中华心血管病杂志
中華心血管病雜誌
중화심혈관병잡지
Chinese Journal of Cardiology
2010年
9期
798-800
,共3页
尤玲%赵春霞%邵娇梅%张珞%汪道文
尤玲%趙春霞%邵嬌梅%張珞%汪道文
우령%조춘하%소교매%장락%왕도문
冠状动脉疾病%非对称性二甲基精氨酸%半胱氨酸蛋白酶抑制剂
冠狀動脈疾病%非對稱性二甲基精氨痠%半胱氨痠蛋白酶抑製劑
관상동맥질병%비대칭성이갑기정안산%반광안산단백매억제제
Coronary disease%Asymmetric dimethylarginine%Cysteine proteinase inhibitors
目的 探讨冠状动脉疾病中血浆非对称性二甲基精氨酸(ADMA)与胱氨酸蛋白酶抑制剂C(Cystatin C)之间的关系.方法 选取冠心病患者87例(其中急性心肌梗死39例,不稳定性心绞痛48例),健康对照组51例;同时,依据Cystatin C水平将冠心病患者分为Cystatin C升高组(51例)与无Cystatin C升高组(36例),采用高效液相色谱法测定血浆中ADMA、对称性二甲基精氨酸(SDMA)、左旋精氨酸(L-Arg)的含量,采用德国BNProSpec全自动速率散色比浊仪测定血浆Cystatin C的含量.结果 冠心病患者血浆ADMA[(0.47±0.15)μmol/L比(0.37±0.15)μmol/L]、SDMA[(0.39±0.19)μmol/L比(0.28±0.12)μmol/L]和Cystatin C浓度[(1.16±0.32)mg/L比(0.73±0.16)mg/L]均高于正常对照组(P均<0.05),L-Arg浓度低于正常对照组[(59.4±19.4)μmol/L比(83.7±19.6)μmol/L,P<0.05];对冠心病组的亚组分析显示血浆ADMA、L-Arg和Cystatin C浓度在心肌梗死组较心绞痛组差异无统计学意义.在Cystatin C<1 mg/L的冠心病患者中血浆ADMA与正常对照组比较,差异无统计学意义;而在Cystatin C>1 mg/L的冠心病患者血浆ADMA高于正常对照组[(0.50±0.17)μmol/L比(0.39±0.15)μmol/L,P<0.05].结论 只有在血浆Cystatin C水平升高的冠心病患者血浆ADMA水平才明显升高,提示冠心病患者血浆ADMA水平的升高并不与冠心病直接相关,可能与冠心病患者伴随轻微肾损害有关.
目的 探討冠狀動脈疾病中血漿非對稱性二甲基精氨痠(ADMA)與胱氨痠蛋白酶抑製劑C(Cystatin C)之間的關繫.方法 選取冠心病患者87例(其中急性心肌梗死39例,不穩定性心絞痛48例),健康對照組51例;同時,依據Cystatin C水平將冠心病患者分為Cystatin C升高組(51例)與無Cystatin C升高組(36例),採用高效液相色譜法測定血漿中ADMA、對稱性二甲基精氨痠(SDMA)、左鏇精氨痠(L-Arg)的含量,採用德國BNProSpec全自動速率散色比濁儀測定血漿Cystatin C的含量.結果 冠心病患者血漿ADMA[(0.47±0.15)μmol/L比(0.37±0.15)μmol/L]、SDMA[(0.39±0.19)μmol/L比(0.28±0.12)μmol/L]和Cystatin C濃度[(1.16±0.32)mg/L比(0.73±0.16)mg/L]均高于正常對照組(P均<0.05),L-Arg濃度低于正常對照組[(59.4±19.4)μmol/L比(83.7±19.6)μmol/L,P<0.05];對冠心病組的亞組分析顯示血漿ADMA、L-Arg和Cystatin C濃度在心肌梗死組較心絞痛組差異無統計學意義.在Cystatin C<1 mg/L的冠心病患者中血漿ADMA與正常對照組比較,差異無統計學意義;而在Cystatin C>1 mg/L的冠心病患者血漿ADMA高于正常對照組[(0.50±0.17)μmol/L比(0.39±0.15)μmol/L,P<0.05].結論 隻有在血漿Cystatin C水平升高的冠心病患者血漿ADMA水平纔明顯升高,提示冠心病患者血漿ADMA水平的升高併不與冠心病直接相關,可能與冠心病患者伴隨輕微腎損害有關.
목적 탐토관상동맥질병중혈장비대칭성이갑기정안산(ADMA)여광안산단백매억제제C(Cystatin C)지간적관계.방법 선취관심병환자87례(기중급성심기경사39례,불은정성심교통48례),건강대조조51례;동시,의거Cystatin C수평장관심병환자분위Cystatin C승고조(51례)여무Cystatin C승고조(36례),채용고효액상색보법측정혈장중ADMA、대칭성이갑기정안산(SDMA)、좌선정안산(L-Arg)적함량,채용덕국BNProSpec전자동속솔산색비탁의측정혈장Cystatin C적함량.결과 관심병환자혈장ADMA[(0.47±0.15)μmol/L비(0.37±0.15)μmol/L]、SDMA[(0.39±0.19)μmol/L비(0.28±0.12)μmol/L]화Cystatin C농도[(1.16±0.32)mg/L비(0.73±0.16)mg/L]균고우정상대조조(P균<0.05),L-Arg농도저우정상대조조[(59.4±19.4)μmol/L비(83.7±19.6)μmol/L,P<0.05];대관심병조적아조분석현시혈장ADMA、L-Arg화Cystatin C농도재심기경사조교심교통조차이무통계학의의.재Cystatin C<1 mg/L적관심병환자중혈장ADMA여정상대조조비교,차이무통계학의의;이재Cystatin C>1 mg/L적관심병환자혈장ADMA고우정상대조조[(0.50±0.17)μmol/L비(0.39±0.15)μmol/L,P<0.05].결론 지유재혈장Cystatin C수평승고적관심병환자혈장ADMA수평재명현승고,제시관심병환자혈장ADMA수평적승고병불여관심병직접상관,가능여관심병환자반수경미신손해유관.
Objective To compare plasma asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase inhibitor, and cystatin C levels in patients with or without coronary artery disease (CAD). Methods We recruited 87 CAD patients (39 with acute myocardial infarction and 48 with unstable angina pectoris ) and 51 non-CAD controls. Plasma ADMA was measured by HPLC, cystatin C by particleenhanced immunonephelometric assay (N Latex cystatin C, Dade Behring) with anephelometer (BNII, Dade Behring). CAD patients were further divided into low cystatin C group ( < 1.0 mg/L, 36 cases) and high cystatin C group ( > 1.0 mg/L, 51 cases). Results ( 1 ) The plasma levels of ADMA [(0. 47 ± 0. 15 )μmol/L vs. (0. 37 ±0. 15) μmol/L], SDMA [(0. 39 ±0. 19) μmol/L vs. (0. 28 ±0. 12) μmol/L] and cystatin C [(1.16 ±0. 32)mg/L vs. (0. 73 ±0. 16)mg/L] were significantly higher in CAD patients than in controls (all P < 0. 05 ). The plasma L-Arg was significantly lower in CAD patients than in controls [(59.4 ± 19.4) μmol/L vs. (83. 7 ± 19. 6) μmol/L, P <0. 05]. (2) Plasma ADMA was similar in CAD patients with low cystatin C level and controls [(0. 42 ±0. 12) μmol/L vs. (0. 39 ±0. 15) μ mol/L, P =0. 251] and Plasma ADMA was significantly higher in CAD patients with high cystatin C level than in controls [(0. 50 ±0. 17) μmol/L vs. (0. 39 ±0. 15) μmol/L, P <0. 05]. Conclusion ADMA levels were significantly increased only in CAD patients with elevated cystatin C levels but not in CAD patients with normal renal function. The reported relationship between coronary heart disease and ADMA may not be direct, but could be secondary due to reduced renal function.
