Circulating levels of dimethylarginines, chronic kidney disease and long-term clinical outcome in non-ST-elevation myocardial infarction.
Circulating levels of dimethylarginines, chronic kidney disease and long-term clinical outcome in non-ST-elevation myocardial infarction.
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DOI：
10.1371/journal.pone.0048499
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发表时间：
2012
期刊：
影响因子：
3.7
通讯作者：
Marenzi G
中科院分区：
文献类型：
--
作者：
Cavalca V;Veglia F;Squellerio I;De Metrio M;Rubino M;Porro B;Moltrasio M;Tremoli E;Marenzi G
慢性肾脏疾病（CKD）与急性冠脉综合征（ACS）不良结局之间的联系机制尚不完全清楚。在潜在的关键参与者中，由于其内源性抑制剂，不对称（ADMA）和对称（SDMA）二甲基精氨酸可能参与减少一氧化氮（NO）的合成。我们测量了精氨酸、ADMA和SDMA的血浆浓度，并研究了它们与CKD和非st段抬高型心肌梗死（NSTEMI）长期预后的关系。我们前瞻性地测量了104例NSTEMI患者入院时的精氨酸、ADMA和SDMA。CKD定义为肾小球滤过率(eGFR) <60 ml/min/1.73 m2。我们在中位随访21个月时考虑了合并心源性死亡和再梗死的主要终点。在CKD （n = 33）和非CKD （n = 71）患者中，精氨酸和ADMA相似，而CKD患者的SDMA明显更高（0.65±0.23 vs. 0.42±0.12µmol/L； P<0.0001）。24例（23%）患者在随访期间发生心脏不良事件：12例（36%）为CKD， 12例（17%）为非CKD （P = 0.02）。当根据精氨酸、ADMA和SDMA中位数对研究人群进行分层时，只有SDMA（中位数0.46µmol/L）与主要终点相关（P = 0.0016）。在校正了年龄、血红蛋白和左心室射血分数的模型中，CKD和SDMA的风险比（HR）都很高（HR 2.93，四分位数范围[IQR] 1.15-7.53, P = 0.02）和HR 6.80, IQR 2.09-22.2, P = 0.001)，但在相互校正后，只有SDMA与主要终点仍然显著相关（HR 5.73, IQR 1.55-21.2, P = 0.009）。在非stemi患者中，SDMA血浆水平升高与CKD和较差的长期预后相关。
Mechanisms linking chronic kidney disease (CKD) and adverse outcomes in acute coronary syndromes (ACS) are not fully understood. Among potential key players, reduced nitric oxide (NO) synthesis due to its endogenous inhibitors, asymmetric (ADMA) and symmetric (SDMA) dimethylarginine could be involved. We measured plasma concentration of arginine, ADMA and SDMA and investigated their relationship with CKD and long-term outcome in non-ST-elevation myocardial infarction (NSTEMI). We prospectively measured arginine, ADMA, and SDMA at hospital admission in 104 NSTEMI patients. CKD was defined as an estimated glomerular filtration rate (eGFR) <60 ml/min/1.73 m2. We considered a primary end point of combined cardiac death and re-infarction at a median follow-up of 21 months. In CKD (n = 33) and no-CKD (n = 71) patients, arginine and ADMA were similar, whereas SDMA was significantly higher in CKD patients (0.65±0.23 vs. 0.42±0.12 µmol/L; P<0.0001). Twenty-four (23%) patients had an adverse cardiac event during follow-up: 12 (36%) were CKD and 12 (17%) no-CKD patients (P = 0.02). When study population was stratified according to arginine, ADMA and SDMA median values, only SDMA (median 0.46 µmol/L) was associated with the primary end-point (P = 0.0016). In models adjusted for age, hemoglobin and left ventricular ejection fraction, the hazard ratio (HR) for CKD and SDMA were high (HR 2.93, interquartile range [IQR] 1.15–7.53; P = 0.02 and HR 6.80, IQR 2.09–22.2; P = 0.001, respectively) but, after mutual adjustment, only SDMA remained significantly associated with the primary end point (HR 5.73, IQR 1.55–21.2; P = 0.009). In NSTEMI patients, elevated SDMA plasma levels are associated with CKD and worse long-term prognosis.
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