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Ann Thorac Surg 2001;72:553-554
© 2001 The Society of Thoracic Surgeons

Invited commentary

David G. Cable, MDa

a Section of Cardiovascular Surgery, Mayo Clinic, 200 First St SW, Rochester, MN 55905, USA

Lazar and colleagues elegantly demonstrate reduced ventricular irritability, improved regional wall motion, preserved endothelial function, and reduced infarct size following angiotensin-converting enzyme (ACE) inhibition in a porcine model of acutely ischemic myocardium. In a randomized, blinded design, the study incorporated 90 minutes of coronary occlusion, 45 minutes of cardioplegic arrest to stimulate three-vessel surgical revascularization, and then permitted 3 hours of reperfusion to allow infarct determination. Despite the clinical correlation, study design, and relevant end-points, detractors will certainly challenge the conclusions. We should address some of these issues.

It is widely known that ACE inhibitors have multiple actions beyond the reduction of systemic blood pressure and angiotensin II generation. In fact, other enzymes such as tissue-plasminogen activator, chymase, cathepsin G, and tonin can also generate angiotensin II. Through inhibition of kininase II, ACE inhibitors also block . . . [Full Text of this Article]


Related Article

High tissue affinity angiotensin-converting enzyme inhibitors improve endothelial function and reduce infarct size
Harold L. Lazar, Yusheng Bao, Samuel Rivers, Theodore Colton, and Sheilah A. Bernard
Ann. Thorac. Surg. 2001 72: 548-553. [Abstract] [Full Text] [PDF]





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