February 10, 2006Cardiovascular Research
Bone marrow molecular alterations after myocardial infarction: Impact on endothelial progenitor cells
Key result
ACE inhibition or statin treatment significantly increased EPC levels in rats post-myocardial infarction, reversing initial reductions to 60±12% and 68±7% (p<0.05).
Why the study?
Does ACE inhibition or statin treatment improve endothelial progenitor cell mobilization and bone marrow molecular alterations in rats post-myocardial infarction?
Population
Rats post-myocardial infarction
Comparison
Angiotensin converting enzyme inhibition or… vs Untreated post-myocardial infarction rats
Design
Preclinical
Follow-up
Up to 10 weeks post-infarction
Authors
Discussion
Loading...
Member takes
Implication
May enhance EPC mobilization post-MI in rats; hypothesis-generating, no practice change warranted.
Structured PICO
Does ACE inhibition or statin treatment improve endothelial progenitor cell mobilization and bone marrow molecular alterations in rats post-myocardial infarction?
P
Population
Rats post-myocardial infarction followed for up to 10 weeks to assess bone marrow molecular alterations and endothelial progenitor cell levels.
I
Intervention
Angiotensin converting enzyme (ACE) inhibition or HMG-CoA reductase inhibition (statin)
C
Comparator
Untreated post-myocardial infarction rats
O
Outcome
Endothelial progenitor cell (EPC) levels and bone marrow molecular pathways (ERK phosphorylation, MMP-9 activity, VEGF protein levels, Akt phosphorylation, eNOS activity, ROS levels)surrogate
Main Result
p-value: p=< 0.05
ACE inhibitors and statins improve endothelial progenitor cell mobilization post-myocardial infarction in rats via distinct bone marrow molecular pathways, correlating with improved cardiac function.
Cite This Study
Thum et al. (2006) studied Myocardial infarction. ACE inhibition or statin treatment was evaluated on Endothelial progenitor cell (EPC) levels and formation of endothelial colony forming units (CFU) (p=< 0.05). ACE inhibition or statin treatment significantly increased EPC levels in rats post-myocardial infarction, reversing initial reductions to 60±12% and 68±7% (p<0.05).