Spectral Doppler imaging of post‐ectopic beat and low‐dose dobutamine stress echocardiography

This case highlights that the valve parameters measured after ventricular ectopic beat are similar to those measured during low-dose dobutamine stress echocardiography (LD-DSE) and may help distinguish between true and pseudo-severe aortic stenosis (AS) in left ventricular (LV) dysfunction. When ventricular bigeminy (VB) causes beat-to-beat variation in stroke volume (SV), post-ectopic spectral Doppler data can help determine the severity of AS, particularly in low-flow, low-gradient AS. In a similar context of SV augmentation by LD-DSE,1 post-extra systolic potentiation (PESP), an intrinsic property of transient increase in myocardial contractility after a premature beat, may also contribute to an increase in SV.2 When there is a low-flow scenario, both PESP and LD-DSE may normalize the SV to differentiate between true and pseudo-severe AS (by a stress aortic valve area (AVA) >1.0 cm2 under a lower stress mean gradient 20% increase in SV, AVA <1.0 cm2 and a projected AVA of 0.75 cm2 (as per the European Society of Cardiology and European Association for Cardio-Thoracic Surgery guidelines3). The patient underwent surgical AV replacement, and at the one-month follow-up, echocardiography showed an improvement in LVEF (from 27% to 35%), normal function of replaced AV, and an increased SV (SV = 60 mL, SV index = 37.2 mL/m2) (Figure 3). The SV decreases following a PVC (due to the shortened diastolic filling time preceding the PVC). However, PESP augments the SV by up to 170% (or even 300%) following a PVC (120% in the present study, 20.8 mL vs. 45.7 mL).4 Unfortunately, it was not possible to measure the baseline SV during normal sinus contraction. Nonetheless, the increase in SV due to PESP following PVC could help refine the correction of AVA using SV changes; the increase in SV during LD-DSE during normal sinus rhythm was 47% (38 mL vs. 56.1 mL). Although the peak velocities in LD-DSE and post-PVC were similar, they were less valuable in evaluating AS severity. Therefore, calculating the projected AVA may be necessary. As for severe LV dysfunction with low SV, even if severe AS with AVA <1.0 cm2 (as per the European Society of Cardiology guidelines) was still observed during LD-DSE, post-ectopic Doppler measurements led to conflicting findings, with AV peak velocity <4.0 m/s.1 With decreased contractile reserve, AV opening becomes inadequate at low flow rates; the AVA is mainly determined by the transvalvular flow rate (ratio of SV to ejection time). Because of the discrepancy between the AVA and peak velocity (or mean pressure gradient), the projected AVA may be necessary for a more accurate estimation of AS severity if the transvalvular flow rate normalizes more than 250 mL/s and increases by more than 15% during LD-DSE.5 Furthermore, SV augmentation with catheter-induced PESP was also validated to correlate with the severity of projected AVA.6 Considering our findings, an increase in SV following PESP may supplement low-flow, low-gradient AS severity assessment in cases where LD-DSE is inconclusive. The informed consent was waived because of the nature of the retrospective study, and we got the permission for publication from our institution. The authors declare no conflicts of interest.