Τίτλος:
Circulating platelet-progenitor cell coaggregate formation is increased in patients with acute coronary syndromes and augments recruitment of cd341 cells in the ischaemic microcirculation
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
Aims The aim of the present study was to evaluate the levels of platelet interaction with circulating CD34+ cells in patients with stable angina pectoris (SAP) and acute coronary syndromes (ACS) and to study the functional consequence of coaggregates formation in vitro and in vivo. Methods and results Platelet binding to circulating progenitor cells was defined by the presence of the platelet-specific marker glycoprotein Ib (CD42b) on the surface of CD34+ cells using flow cytometry. The percentage of CD34+/CD42b+ cell coaggregates was increased in patients with ACS (n 1/4 162), and especially in patients with ST-elevation myocardial infarction (STEMI) (n 1/4 44), compared with patients with SAP (n 1/4 116; P , 0.001). In the ANCOVA analysis, platelet/ CD34+ cell coaggregates were independently increased in ACS after adjustment for possible confounders. In a subgroup of our cohort, we also evaluated the levels of CD34+/CD133+/CD42b+ cell coaggregates, which were also significantly increased in ACS, and especially in STEMI (P , 0.05). Platelet/CD34+ cell coaggregates formation correlated with platelet activation (P 1/4 0.001). In a prospective pilot study of patients with AMI (n 1/4 40) using cardiac MRI, patients with increased baseline platelet/CD34+ cell coaggregates presented with a less myocardial infarct size and better left ventricular function at a 3-month follow-up compared with patients with lower coaggregates (P , 0.05 for all). The adhesion of platelet/CD34+ cell coaggregates onto the extracellular matrix and to endothelial monolayer was enhanced compared with CD34+ under high shear rates in vitro (P , 0.05) and within the microcirculation in mice after ischaemia/reperfusion injury as assessed by intravital microscopy (P , 0.05). Conclusions These findings imply that circulating platelet/CD34+ cell coaggregate levels are increased in ACS, especially in STEMI, which may be a novel mechanism of domiciliation of CD34+ progenitor cells to the injured microvasculature after acute myocardial infarction. © 2013 The Author.
Συγγραφείς:
Stellos, K.
Bigalke, B.
Borst, O.
Pfaff, F.
Elskamp, A.
Sachsenmaier, S.
Zachmann, R.
Stamatelopoulos, K.
Schönberger, T.
Geisler, T.
Langer, H.
Gawaz, M.
Περιοδικό:
EUROPEAN HEART JOURNAL-CARDIOVASCULAR PHARMACOTHERAPY
Λέξεις-κλειδιά:
acetylsalicylic acid; C reactive protein; CD34 antigen; clopidogrel; collagen; creatine kinase; glycoprotein Ib alpha; PADGEM protein; stromal cell derived factor 1; troponin I, acute coronary syndrome; acute heart infarction; article; cardiac patient; cardiovascular magnetic resonance; cardiovascular risk; cell adhesion; comparative study; controlled study; extracellular matrix; flow cytometry; fluorescence microscopy; follow up; heart infarction size; heart left ventricle ejection fraction; heart left ventricle function; heart muscle contractility; heart muscle ischemia; heart stroke volume; human; human cell; in vitro study; in vivo study; major clinical study; microcirculation; non ST segment elevation myocardial infarction; priority journal; reperfusion injury; shear rate; shear stress; ST segment elevation myocardial infarction; stable angina pectoris; stem cell; thrombocyte; thrombocyte activation; thrombocyte aggregation, Acute coronary syndrome; Microcirculation; Platelets; Progenitor cells, Acute Coronary Syndrome; Aged; Angina, Stable; Animals; Antigens, CD34; Blood Platelets; Extracellular Matrix Proteins; Female; Humans; Leukocytes, Mononuclear; Male; Mice; Microcirculation; Myocardial Infarction; Pilot Projects; Platelet Activation; Platelet Aggregation Inhibitors; Risk Factors; Stem Cells
DOI:
10.1093/eurheartj/eht131
