Mitral Stenosis
The physiological mitral orifice extent is between 4cm2 to 6cm2, the valve will open throughout the ventricular diastole to facilitate the blood filling of the left ventricle. Constriction less than 2cm2 can cause an impediment of blood flow to the ventricle thereby resulting in increased pressure exerted on the walls of the left atrium.15 The main etiology of this constriction is rheumatic fever, where a group A beta-hemolytic streptococcus infects the patient in early life. The initial pharyngeal infection promotes the innate immune system to activate T and B cells. CD4+ T cells will promote the production of complementary IgG and IgM antibodies. However, the structural resemblance between the infectious material and human proteins results in tissue damage. From a cardiovascular perspective, antibody binding and dissemination of T cells will cause carditis.16
Genetic susceptibility to the development of acute rheumatic fever was initially considered in 1986. A 2011 systematic review seemed to confirm this hypothesis, suggesting heritability of 60%. Some studies have reported associations to class 2 HLA whilst other studies have discussed an association to non-HLA proteins, but a definite link is yet to be confirmed.17-19
Clinically, mitral stenosis will cause massive rises in left atrial pressure thereby resulting in reactive pulmonary hypertension. As the pressure remains elevated the atrium will begin to dilate in an attempt to accommodate the increasing volumes of blood. This dilation puts the patient at risk of atrial arrhythmias. This sequence of events will eventually result in congestive heart failure which is measurable via the New York Heart Association (NYHA) Classification.15