Secondary Prevention of CAD with ACE Inhibitors: A Struggle Between Life and Death of the Endothelium |
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Authors: | Roberto Ferrari Gabriele Guardigli Claudio Ceconi |
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Institution: | (1) Chair of Cardiology, University of Ferrara, Cardiovascular Institute, Arcispedale S. Anna Hospital, C.rso Giovecca 203, Ferrara, 44100, Italy;(2) Cardiovascular Research Centre, Salvatore Maugeri Foundation, IRCCS, Ferrara, Italy;(3) University Hospital of Ferrara, Ferrara, Italy |
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Abstract: | Angiotensin-converting enzyme (ACE) inhibitors improve outcomes in patients with coronary artery disease (CAD), heart failure,
and hypertension. This short review examines clinical evidence for such effects and the underlying mechanism of action. One
potential mode of action for ACE inhibitors in CAD is blood pressure reduction. However, recent data suggest that the effects
of ACE inhibitors on the endothelium may also be relevant in attenuating the progression of atherosclerosis. In CAD, chronic
overexpression of tissue ACE disrupts the angiotensin II/bradykinin balance with a net result of endothelial dysfunction,
mainly due to an increased rate of apoptosis. An imbalance between endothelial apoptosis (death) and its renewal from the
bone marrow (life) causes discontinuity of the endothelial layer, favoring the initiation and progression of a biochemical
sequence that leads to atherosclerosis, plaque rupture, and eventually acute coronary syndromes. There is clinical and experimental
evidence that ACE inhibition improves the life and death cycle of the endothelium. By restoring the bradykinin/angiotensin
II balance, ACE inhibition reduces the rate of endothelial apoptosis and experimental results suggest that ACE inhibition
can also improve the production and mobilization of endothelial progenitor cells from bone marrow. We report our experience
in this context with perindopril. |
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