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J Am Coll Cardiol, 2000; 36:1437-1438
© 2000 by the American College of Cardiology Foundation
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LETTER TO THE EDITOR

Reply

Christian A. Schneider, MDa, Frank M. Baer, MDa and Erland Erdmann, MDa

a Klinik III für Innere Medizin, Universität zu Köln, Köln, Germany


We appreciate the interest of Dr. Langobardi and his colleagues concerning our analysis of the antiischemic effect of 10 mg quinapril (intravenous) assessed by 15O water positron emission tomography (PET) (1) and questioning the clinical value of our observation. The clear advantage of the PET technique we have used is the noninvasive, quantitative analysis of changes in regional myocardial blood flow, which is currently only possible with positron tracers. Using this technique a significant improvement in myocardial blood flow after quinaprilat intravenous could be demonstrated. We agree with Dr. Langobardi that the incidence of clinical signs of ischemia was low in our patient population as it was observed by others in patients with coronary artery disease undergoing dobutamine-stress (2). However, the PET technique enabled us to detect very early changes in myocardial blood flow before these clinical signs of ischemia eventually developed. Since we know that the presence of clinical signs of ischemia are inconsistent, subjective and variable in the same patient, we decided to focus on quantifiable, regional measures of myocardial blood flow.

In contrast to Dr. Langobardi’s statement, there are data about the anti-ischemic effect of quinapril on clinical variables of myocardial ischemia in patients with coronary artery disease. Bussmann et al. (3) have previously reported the results of a randomized, double-blind, cross-over study of 16 men with coronary artery disease receiving oral quinapril or placebo. They were able to show that quinapril (10 mg) lead acutely, and after two weeks of treatment, to a significant reduction in the extent of ST depression during exercise electrocardiogram.

Taken together these data indicate that quinapril has an anti-ischemic potential. However, we agree with Dr. Langobardi and have this clearly stated in our paper, that we do not treat myocardial blood flow values but patients with coronary artery disease. Therefore, the unique, anti-ischemic potential of quinapril in the treatment of patients with coronary artery disease must be substantiated in large clinical trials. From our data quinapril seems to be a promising choice for such studies.


    References
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 References
 

  1. Schneider CA, Voth E, Moka D, et al. Improvement of myocardial blood flow to ischemic regions by angiotensin-converting enzyme inhibition with quinaprilat intravenous. J Am Coll Cardiol. 1999;34:1005–1011[Abstract/Free Full Text]
  2. Skopicki HA, Abraham SA, Picard MH, Alpert NM, Fischman AJ, Gewirtz H. Effects of dobutamine at maximally tolerated dose on myocardial blood flow in humans with ischemic heart disease. Circulation. 1997;96:3346–3352[Abstract/Free Full Text]
  3. Bussmann WD, Wittig RA, Brunner I, Bahrmann H. The angiotensin-converting enzyme inhibitor in the treatment of angina pectoris. Dtsch Med Wschr. 1992;117:603–606[Medline]




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