Looking backwards: is it time to assess veno-atrial interactions in pulmonary arterial hypertension?

Abstract

@ERSpublications Vena cava backflow measured using CMR imaging is a novel marker to assess veno-atrial interactions in patients with pulmonary arterial hypertension Right ventricular (RV) function is the major determinant of mortality in patients with pulmonary arterial hypertension (PAH). As a result, much of recent research has focused on right ventricular-pulmonary arterial coupling and, specifically, RV systolic function. As research on diastolic RV and right atrial function is beginning to emerge, the effect of the venous system on right ventricular function has been largely ignored. While observations regarding the effect of right ventricular function on venous return date to Aristotle (circa 380 BC), one of the earliest pathological descriptions came in 1873 when Kussmaul described a paradoxical rise in jugular venous pressure during inspiration in constrictive pericarditis [1][2][3]. This phenomenon can be explained by venous backflow in the setting of an elevated right atrial pressure and a noncompliant RV. To this day the determinants of venous backflow have yet to be worked out, but there is a strong clinical relevance, including the effects on RV workload and venous congestion mediated hepatic and renal dysfunction [4,5].With normal right ventricular function, ventricular contraction results in the movement of blood from the ventricle into the pulmonary circulation for oxygenation and subsequent delivery to the rest of the body (figure 1a). Invasive assessments of normal venous blood flow in dogs and healthy individuals demonstrate that the flow is remarkably pulsatile [1,6]. Venous blood flow to the heart is slowed during atrial systole and increases during ventricular systole [6]. Tricuspid insufficiency is one of the pathophysiological conditions that can lead to vena cava backflow. In an early study of vena cava blood flow, WEXLER et al.[6] observed marked backflow instead of forward flow during ventricular systole in a patient with tricuspid insufficiency. More contemporary evidence of this comes from cardiac magnetic resonance (CMR) imaging studies of patients with PAH and severe tricuspid regurgitation, where volumetric assessment of stroke volume (difference between RV end-diastolic volume and end-systolic volume) overestimates cardiac output compared to pulmonary artery and aortic flow measurements [7,8]. These differences were not observed in healthy volunteers or patients with mild tricuspid regurgitation suggesting that increasing tricuspid regurgitation can be a contributor to backflow into the right atrium from the RV. The contribution of right atrial contraction to venous backflow remains unknown.