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Original research
Absolute coronary flow and microvascular resistance reserve in patients with severe aortic stenosis
  1. Pasquale Paolisso1,2,
  2. Emanuele Gallinoro1,
  3. Marc Vanderheyden1,
  4. Giuseppe Esposito1,2,
  5. Dario Tino Bertolone1,2,
  6. Marta Belmonte1,3,
  7. Niya Mileva1,
  8. Konstantinos Bermpeis4,
  9. Cristina De Colle1,2,
  10. Davide Fabbricatore1,2,
  11. Alessandro Candreva1,
  12. Daniel Munhoz1,2,
  13. Ivan Degrieck5,
  14. Filip Casselman5,
  15. Martin Penicka4,
  16. Carlos Collet1,
  17. Jeroen Sonck1,
  18. Fabio Mangiacapra6,
  19. Bernard de Bruyne1,
  20. Emanuele Barbato1,2
  1. 1 Hartcentrum OLV Aalst, Aalst, Belgium
  2. 2 Department of Advanced Biomedical Sciences, Federico II University Hospital, Napoli, Campania, Italy
  3. 3 Centro Cardiologico Monzino Istituto di Ricovero e Cura a Carattere Scientifico, Milano, Lombardia, Italy
  4. 4 Cardiology, Hartcentrum OLV Aalst, Aalst, Flanderen, Belgium
  5. 5 Cardiovascular and Thoracic Surgery, Hartcentrum OLV Aalst, Aalst, Belgium
  6. 6 Campus Bio-Medico University, Roma, Lazio, Italy
  1. Correspondence to Dr Emanuele Barbato, Advanced Biomedical Sciences, Federico II University Hospital, 80131 Napoli, Italy; barba22{at}


Background Development of left ventricle (LV) hypertrophy in aortic stenosis (AS) is accompanied by adaptive coronary flow regulation. We aimed to assess absolute coronary flow, microvascular resistance, coronary flow reverse (CFR) and microvascular resistance reserve (MRR) in patients with and without AS.

Methods Absolute coronary flow and microvascular resistance were measured by continuous thermodilution in 29 patients with AS and 29 controls, without AS, matched for age, gender, diabetes and functional severity of epicardial coronary lesions. Myocardial work, total myocardial mass and left anterior descending artery (LAD)-specific mass were quantified by echocardiography and cardiac-CT.

Results Patients with AS presented a significantly positive LV remodelling with lower global longitudinal strain and global work efficacy compared with controls. Total LV myocardial mass and LAD-specific myocardial mass were significantly higher in patients with AS (p=0.001). Compared with matched controls, absolute resting flow in the LAD was significantly higher in the AS cohort (p=0.009), resulting into lower CFR and MRR in the AS cohort compared with controls (p<0.005 for both). No differences were found in hyperaemic flow and resting and hyperaemic resistances. Hyperaemic myocardial perfusion (calculated as the ratio between the absolute coronary flow subtended to the LAD, expressed in mL/min/g), but not resting, was significantly lower in the AS group (p=0.035).

Conclusions In patients with severe AS and non-obstructive coronary artery disease, with the progression of LV hypertrophy, the compensatory mechanism of increased resting flow maintains adequate perfusion at rest, but not during hyperaemia. As a consequence, both CFR and MRR are significantly impaired.

  • Aortic stenosis
  • Coronary Artery Disease

Data availability statement

Data are available on reasonable request.

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Data availability statement

Data are available on reasonable request.

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  • Twitter @P_Paolisso, @EGallinoro, @BernardBruyne

  • PP and EG contributed equally.

  • Contributors PP and EG contributed to conception and design of the study. PP, EB, GE, DTB, MB, NM, KB, CDC, DF, AC and DM organised the database and collected data. EG, PP and FM performed the statistical analysis. PP and EG wrote the first draft of the manuscript. MV, BdB and EB wrote sections of the manuscript. ID, FC, MP, CC, JS, FM, BdB and EB revised the article and approved the final version of the manuscript. All authors contributed to manuscript revision, read and approved the submitted version. Statement of guarantor: EB is the guarantors of the research and, as such, had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.

  • Funding PP, GE, DF and JS are supported by a research grant from the CardioPaTh PhD Programme. CC reports receiving research grants from Biosensor, Coroventis Research, GE Healthcare, Medis Medical Imaging, Pie Medical Imaging, Cathworks, Boston Scientific, Siemens, HeartFlow Inc. and Abbott Vascular and consultancy fees from Heart Flow Inc, Opsens, Pie Medical Imaging, Abbott Vascular and Philips Volcano. BdB has a consulting relationship with Boston Scientific, Abbott Vascular, CathWorks, Siemens and Coroventis Research; receives research grants from Abbott Vascular, Coroventis Research, Cathworks, Boston Scientific and holds minor equities in Philips-Volcano, Siemens, GE Healthcare, Edwards Life Sciences, HeartFlow, Opsens and Celiad. EB declares speaker’s fees from Abbott Vascular, Boston Scientific and GE.

  • Competing interests None declared.

  • 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.

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