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. © 2011 Adis Data Information BV. All rights reserved.

ACE inhibition modulates endothelial apoptosis and renewal via endothelial progenitor cells in patients with acute coronary syndromes

CAMPO, Gianluca Calogero;FORTINI, Cinzia;CECONI, Claudio;FERRARI, Roberto
2011

Abstract

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. © 2011 Adis Data Information BV. All rights reserved.
2011
Cangiano, E.; Marchesini, J.; Campo, Gianluca Calogero; Francolini, G.; Fortini, Cinzia; Carrà, G.; Miccoli, M.; Ceconi, Claudio; Tavazzi, L.; Ferrari...espandi
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11392/1460115
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