The pathophysiology of mitral regurgitation.

The results of treatment of heart valve disease have improved steadily during the past 20 years. In aortic stenosis, although postoperative survival rates approximated those of age-matched controls, the outcome of surgery to treat ischemic and non-ischemic mitral regurgitation was grave. The reasons for this were two-fold: first, patients were referred for surgery late in the course of their disease, when irreversible left ventricular (LV) dysfunction prevented postoperative restoration of contractile function. Second, the value of the mitral valve apparatus in facilitating LV contraction was unrecognized, and this structure was often removed at surgery, in turn worsening pre-existent LV dysfunction. Consequently, patients with LV dysfunction due to mitral regurgitation underwent surgery that caused further damage to the left ventricle. Not surprisingly, postoperative LV function was poor, congestive heart failure persistent, and lifespan shortened. More recently, however, substantial insight has been gained into the value of the mitral valve apparatus, the causes of LV dysfunction in mitral regurgitation, and into the objective markers of LV function that permit the clinician to recommend surgery before muscle dysfunction has become severe and irreversible.