ABSTRACT
The central pathophysiologic mechanism in MS is obstruction at the mitral valve level during diastolic left ventricular filling leading to increased left atrial pressure and secondary changes in the pulmonary circulation. The hemodynamic hallmark of severe MS is the presence of a diastolic gradient between the LA and LV which persists at end diastole. The LA pressure trace is marked by a prominent a wave in the presence of sinus rhythm. A prominent v wave may be present in long standing MS due to decrease in atrial compliance. Left ventricular end diastolic pressure is usually normal in MS but when elevated, points to the presence of LV systolic or diastolic dysfunction. Gorlin’s formula can be used to calculate the valve area with fair accuracy but is unreliable in the presence of significant MR. Acute MR is an important complication of PTMC and can be easily diagnosed in the catheterization laboratory from a careful inspection of the LA pressure trace. Elevated PA pressures are expected to fall immediately after a successful PTMC, although normalization may take more time in patients with greater severity of MS and severe PAH to begin with.
