Mitral stenosis anatomy and pathophysiology
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Mohammed A. Sbeih, M.D. [2]; Cafer Zorkun, M.D., Ph.D. [3]
Overview
Mitral stenosis (MS) is most commonly secondary to acute rheumatic fever. Generally, the initial valvulits is associated with valvular regurgitation but over a period of 2 or more years, the commissures fuse and the valves thicken and calcify. The chordal supporting structure also calcifies and retracts. The result is the typical “fish mouth deformity”. 70% of the time; the mitral valve is involved in isolation, and 25% of the time; the aortic valve is involved as well. The tricuspid and pulmonic valves are involved less commonly.
The normal mitral valve orifice area is 4-6 cm2. Mitral stenosis occurs when the orifice area is reduced to at least 2.2 cm2. This result in a gradient across the mitral valve which is the haemodynamic hallmark of the disease.
Anatomy
The mitral valve is typically 4–6 cm² in area. It has two cusps, or leaflets, (the anteromedial leaflet and the posterolateral leaflet) that guard the opening. The opening is surrounded by a fibrous ring known as the mitral valve annulus [1]. The anterior cusp protects approximately two-thirds of the valve (imagine a crescent moon within the circle, where the crescent represents the posterior cusp). Note that although the anterior leaflet takes up a larger part of the ring and rises higher, the posterior leaflet has a larger surface area. These valve leaflets are prevented from prolapsing into the left atrium by the action of tendons attached to the posterior surface of the valve, chordae tendineae.
The inelastic chordae tendineae are attached at one end to the papillary muscles and the other to the valve cusps. Papillary muscles are fingerlike projections from the wall of the left ventricle. Chordae tendineae from each muscle are attached to both leaflets of the mitral valve. Thus, when the left ventricle contracts, the intraventricular pressure forces the valve to close, while the tendons keep the leaflets coapting together and prevent the valve from opening in the wrong direction (thus preventing blood to flow back to the left atrium). Each chord has a different thickness. The thinnest ones are attached to the free leaflet margin, whereas thickest ones are attached quite away from the free margin. This disposition has important effects on systolic stress distribution physiology [2].
Pathophysiology
When the mitral valve area goes below 2 cm2, the valve causes an impediment to the flow of blood into the left ventricle, creating a pressure gradient across the mitral valve. This gradient may be increased by increases in the heart rate or cardiac output. As the gradient across the mitral valve increases, the amount of time necessary to fill the left ventricle with blood increases. Eventually, the left ventricle requires the atrial kick to fill with blood. As the heart rate increases, the amount of time that the ventricle is in diastole and can fill up with blood (called the diastolic filling period) decreases. When the heart rate goes above a certain point, the diastolic filling period is insufficient to fill the ventricle with blood and pressure builds up in the left atrium, leading to pulmonary congestion.
When the mitral valve area goes less than 1 cm2, there will be an increase in the left atrial pressures (required to push blood through the stenotic valve). Since the normal left ventricular diastolic pressures is about 5 mmHg, a pressure gradient across the mitral valve of 20 mmHg due to severe mitral stenosis will cause a left atrial pressure of about 25 mmHg. This left atrial pressure is transmitted to the pulmonary vasculature and causes pulmonary hypertension. Pulmonary capillary pressures in this level cause an imbalance between the hydrostatic pressure and the oncotic pressure, leading to extravasation of fluid from the vascular tree and pooling of fluid in the lungs (congestive heart failure causing pulmonary edema).
Increases in the heart rate will allow less time for the left ventricle to fill, also causing an increase in left atrial pressure and pulmonary congestion.
The constant pressure overload of the left atrium will cause the left atrium to increase in size. As the left atrium increases in size, it becomes more prone to develop atrial fibrillation. When atrial fibrillation develops, the atrial kick is lost (since it is due to the normal atrial contraction).
In individuals with severe mitral stenosis, the left ventricular filling is dependent on the atrial kick. The loss of the atrial kick due to atrial fibrillation can cause a precipitous decrease in cardiac output and sudden congestive heart failure.
References
- ↑ Shinoda H, Stern PH (1992). "Diurnal rhythms in Ca transfer into bone, Ca release from bone, and bone resorbing activity in serum of rats". Am J Physiol. 262 (2 Pt 2): R235–40. PMID 1539731.
- ↑ Nazari S, Carli F, Salvi S, Banfi C, Aluffi A, Mourad Z; et al. (2000). "Patterns of systolic stress distribution on mitral valve anterior leaflet chordal apparatus. A structural mechanical theoretical analysis". J Cardiovasc Surg (Torino). 41 (2): 193–202. PMID 10901521.