Mitral Stenosis

Most commonly caused by rheumatic fever, mitral stenosis appears clinically relevant usually after several decades, when the normal mitral orifice area of 4-6 cm² is less than 2 square centimeters, significantly impeding blood flowing from the left atrium into the left ventricle. As the pressure gradient across the mitral valve increases, the left ventricle requires the atrial impetus to fill with blood. Mitral valve area < 1 cm² causes an increase in left atrial pressure, which is transmitted to the pulmonary vasculature. As left atrial pressure remains elevated, the left atrium will increase in size, with a greater chance of developing atrial fibrillation, loss of atrial impetus with a decrease in cardiac output and sudden development of congestive heart failure.¹

Clinical heralding events:

  • dyspnoea, cough, ± haemoptysis – i.e. pulmonary oedema
  • embolic phenomena (atrial thrombus)

Auscultation

  • loud ± palpable S1
  • loud P2 (pulmonic) component of second heart sound (S2) where severe pulmonary hypertension has developed
  • opening snap (OS) followed by mid-diastolic rumbling murmur with presystolic accentuation best heard with bell of stethoscope at the apex

Advanced mitral stenosis, presents with signs of right-sided heart failure (jugular venous distension, parasternal heave, hepatomegaly, ascites) and/or pulmonary hypertension.

Differential Diagnosis

  • tricuspid stenosis
  • left atrial myxoma
  • Austin-Flint murmur of aortic incompetence
  • hypertrophic cardiomyopathy – loud S1

ECG: left atrial hypertrophy

CXR:

  • normal heart size, straightening left border of cardiac silhouette, prominent main pulmonary arteries, dilatation upper pulmonary veins, displacement of esophagus (early)
  • enlargement of all cardiac chambers, pulmonary arteries, and pulmonary veins (late)

ECHO: left atrial hypertrophy

  • mobility, thickness, calcification, impairment of subvalvular apparatus, + commissural calcification

The classification of moderate mitral stenosis:

  • Mean gradient (mmHg) 5 to 10
  • Pulmonary artery systolic pressure (mmHg) 30 to 50
  • Valve area (cm2) 1.0 to 1.5

Management

  • medical therapy – endocarditis prophylaxis, decreasing new cases of rheumatic fever, improving symptoms, and decreasing the thromboembolic risk
    • NSR: relieve congestion with diuretics and minimise exertional symptoms with  beta-blockers and/or calcium channel blockers
    • AF:
      • first control rate using AV node blocking agents (beta-blockers, calcium channel blockers, and/or digitalis) or DC cardioversion if unstable
        • if unable to revert, aim for rate control
    • Anticoagulate
  • percutaneous mitral valvuloplasty
  • surgical therapy for symptomatic moderate / severe mitral disease where percutaneous balloon valvuloplasty contraindicated
    • MVR: porcine vs prosthetic (lifelong anticoagulation)

Endocarditis prophylaxis should only be given to high-risk patients (prosthetic valve or material used for valve repair, previous endocarditis, cardiac valvuloplasty) before dental procedures that involve manipulation of gingival tissue or perforation of the oral mucosa. 


References

  1. Shah SN, Sharma S. Mitral Stenosis. [Updated 2020 Dec 14]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK430742/.

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