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Updated: Aug 25, 2025

Studying Left Ventricular Reverse Remodeling by Aortic Debanding in Rodents
Published on: July 14, 2021
Long-term changes in coronary physiology after aortic valve replacement
Muhammad Sabbah1, Niels T Olsen2,3, Lene Holmvang1
1Department of Cardiology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.
Insights
Coronary flow reserve (CFR) improved after aortic valve replacement, driven by reduced resting flow, not increased hyperemic flow. This improvement correlated with decreased left ventricular stroke work, suggesting beneficial cardiac remodeling.
Area of Science:
- Cardiology
- Cardiovascular Physiology
- Medical Imaging
Background:
- Severe aortic stenosis (AS) can cause left ventricular hypertrophy (LVH) and impair coronary flow reserve (CFR).
- The reversibility of these effects after aortic valve replacement (AVR) is not fully understood.
Purpose of the Study:
- To assess changes in LAD CFR post-AVR and their relation to hyperemic flow (QLAD) and microvascular resistance (Rμ,LAD).
- To examine the correlation between CFR changes and alterations in left ventricular mass (LVM) and stroke work (LVSW).
Main Methods:
- Intracoronary thermodilution measured CFR, QLAD, and Rμ,LAD before and 6 months after AVR.
- Cardiac MRI quantified LVM and LVSW.
Main Results:
- CFR significantly increased post-AVR (p=0.005), despite unchanged QLAD and Rμ,LAD.
- Indexed QLAD increased by 39% (p<0.001).
- CFR improvement correlated with reduced LVSW (r=-0.39, p=0.047).
Conclusions:
- Aortic valve replacement improves CFR in the LAD, primarily due to a decrease in resting flow.
- The observed CFR improvement is linked to a reduction in left ventricular stroke work.
Background:
The detrimental effects of long-standing severe aortic stenosis (AS) often include left ventricular hypertrophy (LVH) and exhaustion of coronary flow reserve (CFR), the reversibility of which is unclear after valve replacement.
Aims:
Our aims were to 1) investigate whether CFR in the left anterior descending artery (LAD) would improve following valve replacement, and if the change was related to changes in hyperaemic coronary flow (QLAD) and minimal microvascular resistance (Rμ,LAD); and 2) investigate the relationship between changes in CFR and changes in left ventricular mass (LVM) and stroke work (LVSW).
Methods:
We measured intracoronary bolus thermodilution-derived CFR, and continuous thermodilution-derived QLAD and Rμ,LAD before and 6 months after aortic valve replacement. Cardiac magnetic resonance imaging was used to quantify left ventricular anatomy and function for the calculation of LVM and LVSW. Results: Thirty-four patients were included (17 patients had transcatheter aortic valve implantation; 14 had surgical valve replacement with a bioprosthesis and 3 with a mechanical prosthesis) who underwent invasive assessment in the LAD. CFR increased from 2.5 (interquartile range [IQR] 1.5-3.3) at baseline to 3.1 (IQR 2.2-5.1) at follow-up (p=0.005), despite no significant change in QLAD (230±106 mL/min to 250±101 mL/min; p=0.26) or Rμ,LAD (347 [IQR 247-463] to 287 [IQR 230-456]; p=0.20). When indexed for LVM, QLAD was 39% (IQR 8-98%) higher at follow-up compared with baseline (p<0.001). The improvement in CFR was correlated with ΔLVSW, r= -0.39; p=0.047. Conclusions: CFR in the LAD increased significantly at follow-up although global hyperaemic flow and minimal microvascular resistance remained unchanged. Thus, a decrease in resting flow was the cause of CFR improvement. CFR improvement was associated with reduction in LVSW.
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