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Original research
Proof of concept study on coronary microvascular function in low flow low gradient aortic stenosis
  1. Roberto Scarsini1,2,
  2. Michele Pighi1,
  3. Andrea Mainardi1,
  4. Leonardo Portolan1,
  5. Paolo Springhetti1,
  6. Concetta Mammone1,
  7. Francesco Della Mora1,
  8. Diego Fanti1,
  9. Domenico Tavella1,
  10. Leonardo Gottin3,
  11. Corinna Bergamini1,
  12. Giovanni Benfari1,
  13. Gabriele Pesarini1,
  14. Flavio Luciano Ribichini1
  1. 1Department of Medicine, Division of Cardiology, University of Verona, Verona, Italy
  2. 2Department of Medicine, Division of Cardiology, Azienda Ospedaliera Universitaria Integrata Verona, Verona, Veneto, Italy
  3. 3Department of Intensive Care and Anesthesiology, University of Verona, Verona, Italy
  1. Correspondence to Dr Roberto Scarsini, Department of Medicine, Division of Cardiology, Azienda Ospedaliera Universitaria Integrata Verona, Verona 37126, Italy; roberto.scarsini{at}aovr.veneto.it

Abstract

Objectives We hypothesised that low flow low gradient aortic stenosis (LFLGAS) is associated with more severe coronary microvascular dysfunction (CMD) compared with normal-flow high-gradient aortic stenosis (NFHGAS) and that CMD is related to reduced cardiac performance.

Methods Invasive CMD assessment was performed in 41 consecutive patients with isolated severe aortic stenosis with unobstructed coronary arteries undergoing transcatheter aortic valve implantation (TAVI). The index of microcirculatory resistance (IMR), resistive reserve ratio (RRR) and coronary flow reserve (CFR) were measured in the left anterior descending artery before and after TAVI. Speckle tracking echocardiography was performed to assess cardiac function at baseline and repeated at 6 months.

Results IMR was significantly higher in patients with LFLGAS compared with patients with NFHGAS (24.1 (14.6 to 39.1) vs 12.8 (8.6 to 19.2), p=0.002), while RRR was significantly lower (1.4 (1.1 to 2.1) vs 2.6 (1.5 to 3.3), p=0.020). No significant differences were observed in CFR between the two groups. High IMR was associated with low stroke volume index, low cardiac output and reduced peak atrial longitudinal strain (PALS). TAVI determined no significant variation in microvascular function (IMR: 16.0 (10.4 to 26.1) vs 16.6 (10.2 to 25.6), p=0.403) and in PALS (15.9 (9.9 to 26.5) vs 20.1 (12.3 to 26.7), p=0.222). Conversely, left ventricular (LV) global longitudinal strain increased after TAVI (−13.2 (8.4 to 16.6) vs −15.1 (9.4 to 17.8), p=0.047). In LFLGAS, LV systolic function recovered after TAVI in patients with preserved microvascular function but not in patients with CMD.

Conclusions CMD is more severe in patients with LFLGAS compared with NFHGAS and is associated with low-flow state, left atrial dysfunction and reduced cardiac performance.

  • transcatheter aortic valve replacement
  • aortic valve stenosis
  • echocardiography
  • cardiac catheterization
  • heart failure, systolic

Data availability statement

Data are available on reasonable request.

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Footnotes

  • RS and MP contributed equally.

  • Contributors All authors have contributed to conception and design or analysis and interpretation of data, or both, to drafting of the manuscript or revising it critically for important intellectual content and to final approval of the manuscript submitted. RS acts as guarantor of the study, accepting full responsibility for the work and/or the conduct of the study, had access to the data, and controlled the decision to publish.

  • Funding This study received a research grant from Abbott Vascular (n.1333-12/2020).

  • Competing interests This study received a research grant from Abbott Vascular (n.1333-12/2020). RS is on advisory boards for Abbott. FR received research grants from Philips and Abbott.

  • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.