Rheumatic Heart Disease

The Mitral valve is a two leaflet valve that separates the left atrium from left ventricle. The commonest cause of its stenosis is a consequence of group A beta haemolytic Streptococcus. The disorder starts most frequently in childhood with an arthropathy and pancarditis after a sore throat. Subcutaneous nodules may be found. Demonstrable valvular or heart disorder may be delayed and appear after several attacks of the systemic symptoms. The pathology is thought to be related to a similarity shared by protein antigens in heart and streptococcus. The mitral valve is involved most frequently followed by aortic and tricuspid valves. Rheumatic pulmonary valve disease can occur, but is less common.

The haemodynamics of mitral stenosis result in a high left atrial pressure with left atrial enlargement and secondary venous congestion in the lungs. The pulmonary veins become enlarged in the upper zones and the lower lung zones may show interstitial pulmonary oedema.

The transmission of the electrical activity through the large atria can be chaotic and unstable with the development of atrial fibrillation. The pulse is then controlled by incomplete conduction of the rapid atrial impulses or by a new origin from irritable cells in the atrio-ventricular conductive bundle ( of His ). The cardiac filling and consequent output can be reduced by a reduced diastolic interval. The development of atrial fibrillation can precipitate an attack of acute pulmonary oedema.

Rather like a computer printer buffer or a large waiting area in a busy outpatient clinic, a large dilated left atrium may partly protect against sudden changes in circulation and onset of oedema, but has a greater risk of mural clot formation.

Chronic stiffening of the lungs with venous engorgement can result in secondary pulmonary arterial hypertension with visible proximal pulmonary arterial dilatation. There may be visible right ventricular hypertrophy. Haemosiderosis can also be found, secondary to chronically elevated pulmonary venous pressures. Ossific nodules are reported in mitral valve disease, but their aetiology is uncertain. There is no direct relationship to the height of the elevated pulmonary venous pressure.

Visible chamber enlargement usually means an increase in the work done and implies an incompetant or regurgitant valve. Thus cardiac enlargement in mitral or aortic valve disease is more often secondary to an increase in stroke volume. Ventricular hypertrophy and wall thickening consequent on hypertension or valvular stenosis is not usually visible on the plain film until failure and dilatation result.