(Circulation. 2001;103:630.)
© 2001 American Heart Association, Inc.
Brief Rapid Communications |
From the Division of Cardiology, Osaka Rosai Hospital, Sakai, Osaka, Japan.
Correspondence to Shiro Hoshida, MD, PhD, Chief, Division of Cardiology, Osaka Rosai Hospital, 1179-3 Nagasone-cho, Sakai, Osaka 591-8025, Japan. E-mail hoshidas{at}orh.go.jp
BackgroundAngiotensin-converting enzyme (ACE) inhibitors are effective in the secondary prevention of ischemic heart disease, but they do not reduce the rate of restenosis. Vascular ACE activity in the culprit coronary lesions of these patients, however, has never been quantified.
Methods and ResultsWe measured the ACE activity of vascular tissue obtained by directional coronary atherectomy in patients with acute coronary syndrome (n=17) and in patients with stable ischemic heart disease (n=36), with and without restenosis. The ACE activity of the culprit coronary lesions was significantly increased in patients with acute coronary syndrome (0.87±0.12 nmol · min1 · mg protein1; P<0.01) but not in patients with ischemic heart disease with restenosis (n=11, 0.19±0.05 nmol · min1 · mg protein1) when compared with those patients with ischemic heart disease without restenosis (n=25, 0.20±0.05 nmol · min1 · mg protein1). There was no difference between the ACE activity of the coronary tissue of the in-stent (n=5) and stent-unrelated (n=6) restenosis patients (0.24±0.10 versus 0.15±0.04 nmol · min1 · mg protein1). Serum ACE activity did not differ significantly among the patients.
ConclusionsThe present study demonstrates increased ACE activity in culprit lesions in acute coronary syndrome, indicating that enhanced ACE activity is related to the causative mechanism of active coronary lesions.
Key Words: heart diseases angiotensin atherosclerosis restenosis
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