Silverberg Daniel, Younis Anan, Savion Naphtali, Harari Gil, Yakubovitch Dmitry, Sheick Yousif Basheer, Halak Moshe, Grossman Ehud, Schneiderman Jacob
The Department of Vascular Surgery, Sheba Medical Center, Tel Hashomer, Israel.
The Department of Internal Medicine D and Hypertension Clinic, Sheba Medical Center, Tel Hashomer, Israel.
J Am Soc Hypertens. 2014 Aug;8(8):571-7. doi: 10.1016/j.jash.2014.04.005. Epub 2014 Apr 18.
Renin-angiotensin system (RAS) has been implicated in the pathogenesis of abdominal aortic aneurysm (AAA). Angiotensin II type 1 receptor blocker (ARB), when given with angiotensin II prevents AAA formation in mice, but found ineffective in attenuating the progression of preexisting AAA. This study was designed to evaluate the effect of chronic RAS blockers on abdominal aortic diameter in hypertensive patients without known aortic aneurysm. Consecutive hypertensive outpatients (n = 122) were stratified according to antihypertensive therapy they received for 12 months or more, consisting of ARB (n = 45), angiotensin converting enzyme inhibitor (ACE-I; n = 45), or nonARB/nonACE-I (control therapy; n = 32). Abdominal ultrasonography was performed to measure maximal subrenal aortic diameter. Eighty-four patients were reexamined by ultrasonography 8 months later. The correlation between the different antihypertensive therapies and aortic diameter was examined. Aortic diameters were significantly smaller in ARB than in control patients in the baseline and follow-up measurements (P = .004; P = .0004, respectively). Risk factor adjusted covariance analysis showed significant differences between ARB or ACE-I treated groups and controls (P = .006 or P = .046, respectively). Ultrasound that was performed 8 months later showed smaller increases in mean aortic diameters of the ARB and ACE-I groups than in controls. Both ARB and ACE-I therapy attenuated expansion of nonaneurysmal abdominal aorta in humans. These results indicate that RAS blockade given before advancement of aortic medial remodeling may slow down the development of AAA.
肾素-血管紧张素系统(RAS)与腹主动脉瘤(AAA)的发病机制有关。血管紧张素II 1型受体阻滞剂(ARB)与血管紧张素II联合使用时可预防小鼠AAA形成,但在减轻已存在的AAA进展方面无效。本研究旨在评估慢性RAS阻滞剂对无已知主动脉瘤的高血压患者腹主动脉直径的影响。连续的高血压门诊患者(n = 122)根据他们接受12个月或更长时间的抗高血压治疗进行分层,包括ARB(n = 45)、血管紧张素转换酶抑制剂(ACE-I;n = 45)或非ARB/非ACE-I(对照治疗;n = 32)。进行腹部超声检查以测量肾动脉以下主动脉的最大直径。84名患者在8个月后通过超声复查。检查了不同抗高血压治疗与主动脉直径之间的相关性。在基线和随访测量中,ARB组的主动脉直径明显小于对照组(分别为P = 0.004;P = 0.0004)。风险因素调整协方差分析显示ARB或ACE-I治疗组与对照组之间存在显著差异(分别为P = 0.006或P = 0.046)。8个月后进行的超声检查显示,ARB组和ACE-I组的平均主动脉直径增加幅度小于对照组。ARB和ACE-I治疗均减轻了人类非动脉瘤性腹主动脉的扩张。这些结果表明,在主动脉中膜重塑进展之前给予RAS阻断可能会减缓AAA的发展。