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BAS/BSCR poster abstract
BAS/BSCR39 Circulating chemical and cellular injury/repair responses are linked to cardiac dysfunction and remodelling in human myocardial infarction
  1. R J McGeoch1,2,
  2. A McGarrity1,
  3. A R Payne1,2,
  4. S Watkins2,
  5. T Steedman2,
  6. A Davie2,
  7. W S Hillis2,
  8. M M Lindsay2,
  9. S D Robb2,
  10. E Rhaume3,
  11. J C Tardif3,
  12. K G Oldroyd2,
  13. C Berry1,2
  1. 1BHF Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, Scotland, UK
  2. 2Golden Jubilee National Hospital, Clydebank, UK
  3. 3Montreal Heart Institute, Montreal, Canada


Background Endogenous regenerative pathways may contribute to cardiovascular repair following ischaemic injury. Based on recent results in experimental studies, we investigated candidate endogenous chemical and cellular injury/repair responses in human myocardial infarction (MI).

Methods Circulating injury (eg, platelets) and repair (circulating CD34+ progenitor cells, serum vascular endothelial growth factor (VEGF) and thymosin β4, and urine acetyl-Ser-Asp-Lys-Pro (AcSDKP)) responses were quantified 2 days and 3 months after acute MI. Progenitor cells in whole blood were quantified using flow cytometry, and cytokines were measured by immunoassay. An automated analyser was used for haematological measurements. Invasive measures of coronary artery microvascular resistance and collateral supply were measured acutely using coronary thermodilution techniques. Cardiac function and remodelling were quantified by magnetic resonance imaging.

Results 35 consecutive patients with MI (mean±SD age 58%±10 years) were included. AcSDKP measured 2 days post-MI negatively predicted left ventricular ejection fraction (R2=0.43; p=0.024) and positively predicted left ventricular end-systolic volume index (R2=0.56; p=0.011) at 3 months. At follow-up, CD34+ count negatively predicted myocardial infarct mass (R2=0.29; p=0.015) and left ventricular end-systolic volume index (R2=0.20; p=0.02). In multivariable analyses, haemoglobin concentration measured 2 days post-MI negatively predicted coronary collateral supply (p=0.006), whereas red cell distribution width (p=0.004) and platelet count (p=0.0001) positively predicted coronary collateral supply. Serum VEGF at 3 months and change in VEGF were negative multivariable predictors of left ventricular end-diastolic volume index at 3 months (p=0.021 and p=0.006, respectively).

Conclusion Circulating chemical and cellular responses participate in myocardial injury and repair and represent targets for therapeutic development.

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