[Usefulness of vasodilator therapy in regurgitant valvular diseases].

Mitral and aortic valve regurgitation both lead to left ventricle volume overload, but have different pathophysiology. Preload is increased in mitral regurgitation whereas afterload is normal since part of the ejection flow goes to the left atrium; however, both preand afterload are increased in aortic regurgitation. When the regurgitations are chronic, the ventricle adapts by increasing the volumes and causing eccentric left ventricular hypertrophy. Nevertheless, when the adaptation mechanisms fail, in the long term left ventricular filling pressures increase and, finally, the ejection fraction decreases, leading to signs and symptoms of heart failure. In acute regurgitations these adaptation mechanisms may not be sufficiently rapid, and although the left ventricle responds with greater hypercontractility, the acute increase in preload can increase filling pressures and trigger pulmonary edema. The regurgitant volume directly depends on the regurgitant orifice, the duration of regurgitation and the pressure gradient between the cavities where regurgitation occurs.1 There are few studies on variations in the regurgitant orifice, but they seem to be associated with the presence or absence of structural valve disease and loading conditions. Although mitral regurgitation is more dynamic than aortic regurgitation, experimental studies have shown that the aortic regurgitant orifice area decreases during diastole and also depends on the loading conditions.2 Clearly, changes in the regurgitant orifice area are associated with the etiology of valvular regurgitation and the degree of structural changes. In aortic regurgitation secondary to valvular thickening or calcification, the Usefulness of Vasodilator Therapy in Regurgitant Valvular Diseases