Patients with atrial septal defects had a lower septal contribution to left ventricular stroke volume at rest compared to healthy controls (-1% vs 7%, P<0.05).
Observational (n=57)
How do regional ventricular pumping mechanisms differ between patients with atrial septal defects, pulmonary regurgitation, and healthy controls, and how do they change after dobutamine stress and ASD closure?
Ventricular pumping mechanisms in right ventricular volume overload are driven by the underlying etiology rather than the degree of right ventricular dilation, and these mechanisms rapidly adapt following ASD closure.
Absolute Event Rate: -1% vs 7%
p-value: p=<0.05
BACKGROUND: Regional ventricular pumping mechanisms in patients with volume-loaded right ventricles (RV) are altered, but the cause is unknown. The aim was to determine whether these changes in ventricular pumping mechanisms are influenced by the RV dilatation itself or the aetiology behind it. METHODS: Seventeen patients with atrial septal defects (ASD) and 10 healthy controls underwent cardiovascular magnetic resonance (CMR) at rest and during dobutamine/atropine stress. Sixteen patients underwent transcutaneous ASD closure. Follow-up CMR at rest was performed the following day. Thirty patients with RV overload due to pulmonary regurgitation (PR) underwent CMR at rest. Cine images were used to measure left ventricular (LV) and RV volumes as well as septal, longitudinal and lateral contributions to LV and RV stroke volume (SV). RESULTS: At rest, septal contribution to LVSV was lower in ASD patients than controls (-1% versus 7%, P<0·05), but there was no difference in longitudinal or lateral contribution to SV. Patients with PR had lower longitudinal contribution to RV with increased lateral and septal contribution. During dobutamine stress, longitudinal contribution to LV and RVSV decreased and lateral contribution increased for ASD patients and controls. The day after ASD closure, septal contribution to LVSV was 6%, longitudinal contribution had increased for RVSV (P<0·05) and decreased for LVSV (P<0·01). CONCLUSION: Pumping mechanisms in patients with RV volume overload depend on the aetiology for the RV dilation and not the size of the RV.
Stephensen et al. (Wed,) conducted a observational in Atrial septal defect and pulmonary regurgitation (n=57). Atrial septal defect (ASD) vs. Healthy controls was evaluated on Septal contribution to left ventricular stroke volume at rest (p=<0.05). Patients with atrial septal defects had a lower septal contribution to left ventricular stroke volume at rest compared to healthy controls (-1% vs 7%, P<0.05).