{"title":"常用抗高血压药物在术前腹主动脉瘤生长中的作用。","authors":"Toko Mitsui, Yasuko K Bando, Akihiro Hirakawa, Kenji Furusawa, Ryota Morimoto, Eiji Taguchi, Akira Kimura, Haruo Kamiya, Naomichi Nishikimi, Kimihiro Komori, Kazuhiro Nishigami, Toyoaki Murohara","doi":"10.1253/circrep.CR-23-0071","DOIUrl":null,"url":null,"abstract":"<p><p><b><i>Background:</i></b> Whether drug therapy slows the growth of abdominal aortic aneurysms (AAAs) in the Japanese population remains unknown. <b><i>Methods and Results:</i></b> In a multicenter prospective open-label study, patients with AAA at the presurgical stage (mean [±SD] AAA diameter 3.27±0.58 cm) were randomly assigned to treatment with candesartan (CAN; n=67) or amlodipine (AML; n=64) considering confounding factors (statin use, smoking, age, sex, renal function), with effects of blood pressure control minimized setting a target control level. The primary endpoint was percentage change in AAA diameter over 24 months. Secondary endpoints were changes in circulating biomarkers (high-sensitivity C-reactive protein [hs-CRP], malondialdehyde-low-density lipoprotein, tissue-specific inhibitor of metalloproteinase-1, matrix metalloproteinase [MMP] 2, MMP9, transforming growth factor-β1, plasma renin activity [PRA], angiotensin II, aldosterone). At 24 months, percentage changes in AAA diameter were comparable between the CAN and AML groups (8.4% [95% CI 6.23-10.59%] and 6.5% [95% CI 3.65-9.43%], respectively; P=0.23]. In subanalyses, AML attenuated AAA growth in patients with comorbid chronic kidney disease (CKD; P=0.04) or systolic blood pressure (SBP) <130 mmHg (P=0.003). AML exhibited a definite trend for slowing AAA growth exclusively in never-smokers (P=0.06). Among circulating surrogate candidates for AAA growth, PRA (P=0.02) and hs-CRP (P=0.001) were lower in the AML group. <b><i>Conclusions:</i></b> AML may prevent AAA growth in patients with CKD or lower SBP, associated with a decline in PRA and circulating hs-CRP.</p>","PeriodicalId":94305,"journal":{"name":"Circulation reports","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2023-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10632072/pdf/","citationCount":"0","resultStr":"{\"title\":\"Role of Common Antihypertensives in the Growth of Abdominal Aortic Aneurysm at the Presurgical Stage.\",\"authors\":\"Toko Mitsui, Yasuko K Bando, Akihiro Hirakawa, Kenji Furusawa, Ryota Morimoto, Eiji Taguchi, Akira Kimura, Haruo Kamiya, Naomichi Nishikimi, Kimihiro Komori, Kazuhiro Nishigami, Toyoaki Murohara\",\"doi\":\"10.1253/circrep.CR-23-0071\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p><b><i>Background:</i></b> Whether drug therapy slows the growth of abdominal aortic aneurysms (AAAs) in the Japanese population remains unknown. <b><i>Methods and Results:</i></b> In a multicenter prospective open-label study, patients with AAA at the presurgical stage (mean [±SD] AAA diameter 3.27±0.58 cm) were randomly assigned to treatment with candesartan (CAN; n=67) or amlodipine (AML; n=64) considering confounding factors (statin use, smoking, age, sex, renal function), with effects of blood pressure control minimized setting a target control level. The primary endpoint was percentage change in AAA diameter over 24 months. Secondary endpoints were changes in circulating biomarkers (high-sensitivity C-reactive protein [hs-CRP], malondialdehyde-low-density lipoprotein, tissue-specific inhibitor of metalloproteinase-1, matrix metalloproteinase [MMP] 2, MMP9, transforming growth factor-β1, plasma renin activity [PRA], angiotensin II, aldosterone). At 24 months, percentage changes in AAA diameter were comparable between the CAN and AML groups (8.4% [95% CI 6.23-10.59%] and 6.5% [95% CI 3.65-9.43%], respectively; P=0.23]. In subanalyses, AML attenuated AAA growth in patients with comorbid chronic kidney disease (CKD; P=0.04) or systolic blood pressure (SBP) <130 mmHg (P=0.003). AML exhibited a definite trend for slowing AAA growth exclusively in never-smokers (P=0.06). Among circulating surrogate candidates for AAA growth, PRA (P=0.02) and hs-CRP (P=0.001) were lower in the AML group. <b><i>Conclusions:</i></b> AML may prevent AAA growth in patients with CKD or lower SBP, associated with a decline in PRA and circulating hs-CRP.</p>\",\"PeriodicalId\":94305,\"journal\":{\"name\":\"Circulation reports\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2023-10-17\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10632072/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Circulation reports\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1253/circrep.CR-23-0071\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2023/11/10 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Circulation reports","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1253/circrep.CR-23-0071","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/11/10 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
摘要
背景:在日本人群中,药物治疗是否能减缓腹主动脉瘤(AAAs)的生长尚不清楚。方法与结果:在一项多中心前瞻性开放标签研究中,术前AAA患者(平均[±SD] AAA直径3.27±0.58 cm)被随机分配到坎地沙坦(CAN;n=67)或氨氯地平(AML;N =64),考虑混杂因素(他汀类药物使用、吸烟、年龄、性别、肾功能),将血压控制效果降至最低,设定目标控制水平。主要终点是24个月内AAA直径的百分比变化。次要终点是循环生物标志物(高敏c反应蛋白[hs-CRP]、丙二醛-低密度脂蛋白、组织特异性金属蛋白酶抑制剂1、基质金属蛋白酶[MMP] 2、MMP9、转化生长因子-β1、血浆肾素活性[PRA]、血管紧张素II、醛固酮)的变化。在24个月时,CAN组和AML组的AAA直径百分比变化具有可比性(分别为8.4% [95% CI 6.23-10.59%]和6.5% [95% CI 3.65-9.43%];P = 0.23)。在亚组分析中,AML减弱了合并慢性肾脏疾病(CKD;P=0.04)或收缩压(SBP)。结论:AML可能阻止CKD或SBP较低患者的AAA生长,并与PRA和循环hs-CRP下降相关。
Role of Common Antihypertensives in the Growth of Abdominal Aortic Aneurysm at the Presurgical Stage.
Background: Whether drug therapy slows the growth of abdominal aortic aneurysms (AAAs) in the Japanese population remains unknown. Methods and Results: In a multicenter prospective open-label study, patients with AAA at the presurgical stage (mean [±SD] AAA diameter 3.27±0.58 cm) were randomly assigned to treatment with candesartan (CAN; n=67) or amlodipine (AML; n=64) considering confounding factors (statin use, smoking, age, sex, renal function), with effects of blood pressure control minimized setting a target control level. The primary endpoint was percentage change in AAA diameter over 24 months. Secondary endpoints were changes in circulating biomarkers (high-sensitivity C-reactive protein [hs-CRP], malondialdehyde-low-density lipoprotein, tissue-specific inhibitor of metalloproteinase-1, matrix metalloproteinase [MMP] 2, MMP9, transforming growth factor-β1, plasma renin activity [PRA], angiotensin II, aldosterone). At 24 months, percentage changes in AAA diameter were comparable between the CAN and AML groups (8.4% [95% CI 6.23-10.59%] and 6.5% [95% CI 3.65-9.43%], respectively; P=0.23]. In subanalyses, AML attenuated AAA growth in patients with comorbid chronic kidney disease (CKD; P=0.04) or systolic blood pressure (SBP) <130 mmHg (P=0.003). AML exhibited a definite trend for slowing AAA growth exclusively in never-smokers (P=0.06). Among circulating surrogate candidates for AAA growth, PRA (P=0.02) and hs-CRP (P=0.001) were lower in the AML group. Conclusions: AML may prevent AAA growth in patients with CKD or lower SBP, associated with a decline in PRA and circulating hs-CRP.