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15 Validation of fractal dimension of the incipient blood clot in stemi and stable coronary artery disease
  1. Ahmed Sabra1,2,3,
  2. Matthew James Lawrence1,2,
  3. Daniel Obaid3,
  4. Alexander Chase3,
  5. Dave Smith3,
  6. Phillip Thomas3,
  7. Karl Hawkins2,
  8. Phylip Rhodri Williams4,
  9. Keith Morris5,
  10. Phillip Adrian Evans1,2,6
  1. 1NISCHR Haemostasis Biomedical Research Unit, Morriston Hospital, ABMU Health Board, Swansea
  2. 2NISCHR Haemostasis Biomedical Research Unit, College of Medicine, Swansea University, Swansea
  3. 3Cardiac Centre, Morriston Hospital, ABMU Health Board, Swansea
  4. 4College of Engineering, Swansea University, Swansea
  5. 5School of Applied Science, Cardiff Metropolitan University, Cardiff
  6. 6Department of Emergency Medicine, Morriston Hospital, ABMU Health Board, Swansea


Background Antithrombotics are the mainstay of management in coronary artery disease (CAD). However, no biomarker is available to assess their global effect on clot formation and structure. We validated a novel biomarker that measures clot microstructure, fractal dimension of incipient blood clot (df), in healthy volunteers, stroke, lung cancer and sepsis.

Aims To validate df in both acute and stable CAD, and assess the effect of therapeutic intervention.

Methods We prospectively recruited 2 groups:

  1. serial venous blood samples were collected on admission, after primary percutaneous coronary intervention (pPCI) and 24 hours in patients with STEMI, and

  2. 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%).

Results In 38 STEMI patients, df after pPCI was lower than df on admission (mean 1.631±0.063 vs 1.751±0.052, p<0.000001) whereas df at 24 hour was similar to that on admission. For group 2, a significant difference in df was observed between obstructive CAD and unobstructive CAD (mean 1.748±0.057 vs 1.732±0.052, p 0.028), where patients with significant CAD produce denser, more tightly packed clots.

Conclusions We characterise clot microstructure, as measured by df, in patients with STEMI and 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.

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