Chronic kidney disease, atherosclerotic plaque characteristics on carotid magnetic resonance imaging, and cardiovascular outcomes.
Chronic kidney disease, atherosclerotic plaque characteristics on carotid magnetic resonance imaging, and cardiovascular outcomes.
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DOI：
10.1186/s12882-021-02260-x
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发表时间：
2021-02-24
期刊：
影响因子：
2.3
通讯作者：
Yuan C
中科院分区：
文献类型：
--
作者：
Beddhu S;Boucher RE;Sun J;Balu N;Chonchol M;Navaneethan S;Chertow GM;Townsend R;Haley W;Cheung AK;Conroy MB;Raj DS;Xu D;George T;Yunis R;Wei G;Canton G;Bates J;Chen J;Papademetriou V;Punzi H;Wiggers A;Wright JT;Greene T;Yuan C
目前尚不清楚动脉粥样硬化的较快进展是否可以解释 CKD 患者心血管事件的较高风险。本研究的目的是 1. 通过颈动脉磁共振成像 (MRI) 表征 CKD 与动脉粥样硬化斑块的存在和形态之间的关系，以及 2. 检查基线 CKD 和颈动脉粥样硬化斑块与后续心血管事件的关系。在收缩压干预试验的一个亚组（N = 465）中。 (SPRINT) 参与者，我们使用 MRI 测量了基线时和 30 个月后颈动脉斑块的存在和形态。我们检查了 CKD（基线 eGFR < 60 ml/min/1.73m2）与颈动脉斑块进展和 SPRINT 心血管终点的关联。一百九十六 (42%) 参与者患有 CKD。非 CKD 和 CKD 亚组的基线 eGFR 分别为 77±14 和 49±8ml/min/1.73m2。 137 名 (29.5%) 参与者存在富含脂质的坏死核心斑块。在 323 名基线和随访 MRI 测量最大壁厚的参与者中，CKD 与最大壁厚的进展无关（OR 0.62，95% CI 0.36 至 1.07，p = 0.082）。在 96 名基线时患有坏死核心斑块并进行有效随访 MRI 的参与者中，CKD 与坏死核心斑块进展的几率较低相关（OR 0.41，95% CI 0.17 至 0.95，p = 0.039）。在 1764 人年的随访中，共发生 28 起心血管事件。在单独的 Cox 模型中，坏死核心斑块（HR 2.59，95% CI 1.15 至 5.85）与心血管事件相关，但由最大壁厚度或斑块成分的存在定义的斑块（HR 1.79，95% CI 0.73 至 4.43）则不然。独立于坏死核心斑块，CKD（HR 3.35，95% CI 1.40 至 7.99）与心血管事件相关。颈动脉斑块中坏死核心的存在而不是斑块本身的存在与心血管事件风险增加相关。我们没有发现 CKD 与坏死核心斑块的更快进展相关，尽管两者都与心血管事件独立相关。因此，CKD 可能主要通过动脉粥样硬化以外的机制（如动脉中膜钙化或硬化）导致心血管疾病。 NCT01475747，注册于 2011 年 11 月 21 日。在线版本包含可在 10.1186/s12882-021-02260-x 获取的补充材料。
It is unclear whether faster progression of atherosclerosis explains the higher risk of cardiovascular events in CKD. The objectives of this study were to 1. Characterize the associations of CKD with presence and morphology of atherosclerotic plaques on carotid magnetic resonance imaging (MRI) and 2. Examine the associations of baseline CKD and carotid atherosclerotic plaques with subsequent cardiovascular events. In a subgroup (N = 465) of Systolic Blood Pressure Intervention Trial. (SPRINT) participants, we measured carotid plaque presence and morphology at baseline and after 30-months with MRI. We examined the associations of CKD (baseline eGFR < 60 ml/min/1.73m2) with progression of carotid plaques and the SPRINT cardiovascular endpoint. One hundred and ninety six (42%) participants had CKD. Baseline eGFR in the non-CKD and CKD subgroups were 77 ± 14 and 49 ± 8 ml/min/1.73 m2, respectively. Lipid rich necrotic-core plaque was present in 137 (29.5%) participants. In 323 participants with both baseline and follow-up MRI measurements of maximum wall thickness, CKD was not associated with progression of maximum wall thickness (OR 0.62, 95% CI 0.36 to 1.07, p = 0.082). In 96 participants with necrotic core plaque at baseline and with a valid follow-up MRI, CKD was associated with lower odds of progression of necrotic core plaque (OR 0.41, 95% CI 0.17 to 0.95, p = 0.039). There were 28 cardiovascular events over 1764 person-years of follow-up. In separate Cox models, necrotic core plaque (HR 2.59, 95% CI 1.15 to 5.85) but not plaque defined by maximum wall thickness or presence of a plaque component (HR 1.79, 95% CI 0.73 to 4.43) was associated with cardiovascular events. Independent of necrotic core plaque, CKD (HR 3.35, 95% CI 1.40 to 7.99) was associated with cardiovascular events. Presence of necrotic core in carotid plaque rather than the presence of plaque per se was associated with increased risk of cardiovascular events. We did not find CKD to be associated with faster progression of necrotic core plaques, although both were independently associated with cardiovascular events. Thus, CKD may contribute to cardiovascular disease principally via mechanisms other than atherosclerosis such as arterial media calcification or stiffening. NCT01475747, registered on November 21, 2011. The online version contains supplementary material available at 10.1186/s12882-021-02260-x.
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DOI：
10.1016/j.jcmg.2016.06.017
发表时间：
2017-03
期刊：
JACC. Cardiovascular imaging
影响因子：
--
作者：
Sun J;Zhao XQ;Balu N;Neradilek MB;Isquith DA;Yamada K;Cantón G;Crouse JR 3rd;Anderson TJ;Huston J 3rd;O'Brien K;Hippe DS;Polissar NL;Yuan C;Hatsukami TS
通讯作者：
Hatsukami TS
DOI：
10.1177/1740774514537404
发表时间：
2014-10
期刊：
Clinical trials (London, England)
影响因子：
--
作者：
Ambrosius WT;Sink KM;Foy CG;Berlowitz DR;Cheung AK;Cushman WC;Fine LJ;Goff DC Jr;Johnson KC;Killeen AA;Lewis CE;Oparil S;Reboussin DM;Rocco MV;Snyder JK;Williamson JD;Wright JT Jr;Whelton PK;SPRINT Study Research Group
通讯作者：
SPRINT Study Research Group
影响因子：
168.9
作者：
Matsushita, Kunihiro;van der Velde, Marije;Astor, Brad C.;Woodward, Mark;Levey, Andrew S.;de Jong, Paul E.;Coresh, Josef;Gansevoort, Ron T.
通讯作者：
Gansevoort, Ron T.
影响因子：
2.8
作者：
Nicholls, Stephen J.;Tuzcu, E. Murat;Nissen, Steven E.
通讯作者：
Nissen, Steven E.
影响因子：
19.6
作者：
Shoji, T;Emoto, M;Nishizawa, Y
通讯作者：
Nishizawa, Y