed above, and should usually be available. Echocardiographic information is particularly essential to assess for the svereity of MS and any complications.
Planning of anaesthetic technique should take into account the CVS impact of MS. In general, the haemodynamic impact of neuraxial anaesthesia makes it a particular;y risky choice.
Intraoperative As with AS, MS represents a fixed cardiac output state. As such, great care needs to be taken with cardiovascular parameters to prevent disastrous CVS dysfunction.
Rate/Rhythm A low normal heart rate is preferred to allow adequate time in diastole for ventricular filling. Sinus rhythm is clear desirable, but the atrial pathology may make this challenging. New perioperative AF may require rapid cardioversion, as rapid decompensation is possible.
Preload Normovolaemic is the target to ensure adequate ventricular filling. However, it is important to bear in mind that the patient may have right heart dysfunction and be at risk of pulmonary oedema.
Afterload A reduction in SVR can result in a drop in coronary perfusion, as the fixed cardiac output state is unable to compensate. Maintenance of a stable afterload is therefore important. Right sided afterload and pulmonary vascular resistance (PVR) is also very important factor to consider, as this may be failing. Avoidable increases in PVR (hypoxia, hypercarbia, acidosis, nitrous oxide) should be dealt with.
Contractility The LV function is generally unaffected, and thus the right side is the challenge. Failure should therefore first focus on optimising PVR. If this is failing, inotropy may be required. Care should be taken with inodilators (such as phosphodiesterase inhibitors) due to the impact of a drop is SVR.
Postoperative Routine optimisation of recovery should be in place to minimise the impact of MS e.g. optimal analgesia to minimise sympathetic stimulation. In all but the most minor procedures, critical care admission for optimal observation is usually needed for significant MS. Caution is needed with fluid therapy.