Kobayashi Nobuaki, Asai Kuniya, Tsurumi Masafumi, Shibata Yusaku, Okazaki Hirotake, Shirakabe Akihiro, Goda Hiroki, Uchiyama Saori, Tani Kenichi, Takano Masamichi, Shimizu Wataru
Division of Intensive Care Unit, Nippon Medical School Chiba Hokusoh Hospital, Chiba, Japan,
Division of Intensive Care Unit, Nippon Medical School Chiba Hokusoh Hospital, Chiba, Japan.
Cardiology. 2018;141(4):190-198. doi: 10.1159/000496053. Epub 2019 Feb 13.
We aimed to examine the relations of very high levels of serum uric acid (sUA) with features of culprit lesion plaque morphology determined by optical coherence tomography (OCT) and adverse clinical outcomes in patients with acute coronary syndrome (ACS).
We retrospectively compared ACS patients according to sUA levels of > 8.0 mg/dL (n = 169), 7.1-8.0 mg/dL (n = 163), 6.1-7.0 mg/dL (n = 259), and ≤6.0 mg/dL (n = 717). Angiography and OCT findings were analyzed in patients with preintervention OCT and the 4 sUA groups (> 8.0 mg/dL, n = 61; 7.1-8.0 mg/dL, n = 72; 6.1-7.0 mg/dL, n = 131; and ≤6.0 mg/dL, n = 348) were compared.
Cardiogenic shock was more prevalent in ACS patients with sUA > 8.0 mg/dL (22% vs. 19% vs. 10% vs. 6%, p < 0.001). Plaque rupture was observed more prevalently by OCT in patients with sUA > 8.0 mg/dL (67% vs. 47% vs. 56% vs. 45%, p = 0.027). At the 2-year follow-up, Kaplan-Meier estimates showed higher cardiac mortality in patients with sUA > 8.0 mg/dL (25% vs. 12% vs. 5% vs. 5%, p < 0.001). After adjusting for traditional cardiovascular risk factors and creatinine levels, patients with sUA > 8.0 mg/dL showed a 4.5-fold increased risk in 2-year cardiac death by multivariate Cox proportional hazard analysis (hazard ratio 4.54, 95% confidence interval 2.98-6.91; p < 0.001).
Very high sUA levels like > 8.0 mg/dL are the primary predictor of 2-year cardiac mortality and could partly be caused by adverse effects of accumulated sUA on plaque morphology in patients with ACS.
我们旨在研究急性冠状动脉综合征(ACS)患者中,血清尿酸(sUA)水平极高与光学相干断层扫描(OCT)所确定的罪犯病变斑块形态特征以及不良临床结局之间的关系。
我们根据sUA水平将ACS患者进行回顾性比较,分为>8.0mg/dL组(n = 169)、7.1 - 8.0mg/dL组(n = 163)、6.1 - 7.0mg/dL组(n = 259)和≤6.0mg/dL组(n = 717)。对干预前接受OCT检查的患者进行血管造影和OCT结果分析,并比较4个sUA组(>8.0mg/dL组,n = 61;7.1 - 8.0mg/dL组,n = 72;6.1 - 7.0mg/dL组,n = 131;≤6.0mg/dL组,n = 348)。
sUA>8.0mg/dL的ACS患者发生心源性休克更为普遍(22%对19%对10%对6%,p<0.001)。OCT观察到sUA>8.0mg/dL的患者斑块破裂更为普遍(67%对47%对56%对45%,p = 0.027)。在2年随访时,Kaplan-Meier估计显示sUA>8.0mg/dL的患者心脏死亡率更高(25%对12%对5%对5%,p<0.001)。在调整传统心血管危险因素和肌酐水平后,多因素Cox比例风险分析显示,sUA>8.0mg/dL的患者2年心脏死亡风险增加4.5倍(风险比4.54,95%置信区间2.98 - 6.91;p<0.001)。
sUA水平>8.0mg/dL这样的极高水平是2年心脏死亡率的主要预测因素,并且部分可能是由于ACS患者中累积的sUA对斑块形态产生的不良影响所致。