Abstract 16146: Renin-Angiotensin Axis Blockade Attenuates Abdominal Aortic Expansion in Humans
Introduction: The renin-angiotensin system (RAS) has been implicated in abdominal aortic aneurysm (AAA) development in mice and in humans. Angiotensin II (Ang II) signaling was suggested to promote medial degeneration and dilatation in aging human aortas. Angiotensin II type 1 receptor blocker (ARB), when given with Ang II, prevents AAA formation in mice, but fails to attenuate progression of pre-existing aortic aneurysms clinically. We sought a possible linkage between ARB, angiotensin converting enzyme inhibitor (ACE-I) or non-ARB/non-ACE-I (as control) antihypertensive therapy, and abdominal aortic diameter in patients without AAA.
Methods: Consecutive hypertensive outpatients (n=116) were prospectively stratified into groups according to medical therapy they had been receiving for 12 months or more, which consisted of either ARB (valsartan) 160[[Unable to Display Character: –]]320 mg/day (n=44), ACE-I (n=42), or control therapy (n=30). All underwent abdominal ultrasonographic measurement of the maximal diameter of the subrenal aorta by one blinded examiner. Differences between duplicate per-patient analyses of aortic diameters were nonsignificant (p=0.926). After 8 months, 84 patients (72%) were re-examined. Demographics and risk factors including age, gender, BMI, DM, IHD, smoking, hypercholesterolemia, and statin therapy were assessed. Univariate and multivariate analyses examined the linkage between the different antihypertensive therapies and aortic diameter.
Results: Univariate analysis revealed significantly smaller aortic diameters after ARB or ACE-I treatment than after control treatment (p=0.0003 or p=0.01, respectively). Covariance analysis adjusted for risk factors showed significant differences between ARB or ACE-I treated groups and controls (p=0.0029 or p=0.024, respectively). Follow-up ultrasound 8 months later showed smaller mean increases in aortic diameters of the ARB and ACE-I groups than in controls (0.51 mm, 0.45 mm, and 0.89 mm, respectively; p=0.07 for ACE-I versus control).
Conclusions: Both ARB and ACE-I therapy attenuate the expansion of non-aneurismal abdominal aorta in humans. This linkage implies that ARB or ACE-I therapy, given prior to the advancement of aortic medial remodeling, may slow down the development of AAA.
- © 2013 by American Heart Association, Inc.