Non-invasive left ventricle strain-volume-pressure loops in asymptomatic patients with significant aortic regurgitation: potential to improve prediction of optimal timing for aortic valve surgery
E K de Oliveira, D Buytaert, A Moya, M Shumkova, R Mistrulli, M Fialova, K Medilek, J Spapen, S Brouwers, G Van Camp, R Kockova, M PenickaAbstract
Background
Severe aortic regurgitation (AR) causes left ventricular (LV) pressure and volume overload with irreversible myocardial damage, which often occurs before meeting the aortic valve surgery indication (AVSi) per guidelines. Developing cost-effective imaging markers to identify the initial effects of pressure-volume overload due to AR is crucial.
Aim
To analyze the performance of the echocardiographic strain-volume-pressure loop surface area (SVPLsa) in predicting the onset of Class I AVSi in asymptomatic individuals with significant AR and preserved LVEF (> 50%) without ESC Guidelines 2025 indications for AV surgery according to the class of indication.
Methods
This multicenter study included 95 consecutive patients [80 (84.2%) male, 45 ± 14 years] with asymptomatic significant AR in sinus rhythm and preserved LVEF > 50%, who did not have any ESC Guidelines 2025 Class I indication for AV surgery. For the second analysis, only the patients without Class I and IIb indications for AV surgery at baseline were included. This subgroup consisted of 77 patients (84.4% male, 44 ± 14 years). Comprehensive echocardiography was analyzed by an experienced operator blinded to the clinical outcome. SVPL and its SVPLsa were analyzed using customized software.
Results
During a median follow-up of 1375 [interquartile range 1041–1783] days, 34 (36%) patients developed class I AVS, i.e., either symptoms or LV dysfunction. At baseline, the group with versus without onset of AVSi showed significantly larger SVPLsa (Delta 22%, p<0.001) while age, gender, LV end-systolic diameter (LVESDi), LVEF, and global longitudinal strain were similar (all non-significant - NS). In multivariable Cox regression analysis, adjusted for age, gender, and BNP, SVPLsa emerged as a strong independent predictor of AVSi (adjusted HR [95% CI 3.400 (1.681-6.878)]; p<0.001). In contrast, the presence of class IIb AVSi (n=18; 19%) patients at baseline, i.e., LVSDi between 22-25 mm/m², LV end-systolic volume index > 45 ml/m² or LVEF between 50-55%, was not a predictor (NS). In the subgroup, 19 (24,7%) patients developed class I AVSi, and who presented an elevated SVPL surface area at baseline still had a higher risk of 3.051 [95% CI 1.327-7.013; p=0.009] of AVSi.
Conclusion
The non-invasive strain-volume-pressure loop detects early changes in LV geometry and function due to pressure-volume overload in significant AR. Patients with larger SVPLsa are at higher risk of faster disease progression and warrant close clinical follow-up, even when accounting for all currently suggested parameters outlined in the guidelines.Figure SVPLsa