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Basic and translational research
Original research article
Characterisation of clot microstructure properties in stable coronary artery disease
  1. Ahmed Sabra1,2,3,
  2. Matthew James Lawrence1,2,
  3. Robert Aubrey1,
  4. Daniel Obaid4,
  5. Alexander Chase4,
  6. Dave Smith4,
  7. Phillip Thomas4,
  8. Sharon Storton1,2,
  9. Gareth R Davies1,2,
  10. Karl Hawkins2,
  11. Phylip Rhodri Williams5,
  12. Keith Morris6 and
  13. Phillip Adrian Evans1,2,7
  1. 1NISCHR Haemostasis Biomedical Research Unit, Morriston Hospital, ABMU Health Board, Swansea, UK
  2. 2NISCHR Haemostasis Biomedical Research Unit, College of Medicine, Swansea University, Swansea, UK
  3. 3Department of Cardiology, Princess of Wales Hospital, ABMU Health Board, Bridgend, UK
  4. 4Cardiac Centre, Morriston Hospital, ABMU Health Board, Swansea, UK
  5. 5College of Engineering, Swansea University, Swansea, UK
  6. 6School of Applied Science, Cardiff Metropolitan University, Cardiff, UK
  7. 7Department of Emergency Medicine, Morriston Hospital, ABMU Health Board, Swansea, UK
  1. Correspondence to Phillip Adrian Evans; phillip.evans2{at}wales.nhs.uk

Abstract

Background Coronary artery disease (CAD) is associated with an increased prothrombotic tendency and is also linked to unfavourably altered clot microstructure. We have previously described a biomarker of clot microstructure (df) that is unfavourably altered in acute myocardial infarction. The df biomarker assesses whether the blood will form denser or looser microstructures when it clots. In this study we assessed in patients with stable chest pain whether df can differentiate between obstructed and unobstructed CAD.

Methods A blood sample prior to angiography was obtained from 251 consecutive patients undergoing diagnostic coronary angiography. Patients were categorised based on angiographic findings as presence or absence of obstructive CAD (stenosis ≥50%). The blood sample was assessed using the df biomarker, standard laboratory markers and platelet aggregometry (Multiplate).

Results A significant difference (p=0.028) in df was observed between obstructive CAD (1.748±0.057, n=83) and unobstructive CAD (1.732±0.052, n=168), where patients with significant CAD produce denser, more tightly packed clots. df was also raised in men with obstructive CAD compared with women (1.745±0.055 vs 1.723±0.052, p=0.007). Additionally df significantly correlated with the platelets response to arachidonic acid as measured by the ASPItest area under the curve readings from platelet aggregometry (correlation coefficient=0.166, p=0.008), a low value of the ASPItest indicating effective aspirin use was associated with looser, less dense clots.

Conclusions For the first time, we characterise clot microstructure, as measured by df, in patients with stable CAD. df can potentially be used to risk-stratify patients with stable CAD and assess the efficacy of therapeutic interventions by measuring changes in clot microstructure.

  • atherosclerosis
  • coronary artery disease
  • coronary angiography
  • coagulation
  • clot microstructure

This is an Open Access article distributed in accordance with the terms of the Creative Commons Attribution (CC BY 4.0) license, which permits others to distribute, remix, adapt and build upon this work, for commercial use, provided the original work is properly cited. See: http://creativecommons.org/licenses/by/4.0/

https://doi.org/10.1136/openhrt-2016-000562

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    Footnotes

    • Contributors AS and MJL contributed to concept and design, performed rheological analysis, analysed data and critical writing. RA, KH and GRD recruited participants, collected and analysed data, and performed rheological experiments, DO, DS, AC and PT performed angiographies, analysed and collected data and contributed to the writing of the article. KM was the statistician of the project and contributed to concept and design and interpreted data. PRW and PAE contributed to concept and design, revised intellectual content and final approval of the version to be published. There is no additional data available for sharing.

    • Funding This translational work was supported by the National Institute of Social Care and Health Research (NISCHR) Biomedical Research Unit grant (BRO1) and the EPSRC grant (EP/L024799/1).

    • Competing interests None declared.

    • Patient consent No identifiable data were used or were reported in the manuscript. All data were anonymised to the researchers.

    • Ethics approval Wales REC 7.

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

    • Data sharing statement There is no additional data available for sharing.