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Combined and independent impact of coronary artery calcification and inflammation on risk for adverse cardiovascular events after percutaneous coronary intervention: Results from a large single-center registry.

冠状动脉钙化和炎症对经皮冠状动脉介入治疗后不良心血管事件风险的联合独立影响: 来自大型单中心登记研究的结果。

  • 影响因子:1.85
  • DOI:10.1002/ccd.28784
  • 作者列表:"Aoi S","Baber U","Kovacic JC","Mehran R","Aquino M","Dangas G","Sweeny J","Vijay P","Shah S","Barman N","Moreno P","Kini AS","Sharma SK
  • 发表时间:2020-02-22
Abstract

PURPOSE:Our study investigated the impact of coronary artery calcification (CAC) and systemic inflammation on risks for major adverse cardiovascular events (MACE) following percutaneous coronary intervention (PCI). BACKGROUND:CAC and systemic inflammation are known to be associated with an increased risk of cardiovascular events. METHODS:A total of 17,711 consecutive patients who underwent PCI in our hospital between January 1, 2009 and December 31, 2015 were categorized according to the degree of CAC (moderate/severe vs. none/mild) and high-sensitivity C-reactive protein (hsCRP) level (≥2 vs. <2 mg/L). MACE was defined as death, myocardial infarction (MI), or target vessel revascularization (TVR) occurring over 1 year. RESULTS:Within the four groups, patients with both moderate/severe CAC and elevated hsCRP (n = 1,814 [10.2%]) were older with more comorbid risk factors compared to those with moderate/severe CAC alone (n = 1,687 [9.5%]), elevated hsCRP alone (n = 7,597 [42.9%]) or neither abnormality (n = 6,613 [37.3%]). The analogous 1-year MACE rates were 21.2, 14.9, 11.5, and 7.8%, respectively (p-trend < .001). Results were unchanged after multivariable adjustment, suggesting synergistic adverse effects in patients with both CAC and elevated hsCRP. CONCLUSIONS:The presence of both moderate/severe CAC and systemic inflammation confers a synergistic effect on risk for MACE following PCI, indicating the need for novel or more intense therapeutic interventions to mitigate risk in such patients.

摘要

目的: 我们的研究调查了冠状动脉钙化 (CAC) 和全身炎症对经皮冠状动脉介入治疗 (PCI) 后主要不良心血管事件 (MACE) 风险的影响。 背景: 已知 CAC 和全身性炎症与心血管事件风险增加有关。 方法: 根据 CAC 程度 (中度/重度 vs.无/轻度) 对 2009年1月1日至 2015年12月31日在我院连续行 PCI 的 17,711 例患者进行分组。和高敏 C 反应蛋白 (hsCRP) 水平 (≥ 2 vs. <2 mg/L)。MACE 定义为 1 年以上发生的死亡、心肌梗死 (MI) 或靶血管血运重建 (TVR)。 结果: 在四组中,同时存在中度/重度 CAC 和 hsCRP 升高的患者 (n = 1,814 [10.2%]) 与单独使用中度/重度 CAC (n = 1,687 [9.5%]) 、单独使用 hsCRP 升高 (n = 7,597 [42.9%]) 相比,合并危险因素更多或无异常 (n = 6,613 [37.3%])。类似的 1 年 MACE 率分别为 21.2 、 14.9 、 11.5 和 7.8% (p 趋势 <.001)。多变量校正后结果无变化,提示 CAC 和 hsCRP 升高患者存在协同不良反应。 结论: 中度/重度 CAC 和全身性炎症的存在对 PCI 术后 MACE 的风险具有协同作用。表明需要新型或更强烈的治疗干预措施来减轻此类患者的风险。

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发表时间:2020-01-02
DOI:10.1172/JCI124708
作者列表:["Jain M","Dhanesha N","Doddapattar P","Chorawala MR","Nayak MK","Cornelissen A","Guo L","Finn AV","Lentz SR","Chauhan AK"]

METHODS::Fibronectin-splice variant containing extra domain A (Fn-EDA) is associated with smooth muscle cells (SMCs) following vascular injury. The role of SMC-derived Fn-EDA in SMC phenotypic switching or its implication in neointimal hyperplasia remains unclear. Herein, using human coronary artery sections with a bare metal stent, we demonstrate the expression of Fn-EDA in the vicinity of SMC-rich neointima and peri-strut areas. In mice, Fn-EDA colocalizes with SMCs in the neointima of injured carotid arteries and promotes neointima formation in the comorbid condition of hyperlipidemia by potentiating SMC proliferation and migration. No sex-based differences were observed. Mechanistic studies suggested that Fn-EDA mediates integrin- and TLR4-dependent proliferation and migration through activation of FAK/Src and Akt1/mTOR signaling, respectively. Specific deletion of Fn-EDA in SMCs, but not in endothelial cells, reduced intimal hyperplasia and suppressed the SMC synthetic phenotype concomitant with decreased Akt1/mTOR signaling. Targeting Fn-EDA in human aortic SMCs suppressed the synthetic phenotype and downregulated Akt1/mTOR signaling. These results reveal that SMC-derived Fn-EDA potentiates phenotypic switching in human and mouse aortic SMCs and neointimal hyperplasia in the mouse. We suggest that targeting Fn-EDA could be explored as a potential therapeutic strategy to reduce neointimal hyperplasia.

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影响因子:4.65
发表时间:2020-01-01
DOI:10.1161/ATVBAHA.119.313602
作者列表:["Lee SY","Ahn JM","Mintz GS","Hong SJ","Ahn CM","Park DW","Kim JS","Kim BK","Ko YG","Choi D","Jang Y","Park SJ","Hong MK"]

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