TY - JOUR
T1 - ACE inhibition modulates endothelial apoptosis and renewal via endothelial progenitor cells in patients with acute coronary syndromes
AU - Cangiano, Elisa
AU - Marchesini, Jlenia
AU - Campo, Gianluca
AU - Francolini, Gloria
AU - Fortini, Cinzia
AU - Carr, Giacomo
AU - Miccoli, Matteo
AU - Ceconi, Claudio
AU - Tavazzi, Luigi
AU - Ferrari, Roberto
PY - 2011
Y1 - 2011
N2 - Background: The equilibrium between endothelial apoptosis and endothelial renewal is altered in acute coronary syndromes and may be related to differences in the beneficial effects of angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists (angiotensin receptor blockers). Methods: We evaluated the effect of treatment on endothelial function in post-myocardial infarction (MI) patients treated with perindopril (group 2, n = 16) or valsartan (group 3, n = 17) at baseline and after 7, 15, and 30 days and in normal controls (group 1, n = 20). Endothelial apoptosis was determined by cultivating serum samples in vitro with human umbilical vein endothelial cells (HUVECs), while endothelial renewal was assessed by mobilization of CD34+ bone marrow cells. Results: At baseline, post-MI patients had significantly elevated rates of apoptosis (16.6 - 5.0% and 16.5 - 8.4%in groups 2 and 3, respectively [both p = 0.01] vs 1.6 - 0.7%in group 1), which declined in group 2 (10.5 - 4.4% at 30 days, p = 0.04), but not in group 3. Similar results and trends were found for the Bax/Bcl-2 ratio. CD34+ mobilization was significantly increased in group 2 (3.0 - 1.0 at baseline to 6.2 - 1.6 at 15 days, p = 0.03), whereas in group 3 CD34+ mobilization did not change significantly. The findings in group 2 were accompanied by an increase in vascular endothelial growth factor at 15 days, and a reduction in tumor necrosis factor-a and its soluble receptors, versus no change in group 3. Similar findings were observed for angiotensin II and bradykinin. Conclusion: Our results indicate that perindopril, but not valsartan, reduces the proapoptotic effect of serum on the endothelium and increases endothelial renewal in patients with acute coronary syndromes.
AB - Background: The equilibrium between endothelial apoptosis and endothelial renewal is altered in acute coronary syndromes and may be related to differences in the beneficial effects of angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists (angiotensin receptor blockers). Methods: We evaluated the effect of treatment on endothelial function in post-myocardial infarction (MI) patients treated with perindopril (group 2, n = 16) or valsartan (group 3, n = 17) at baseline and after 7, 15, and 30 days and in normal controls (group 1, n = 20). Endothelial apoptosis was determined by cultivating serum samples in vitro with human umbilical vein endothelial cells (HUVECs), while endothelial renewal was assessed by mobilization of CD34+ bone marrow cells. Results: At baseline, post-MI patients had significantly elevated rates of apoptosis (16.6 - 5.0% and 16.5 - 8.4%in groups 2 and 3, respectively [both p = 0.01] vs 1.6 - 0.7%in group 1), which declined in group 2 (10.5 - 4.4% at 30 days, p = 0.04), but not in group 3. Similar results and trends were found for the Bax/Bcl-2 ratio. CD34+ mobilization was significantly increased in group 2 (3.0 - 1.0 at baseline to 6.2 - 1.6 at 15 days, p = 0.03), whereas in group 3 CD34+ mobilization did not change significantly. The findings in group 2 were accompanied by an increase in vascular endothelial growth factor at 15 days, and a reduction in tumor necrosis factor-a and its soluble receptors, versus no change in group 3. Similar findings were observed for angiotensin II and bradykinin. Conclusion: Our results indicate that perindopril, but not valsartan, reduces the proapoptotic effect of serum on the endothelium and increases endothelial renewal in patients with acute coronary syndromes.
KW - ACE inhibition
KW - acute coronary syndromes
KW - angiotensin II receptor blocker
KW - apoptosis
KW - endothelial progenitor cells
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U2 - 10.2165/11589400-000000000-00000
DO - 10.2165/11589400-000000000-00000
M3 - Article
C2 - 21619382
AN - SCOPUS:79957812722
VL - 11
SP - 189
EP - 198
JO - American Journal of Cardiovascular Drugs
JF - American Journal of Cardiovascular Drugs
SN - 1175-3277
IS - 3
ER -