Mitral Stenosis

Summary of Values

Overview

Mitral stenosis is rarely seen now in the UK with the leading cause internationally being rheumatic heart disease which tends to be associated with lower-income in developing countries. Other causes include endocarditis and mitral annular calcification in the elderly (senile MS). The incidence in the US is 0.1% and it contributed to 12% of all valvular heart disease in the Euroheart Survey. 20% of patients with rheumatic mitral disease have multiple valves affected. [1]

In rheumatic mitral disease repeated inflammatory episodes of the valve results in a hypertrophic and irregular valve appearance with tethering, poor coaptation and poor opening. Calcification and thickening of the subvalvular apparatus can also be seen on echo.

Inflammation is due to recurrent streptococcus throat infections with the "M-protein" causing an inflammatory reaction on the heart valves and synovium.

Progression is often slow at 0.1-0.3cm2 per year as the normal valve area (4-6cm2) gradually reduces. As a general rule non-cardiac surgery in asymptomatic patients with PASP <50mmHg is deemed safe [2]

Causes

1. Rheumatic heart disease
2. Severe mitral annular calcification (MAC) Most commonly affecting the posterior leaflet and sparing the leaflet tips.
3. Atrial myxoma (stenosis can be dynamic as the myxoma obstructs LV inflow)
4. Atrial thrombus
5. Congenital abnormalities
• Parachute MV
• MV inflow ring
• Cortriatriatum sinister
6. Thrombosis or obstruction of a prosthetic mitral valve replacement
7. Inflammatory diseases (RA / SLE)

Pathology

An increased pressure gradient is required to move blood from the LA into the LV through a stenotic mitral valve. In normality the mitral valve orifice should be 4-6cm2. The LA gradually dilates over time to compensate for the increased LAP required to generate forward flow.

Concommitant MR is often also present due to coaptation defects resulting from the irregular closure of a heavily calcified or rheumatic valve. AF is present in 40% of patients and patients are often on anticoagulation for this so careful planning is required to bridge anticoagulation therapy in the perioperative phase.

Over time elevated LAP leads to pulmonary hypertension and compensatory RV hypertrophy. Pulmonary regurgitation can develop as a consequence of the elevated PASP. Elevated PA pressures can be estimated on echo from the TR jet and pulmonary pressures can approach those of the systemic circulation in very severe cases.

Pre-operative severity Assessment

1. Clinical - evidence of exertional dyspnoea, CCF or RV failure (high JVP, deranged LFT's, peripheral oedema) should lead to postponing of elective surgery pending cariology review
2. Pressure gradient (LAP to LVEDP)
1. Prolonged E-wave (pressure gradient maintained for much longer in order to fill the ventricle
3. Valve orifice area (EROA) - Generally calculated indirectly as tracing the valve area is often unreliable unless 3D imaging is used.
4. Associated features on TOE:

• LA dilatation (non-specific and occurs in diastolic dysfunction, AF, MR etc…
• Reduced LA blood velocities with SEC or thrombus present, especially in the LAA
• Thrombus in LAA
• RV dilatation and features of pulmonary hypertension
• Calcification of the subvalvular apparatus or mitral annulus (MAC)

Grading of Mitral Stenosis Severity

Mean Pressure

This is calculated by tracing the outline of the diastolic inflow velocity profile (E and A-wave) using the CWD or the PWD at the mitral valve leaflet tips during diastole. ESC guidelines recommend CWD to avoid missing high velocities through the valve. Using the simplified Bernoulli equation P = 4v2, the area under the velocity curve correlates with mean pressure gradient through the valve. An average of 5 readings should be taken if the patient is in AF.

Mild = 1-5mmHg

Moderate = 6-10mmHg

Severe = >10mmHg

Pressure half time

The time taken from peak velocity of the mitral E-wave to half of that value. This gives a measure of how rapidly velocities through the valve fall. Longer half times correlate with higher grade stenosis. Be wary that the pressure half-time can be artificially shortened in patients with concomitant AR and is less reliable in patients with diastolic dysfunction where LVEDP is elevated.

Pressure half time can be used to calculate MVA using the equation:

MVA = 220 / PHT

In severe MS the E-wave will not return to baseline prior to the a-wave as it is so prolonged and “E-A fusion” occurs, even at normal heart rates.

Three readings should be averaged to give an accurate result.

Deceleration Time

• Generally longer pressure half times and deceleration times result in a smaller MVA estimate)

Normal = MVA >4cm2

Mild = MVA 2.5-4.0 cm2

Moderate = MVA 1.0-2.5cm2

Severe = MVA < 1cm2

MVA by PISA Method

PISA method can be performed in a similar manner to that for MR assessment.

PISA is measured on the LA side of the valve

Alpha - correction angle is added to correct for the "funnel" shape of the MV orifice and is measured at end-diastole.

NL should be adjusted to 40cm/sec to achieve an accurate PISA envelope

MVA = PISA area x NL x [alpha/180] / Velocity E-wave peak

*Note: Not valid in patients with AF or MR.

Overall PISA is rarely used to assess MS severity.

3D Assessment of MS orifice area (3D planimetry):

3D planimetry is the gold standard for assessing severity of MS.

Perioperative Management 

Haemodynamic goals are similar to those of aortic stenosis although consideration to keeping PA pressures low should also be taken. • Maintain SVR (Low SVR reduces coronary perfusion pressure)  • Maintain sinus rhythm  • Low to normal heart rate (Faster rates raise LAP)  • Avoid increases in PVR (hypoxia, hypercarbia, acidosis, pyrexia, nitrous oxide)  Neuraxial blockade should generally be avoided (risk of catastrophic reduction in SVR) The patient is also likely to be anticoagulated.

References

1. Euroheart survey. Bernard Iung, Gabriel Baron, Eric G. Butchart, François Delahaye, Christa Gohlke-Bärwolf, Olaf W. Levang, Pilar Tornos, Jean-Louis Vanoverschelde, Frank Vermeer, Eric Boersma, Philippe Ravaud, Alec Vahanian, A prospective survey of patients with valvular heart disease in Europe: The Euro Heart Survey on Valvular Heart Disease, , Volume 24, Issue 13, 1 July 2003, Pages 1231–1243

European Heart Journal

2. DiNardo JA, Zvara DA. Anesthesia for Cardiac Surgery. Wiley-Blackwell, Oxford, UK: John Wiley & Sons, 2008
3. Baumgartner H, Hung J, Bermejo J, et al. Echocardiographic assessment of valve stenosis: EAE/ASE recommendations for clinical practice. Journal of the American Society of Echocardiography : Official Publication of the American Society of Echocardiography. 2009 Jan;22(1):1-23