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