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Tsung O. Cheng, MD
Washington, DC

Arch Intern Med. 1991;151(8):1670.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.—

The recent article on angiotensin-converting enzyme (ACE) inhibitors in congestive heart failure by Deedwania¹ brings into focus the fact that all ACE inhibitors are not alike.

Besides the more prolonged and greater reduction in renal perfusion pressure and symptomatic hypotension by the long-acting ACE inhibitors, ie, enalapril and lisinopril, than by the short-acting ACE inhibitor, ie, captopril, as pointed out by Deedwania, captopril has one additional advantage. The cardioprotective effect of captopril— which like glutathione, a well-recognized free radical scavenger,² also contains a sulfhydryl grouphas been fur ther attributed to its capacity to act also as a free radical scavenger.^3,4 Ther is recently published^5,6 evidence for enhanced free radical activity in congestive heart failure due to coronary artery disease.

In addition, experimental studies in rats' showed that the ACE inhibitors reduce intimal proliferation and, thus, are of further benefit in reducing or preventing . . . [Full Text PDF of this Article]

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