Left ventricular pressure-strain-volume-loop and myocardial work patterns in asymptomatic severe aortic regurgitation with early disease decompensation

Severe aortic regurgitation (AR) is associated with left ventricular (LV) pressure and volume overload, leading to irreversible myocardial damage often before the onset of guidelines triggers for aortic valve surgery. Therefore, the development of sensitive imaging markers to detect the early impact of pressure-volume overload imposed by AR on LV geometry and function is needed.

To describe patterns of LV pressure-strain-volume loops, their components and myocardial work in asymptomatic patients with significant AR and preserved LV ejection fraction with early disease progression.

This multicenter study consisted of 95 consecutive patients (84.1% male, 45±14 years) with asymptomatic significant AR, in sinus rhythm, and preserved LV ejection fraction (EF) >50%, who did not have any indication for aortic valve surgery as per current guidelines. Comprehensive echocardiography was analyzed by an experienced operator blinded to clinical outcome. Pressure-strain-volume loops (PSVL), their components, and myocardial work were analyzed using customized software.

During a median follow-up of 1375 [interquartile range 1041-1783] days, a total of 34 (36%) patients developed the class I indication for aortic valve surgery, i.e. either symptoms or LV dysfunction (AVsurg group). At baseline, LVEF (64±5% vs. 64±7%;p=0.748), global longitudinal strain (-17.6 ± -2.4% vs. -18.5 ± -2.4%; p=0.112), global myocardial work index (1963±429 vs.1900±340 mmHg%; p=0.429) or global constructive work (2371±495 vs. 2287±368 mmHg%; p=0.390) did not differ significantly between groups. In contrast, global wasted work was significantly higher (149[90-204] vs.106[80-152] mmHg%; p=0.031) in the Avsurg group compared to the patients without progression for AV surgery indication (CON group). Moreover, the AVsurg group showed a larger PSVL area than the CON group probability due to the larger strain-volume (234 [129-380] vs.155 [88-216] %mL; p=0.021) and pressure-volume (12504 [9318- 15073] vs. 10192 [8004-11918] mmHg.mL; p=0.002) component, while the pressure-strain loop was similar between groups (Figure 1).

Non-invasive pressure-strain-volume loop reflects early changes in LV geometry and function due to chronic pressure-volume overload in significant AR. Patients with early disease decompensation show larger PSVL than stable individuals. The clinical utility of this index needs to be investigated in future studies.

Figure 1