Haemodynamic left-ventricular changes during dobutamine stress in patients with atrial septal defect assessed with magnetic resonance imaging-based pressure-volume loops.

Background: Atrial septal defect (ASD) results in a left-to-right shunt causing right-ventricular (RV) volume overload and decreased cardiac output from the left ventricle. Pressure-volume (PV) loops enable comprehensive assessment of ventricular function and might increase understanding of the pathophysiology of ASD. The aim of this study was to investigate if left-ventricular (LV) haemodynamic response to stress in patients with ASD differs from controls.
Material and Methods: Patients with ASD (n = 18, age 51 ± 18) and healthy controls (n = 16, age 35 ± 13) underwent cardiac magnetic resonance (CMR) and brachial cuff pressure measurements at rest and during dobutamine stress. An in-house, validated method was used to compute PV loops.
Results: Patients had lower stroke work, potential energy and external power at rest than controls (p < 0.001; p < 0.05; p < 0.05). Stroke work and external power increased and potential energy decreased during stress in patients (p < 0.05; p < 0.0001; p < 0.01) and controls (p < 0.0001; p < 0.001; p < 0.01). Contractility and arterial elastance at rest were higher in patients than controls (p < 0.01; p < 0.01). Contractility increased during stress in both groups (p < 0.0001; p < 0.001). There was no difference between patients and controls in arterio-ventricular coupling.
Conclusion: LV haemodynamic response to stress can be assessed using noninvasive PV loops derived from CMR and brachial blood pressure. Patients with ASD had normal LV energy efficiency, in contrast to other patient groups with decreased cardiac output. Data suggest that patients with ASD had an increased inotropic level at rest with high contractility and heart rate but were able to respond with a further increase during stress, albeit to not as high a cardiac output as controls.
(© 2022 The Authors. Clinical Physiology and Functional Imaging published by John Wiley & Sons Ltd on behalf of Scandinavian Society of Clinical Physiology and Nuclear Medicine.)