Interventions for valvular disease and heart failure

Long-term changes in coronary physiology after aortic valve replacement

EuroIntervention 2023;18:1156-1164. DOI: 10.4244/EIJ-D-22-00621

Muhammad Sabbah
Muhammad Sabbah1, MD, PhD; Niels T. Olsen2,3, MD, PhD; Lene Holmvang1, MD, PhD; Hans-Henrik Tilsted1, MD, PhD; Frants Pedersen1, MD, PhD; Francis Richard Joshi1, MD, PhD; Rikke Sørensen1, MD, PhD; Reza Jabbari1, MD, PhD; Ketina Arslani1, MD; Lars Sondergaard1,3, MD, DMSc, PhD; Thomas Engstrøm1,3, MD, DMSc, PhD; Jacob Thomsen Lønborg1, MD, DMSc, PhD
1. Department of Cardiology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark; 2. Department of Cardiology, Copenhagen University Hospital – Herlev and Gentofte, Copenhagen, Denmark; 3. Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark

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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clinical researchcoronary artery diseasefractional flow reserveNormal coronary arteries
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