[The mechanism of remodelling in left ventricular volume overload].

We studied 60 people who were separated into three groups. Group A: 11 patients with pure, severe mitral regurgitation (MR); Group B: 18 patients with pure, severe aortic regurgitation (AR) [this group was divided into two: I) with normal ejection fraction (EF) and II) with low EF]. The third group was a control one with 31 healthy people. Through 2-D Echocardiography (2-D Echo) we got: diameters of the cavities, thickness of the wall, ventricular function, h/r ratio, and systolic wall stress (S). Patients with MR showed left atrial and ventricular enlargement with low h/r ratio, normal ventricular function and raised S. The group I of AR had left ventricular enlargement and hypertrophy, with normal h/r ratio and EF, and with raised S, while the group II of AR showed left ventricular enlargement, low h/r ratio and EF with very high S. In MR volumetric overload causes different anatomic and functional changes on the left ventricle than in the AR. In MR there is a systolic leak toward left atrium. This causes the low S in the beginning of the illness and is not the mechanism that trigger left ventricular hypertrophy (LVH). The absence of LVH causes excessive enlargement of the myofibril and with time there is structural damage and contractile failure which raises the systolic volume and S. Later on, hypertrophy develops. On the other hand, since the beginning AR has high S which causes adequate hypertrophy (normal h/r ratio) and later it produces huge ventricular enlargement decreases the h/r ratio (inadequate hypertrophy) with contractile failure. We conclude: the time of surgery in MR is when the patient raises S and in the AR when inadequate hypertrophy appears (low h/r) but when EF is still normal.