Medical Service, Veterans Affairs Salt Lake City Health Care System, Salt Lake City, USA.
Division of Nephrology & Hypertension, University of Utah School of Medicine, 85 North Medical Drive East, Room 201, Salt Lake City, UT, 84112, USA.
BMC Nephrol. 2021 Feb 24;22(1):69. doi: 10.1186/s12882-021-02260-x.
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/1.73m) 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 m, 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.
目前尚不清楚动脉粥样硬化的进展是否可以解释 CKD 患者心血管事件风险增加。本研究的目的是 1. 描述 CKD 与颈动脉磁共振成像(MRI)上动脉粥样硬化斑块的存在和形态之间的关系;2. 探讨基线 CKD 和颈动脉粥样硬化斑块与随后心血管事件的关系。
在 Systolic Blood Pressure Intervention Trial. (SPRINT) 参与者的一个亚组(N = 465)中,我们在基线和 30 个月时使用 MRI 测量颈动脉斑块的存在和形态。我们研究了 CKD(基线 eGFR < 60 ml/min/1.73m)与颈动脉斑块进展和 SPRINT 心血管终点的关系。
196 名(42%)参与者患有 CKD。非 CKD 和 CKD 亚组的基线 eGFR 分别为 77 ± 14 和 49 ± 8 ml/min/1.73m。137 名(29.5%)参与者存在富含脂质的坏死核心斑块。在 323 名基线和随访时均进行最大壁厚度 MRI 测量的参与者中,CKD 与最大壁厚度的进展无关(OR 0.62,95%CI 0.36 至 1.07,p = 0.082)。在 96 名基线存在坏死核心斑块且有有效随访 MRI 的参与者中,CKD 与坏死核心斑块进展的可能性降低相关(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 例心血管事件。在单独的 Cox 模型中,坏死核心斑块(HR 2.59,95%CI 1.15 至 5.85)而不是斑块定义的最大壁厚度或斑块成分的存在(HR 1.79,95%CI 0.73 至 4.43)与心血管事件相关。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非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 与坏死核心斑块的进展更快有关,尽管两者都与心血管事件独立相关。因此,CKD 可能主要通过动脉中层钙化或僵硬等动脉粥样硬化以外的机制导致心血管疾病。
NCT01475747,于 2011 年 11 月 21 日注册。