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Progenitor cell mobilisation in patients with acute and chronic coronary artery disease
  1. A Gaspardone1,
  2. F Menghini1,
  3. V Mazzuca1,
  4. O Skossyreva1,
  5. G Barbato1,
  6. P de Fabritiis2
  1. 1Divisione di Cardiologia, Ospedale S Eugenio, Rome, Italy
  2. 2Ematologia, University Tor Vergata, Rome, Italy
  1. Correspondence to:
    Dr Achille Gaspardone
    U O C di Cardiologia, Ospedale S Eugenio, ASL Rm C, Piazzale dell’Umanesimo 10, 00144 Rome, Italy; a_gaspardone{at}yahoo.com

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Tissue ischaemia is considered to be a major trigger for progenitor cell mobilisation because of the massive release of reactive molecules caused by myocardial necrosis and tissue inflammation.1,2 Surprisingly, despite the growing number of clinical investigations of the effects of stem cell administration to patients with acute myocardial infarction (AMI), very little is known about the spontaneous mobilisation of progenitor cells in patients with different clinical manifestations of ischaemic heart disease.3,4 To understand better the biology of progenitor cell mobilisation in the clinical setting, we measured the concentration of circulating haematopoietic progenitor cell associated antigen CD34+ in patients with AMI or chronic stable angina (CSA) and in healthy controls. Furthermore, we correlated the magnitude of progenitor cell mobilisation with a variety of demographic, clinical, and biochemical variables.

METHODS

Forty five consecutive patients with AMI (25 with ST segment elevation and 20 with non-ST elevation AMI), 33 patients with CSA and significant coronary artery disease, and 30 healthy controls were enrolled in the present study. Patients with ST elevation AMI were thrombolysed with recombinant tissue plasminogen activator according to the GUSTO (global utilisation of streptokinase and t-PA for occluded coronary arteries) protocol. Patients with CSA had evidence of inducible ischaemia at non-invasive stress test and significant stenoses at coronary angiography but no history of AMI or acute coronary syndromes …

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Footnotes

  • This study was funded by a grant from the Associazione per lo Studio delle Malattie Cardiovascolari CARDIVA ONLUS No 73474, June 2004, Rome, Italy