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The impact of mitral regurgitation (MR) on left ventricular (LV) function and remodelling has been typically described in terms of a pure volume overload. In fact, LV afterload in MR is sometimes believed to be below normal ‘because the regurgitant orifice allows blood to exit the ventricle with little opposition’. Moreover, this argument sometimes is followed by the idea that a low-afterload leads to overestimate intrinsic LV systolic function in MR. Remarkably, despite a number of authors have emphasised that afterload is not reduced in chronic MR,1 ,2 the idea is still prevalent. Describing MR merely as a volume overload condition also overlooks other biomechanical consequences of MR, which deserve discussion.
Afterload in MR
The LV is capable of maintaining stroke volume in chronic MR until advanced stages of the disease because, following the Frank-Starling law, diastolic lengthening increases shortening of the sarcomere. If the regurgitant leak were unrestrictive, this compensating mechanism would be insufficient to maintain forward flow because the preload-recruited stroke volume would be mostly pumped towards the left atrium. In chronic MR, the regurgitant lesion always imposes a significant opposition to backflow. Although its area may vary during systole, in fluid-mechanical terms, the regurgitant lesion in MR behaves as a small, flat and restrictive orifice. Very large free regurgitant lesions, as sometimes found in severe tricuspid insufficiency—showing a laminar regurgitant flow and a very low transtricuspid pressure gradient—are virtually never seen in chronic MR. Furthermore, even in advanced stages of the disease, any decline in cardiac output is compensated by vasomotor reflexes. Consequently, systolic blood pressure remains normal in chronic MR.1
Ventricular pressure translates to afterload by means of wall-stress. Governed by Laplace's law, systolic wall-stress is directly proportional to systolic LV pressure. But systolic wall-stress is also directly proportional to the degree of wall curvature (radius), …
Contributors PM-L, RY and JB: conception and design of manuscript, prepared figures; drafted manuscript; approved final version of manuscript.
Funding This study was supported by grants PIS015/02211 and RD12/0042 (Red de Investigación Cardiovascular), from the Instituto de Salud Carlos III, and the Juan de la Cierva-incorporación fellowship (IJCI-2014-19507) (to PM-L), Ministerio de Economía y Competitividad, Spain and by the EU—European Regional Development Fund.
Competing interests None declared.
Provenance and peer review Commissioned; internally peer reviewed.
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