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(Hypertension. 2002;40:e5.)
© 2002 American Heart Association, Inc.

Letters to the Editor

Can ACE Inhibitors Promote Detrimental Vascular Effects After Percutaneous Injury?

Division of Cardiology, University of Piemonte Orientale, Novara, Italy, E-mail flavio_ribichini@hotmail.com

William Wijns

Cardiovascular Center OLVZ, Aalst, Belgium

Giuseppe Matullo; Alberto Piazza

Institute of Human Genetics, University of Turin, Turin, Italy

Eugenio Uslenghi

Department of Cardiology, Ospedale Santa Croce, Cuneo, Italy

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

Zhuo et al¹ reported interesting observations in vivo about the effects of angiotensin-converting enzyme (ACE) inhibition with perindopril on plasma ACE levels and cellular expression of ACE, AT₁ receptors, and nitric oxide synthase (NOS) isoforms in human blood vessels.

Oral ACE inhibition at conventional doses (perindopril 4 mg/d) decreased plasma ACE activity by 70% and vascular ACE immunoactivity to 65% of control subjects detected by immunocytochemistry, and increased endothelial NOS (eNOS) and inducible NOS (iNOS) expression in the vascular wall. However, the authors also observed a dramatic 80% increment of the AT₁ receptor binding in vascular smooth muscle cells, which might increase the potential of these receptors to counterbalance the beneficial effects of suppressed angiotensin II formation if AT₁ receptors were activated by alternative sources of angiotensin II.

Whether the overexpression of AT₁ receptors may somehow limit, or even reverse, the beneficial effects of ACE inhibitors in specific clinical situations of vascular disease has stimulated the following comments.

So far, mostly beneficial vascular effects have been reported in patients treated with ACE inhibitors.^2,3 However, 2 recent publications have shown that oral administration of ACE inhibitors following stented angioplasty actually augmented the incidence of restenosis instead of reducing it.^4,5 Conversely, the administration of AT₁ antagonist valsartan in the VAL-PREST Trial reduced the occurrence of stent restenosis in a small but placebo-controlled randomized trial.⁶ Although these studies were not aimed at evaluating the clinical outcome, the angiographic findings are consistent with an opposite-to-the-expected effect of ACE inhibitors and a possible favorable outcome . . . [Full Text of this Article]

Jia L. Zhuo

Division of Hypertension and Vascular Research, Henry Ford Hospital, Detroit, Michigan, E-mail jzhuo1@hfhs.org

Frederick A.O. Mendelsohn

Howard Florey Institute, University of Melbourne, Victoria, Australia

Mitsuru Ohishi

Department of Geriatric Medicine, Osaka University Medical School, Osaka, Japan