Disparate impact of severe aortic and mitral regurgitation on left ventricular dilation

In asymptomatic severe aortic (AR) and mitral regurgitation (MR), left ventricular (LV) dimension criteria were established to guide timing of valve replacement to prevent irreversible LV dysfunction. Given both lesions are primary LV volume overload ''leaks'', it might be expected that both lesions would induce similar impact on the LV and result in equivalent dimension criteria for intervention. However, the dimension-based intervention criteria for AR versus MR (developed through natural history studies), differ markedly. The pathophysiological foundations for such discordance have neither been fully elucidated nor emphasized. This case-based treatise compares the two regurgitant lesions with respect to: (a) ''total regurgitant circuits''; (b) ''driving pressures'' resulting in LV volume overload from each respective ''leak''; and (c) volume and afterload wall stresses imposed on the LV.Key points The ''total circuits'' of volume overload differ: The AR circuit includes the LV and systemic vasculature, whereas MR includes the LV ejecting into the left atrium/pulmonary veins and systemic circulation. The ''driving pressure'' of regurgitation and afterload are high with AR and low with MR. Differing ''total circuits'' and ''driving pressures'' impose disparate wall stresses upon the LV. Parallel and serial sarcomere replication occurs in AR, while only serial replication occurs in MR. It therefore follows that for regurgitation of similar severities, AR results in greater LV dilation at the point of irreversible myocardial dysfunction compared to MR. These considerations may explain, at least in part, the disparate dimension criteria employed for valve intervention for severe AR vs MR.