Effects of myocardial postconditioning on the recruitment of endothelial progenitor cells
Christian Jung1, Peder Sörensson, Nawsad Saleh
1Department of Medicine, Division of Cardiology, Karolinska Institutet, Stockholm, Sweden. christian.jung@ki.se
Insights
Ischemic postconditioning (PostC) did not improve endothelial progenitor cell (EPC) mobilization in patients with ST-elevation myocardial infarction (STEMI). EPC recruitment appears linked to ischemia duration, not infarct size, suggesting further research into PostC
Area of Science:
- Cardiovascular Medicine
- Regenerative Medicine
- Interventional Cardiology
Background:
- Ischemic postconditioning (PostC) may protect the myocardium in ST-elevation myocardial infarction (STEMI) by improving endothelial function and altering cytokine release.
- These mechanisms are crucial for endothelial progenitor cell (EPC) recruitment, vital for re-endothelialization and neoangiogenesis.
- The study investigates PostC's effect on EPC recruitment in STEMI patients.
Purpose of the Study:
- To determine if ischemic postconditioning (PostC) influences endothelial progenitor cell (EPC) mobilization in patients with ST-elevation myocardial infarction (STEMI).
- To explore the relationship between PostC, EPC subpopulations, and infarct size.
- To assess the correlation between symptom-to-balloon time and progenitor cell mobilization.
Main Methods:
- 20 STEMI patients were randomized to PostC or conventional percutaneous coronary intervention (PCI).
- EPC subpopulations were quantified using flow cytometry immediately and on day 4.
- Myocardial risk and infarct size were assessed using cardiovascular magnetic resonance.
Main Results:
- PostC did not significantly alter the number of analyzed EPC subpopulations (CD34+, CD133+, CD34+CD133+, CD34+KDR+, CD34-CD133+KDR+, CD34+CD133+KDR+).
- Left ventricular ejection fraction, myocardium at risk, and infarct size showed no correlation with EPC mobilization.
- Shorter symptom-to-balloon times correlated inversely with mobilization of CD34+, CD133+, and CD34+CD133+ cells.
Conclusions:
- Ischemic PostC did not enhance EPC mobilization in STEMI patients.
- Progenitor cell recruitment appears more dependent on ischemia duration than the size of the ischemic area.
- Further research is needed to elucidate PostC's impact on endothelial surface markers and their role in EPC recruitment and homing.
Background:
Ischemic postconditioning (PostC), brief repetitive cycles of ischemia and reperfusion during early reperfusion, is suggested to protect the myocardium in patients with stent thrombosis-elevation myocardial infarction (STEMI) by improved endothelial dysfunction and alteration of cytokine release. These mechanisms are also of importance for the recruitment of endothelial progenitor cells (EPC), an endogenous repair mechanism for re-endothelialization and neoangiogenesis. The aim of this study was to investigate the effect of PostC on recruitment of EPC.
Methods:
EPC were analyzed in 20 patients with STEMI randomized to receive four cycles of PostC following percutaneous coronary intervention (PCI) or conventional PCI. Different subpopulations of EPC were quantified immediately and on day 4 using flow cytometry. Myocardium at risk, and infarct size was determined by cardiovascular magnetic resonance.
Results:
There was no influence of PostC on the number of different EPC (CD34(+) , CD133(+) , CD34(+) CD133(+) , CD34(+) KDR(+) , CD34(-) CD133(+) KDR(+) , CD34(+) CD133(+) KDR(+) ). Left ventricular ejection fraction, myocardium at risk, and infarct size did not correlate to the mobilization of EPC. There was an inverse correlation between the symptom-to-balloon time and the mobilization of progenitor precursor cells (CD34(+) cells: R =-0.527, P = 0.02; CD133(+) cells: R =-0.624, P = 0.004; CD34(+) CD133(+) cells: R =-0.466, P = 0.04).
Discussion:
Ischemic PostC did not result in improved mobilization of EPC in STEMI patients. The recruitment of progenitor cells seems to be related to the duration of ischemia rather than the size of the ischemic myocardial area. More effort is needed to understand the changes of endothelial surface markers by PostC and their role in EPC recruitment and homing.
