Physiological Reports (Oct 2021)
Left atrial conduit function: A short review
Abstract
Abstract Three‐dimensional echocardiography can elucidate the phasic functions of the left atrium if a simultaneous acquisition of a pyramidal full‐volume dataset, as gathered from the apical window and containing the entire left atrial and left ventricular cardiac sections, is obtained. Hence, conduit can be quantified as the integral of net, diastolic, instantaneous difference between synchronized atrial and ventricular volume curves, beginning at minimum ventricular cavity volume and ending just before atrial contraction. Increased conduit can reflect increased downstream suction, as conduit would track the apex‐to‐base intracavitary pressure gradient existing, in early diastole, within the single chamber formed by the atrium and the ventricle, when the mitral valve is open. Such a gradient increases in response to adrenergic stimulation or during exercise and mediates an increment in passive flow during early diastole, with the ventricle being filled from the atrial reservoir and, simultaneously, from blood drawn from the pulmonary veins. In this context conduit, and even more conduit flow rate, expressed in ml/sec, can be viewed as an indirect marker of left ventricular relaxation. It is well known, however, that a large amount of conduit (in relative terms) is also supposed to contribute to LV stroke volume in conditions of increased resistance to LV filling, when diastolic function significantly worsens. Stiffening of the atrio‐ventricular complex implies increments in LA pressure more pronounced in late systole, causing markedly elevated “v” waves, independently of the presence of mitral insufficiency. The combination of increased atrio‐ventricular stiffness and conduit flow is associated with an elevation of the right ventricular pulsatile relative to resistive load that negatively impacts on exercise capacity and survival in these patients. Atrial conduit is an “intriguing” parameter that conveys a noninvasive picture of the complex atrioventricular coupling condition in diastole and its backward effects on the right side of the heart and the pulmonary circulation. Given the easiness associated with its correctly performed quantification in the imaging laboratory, I am sure that conduit will survive the competitive access to the list of valuable parameters capable of deciphering, although not necessarily simplifying, the complex diastolic scenario in health and disease.