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Editor's Correspondence |

Vascular Protection of ACE Inhibitors

Franz H. Messerli, MD
Arch Intern Med. 2003;163(22):2791-2792. doi:10.1001/archinte.163.22.2791-a.
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In their enthusiastic review on the renin-angiotensin system and atherothrombotic disease,1 Jacoby and Rader state that

This statement represents a misinterpretation of the PROGRESS data.2 Despite lowering systolic pressure by 5 mm Hg, monotherapy with perindopril did not reduce the primary end point or the secondary end point in this study, as was clearly emphasized by Staessen et al.3 Only when indapamide was added to perindopril was there a significant reduction in these end points. In contrast, for the same systolic pressure reduction of 5 mm Hg, monotherapy with indapamide reduced the risk of strokes by an impressive 29% in 2841 patients in the Post-stroke Antihypertensive Treatment (PATS) study.4 Conceivably, most if not all of the benefits in PROGRESS can be attributed to indapamide. This could indicate that diuretics have a specific cerebroprotective effect that is not shared by other drug classes, such as ACE inhibitors or β-blockers.5 Thus, PROGRESS,2 like the Quinapril Ischemic Event Trial (QUIET),6 the Simvastatin/Enalapril Coronary Atherosclerosis Trial (SCAT),7 and the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT),8 and even the HOPE trial,9 do not attest to any blood pressure–independent effect of ACE inhibitors on cardiovascular morbidity and mortality or atherothrombosis.10 Only the recent EUROPA study seems to suggest some vasculoprotective properties of perindopril in patients with coronary artery disease.

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