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J Thorac Cardiovasc Surg 2003;125:974-975
© 2003 The American Association for Thoracic Surgery

Letters to the Editor

Quinaprilat during cardioplegic arrest

Professor of Cardiothoracic Surgery, Boston Medical Center, Cardiothoracic Surgery, Boston, MA 02118

To the Editor:

I read with interest the recent article by Korn and his coworkers ¹ concerning quinaprilat during cardioplegic arrest to prevent ischemia-reperfusion injury. They have demonstrated that quinaprilat enhances recovery of the ischemic myocardium and suggests that its protective mechanism may be due to the increased coronary blood flow during the early reperfusion period. My group at the Boston Medical Center has recently published a study that helps to identify the mechanisms for the beneficial effects of quinaprilat. ²

In an intact porcine model involving ischemia and reperfusion with cardioplegic arrest on cardiopulmonary bypass, hearts treated with the high-affinity tissue angiotensin-converting enzyme (ACE) inhibitor quinaprilat had significantly better recovery of regional wall motion, a lower incidence of ventricular arrhythmias, and a smaller infarct size than controls. When the low-affinity tissue ACE inhibitor enalaprilat was administered, the decrease in infarct size was less (24% enalaprilat vs 14% quinaprilat; P < .0001). The beneficial effects of quinaprilat's action could be explained by its superior preservation of endothelial function, since quinaprilat-treated hearts had significantly greater coronary arterial relaxation in response to bradykinin (66% quinaprilat vs 32% enalaprilat; P < .0001). When the bradykinin antagonist HOE140 was added to the quinaprilat-treated hearts, the protective effect on endothelial function was abolished and these hearts had a significant increase in infarct size (48% quinaprilat + HOE vs 14% quinaprilat; P < .0001).

I agree that ACE inhibitors enhance myocardial protection during cardioplegic arrest. However, ACE inhibitors are not all equally protective. ACE inhibitors with high tissue ACE inhibition such as quinaprilat result in better preservation of endothelial function, which decreases ischemic necrosis. This improvement in endothelial function appears to be bradykinin-mediated. I concur with Korn and coworkers that high-affinity tissue ACE inhibitors may play an important role in enhancing cardioplegic protection during coronary revascularization. ^2,3

References

1. Korn P, Kröner A, Schirnhofer J, Hallström S, Bernecker O, Mallinger R, et al. Quinaprilat during cardioplegic arrest in the rabbit to prevent ischemia-reperfusion injury. J Thorac Cardiovasc Surg. 2002;124:352-60.[Abstract/Free Full Text]
   
2. Lazar HL, Bao Y, Rivers S, Colton S, Bernard SA. High tissue affinity angiotensin-converting enzyme inhibitors improve endothelial function and reduce infarct size. Ann Thorac Surg. 2001;72:548-54.[Abstract/Free Full Text]
   
3. Lazar HL, Bao Y, Rivers S, Bernard SA. Pretreatment with angiotensin-converting inhibitors attenuates ischemic reperfusion injury during coronary revascularization. Ann Thorac Surg. 2002;73:1522-7.[Abstract/Free Full Text]
   

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Harold L. Lazar Permission Requests Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Lazar, H. L. Search for Related Content PubMed PubMed Citation Articles by Lazar, H. L.