中华临床医师杂志(电子版)
中華臨床醫師雜誌(電子版)
중화림상의사잡지(전자판)
CHINESE JOURNAL OF CLINICIANS(ELECTRONIC VERSION)
2014年
15期
2766-2770
,共5页
心肌梗死%预后%抵抗素%女(雌)性
心肌梗死%預後%牴抗素%女(雌)性
심기경사%예후%저항소%녀(자)성
Myocardial infarction%Prognosis%Resistin%Female
目的:研究绝经后女性急性心肌梗死患者血清抵抗素水平的变化,探讨血清抵抗素水平与急性心肌梗死发病和预后的关系。方法入选2005年3~8月住院的绝经后女性患者67例,其中急性心肌梗死患者30例,非冠心病患者37例。收集所有患者的临床资料,包括病史、身高、体重、血压、空腹血糖、血脂、纤维蛋白原、白细胞计数、高敏C反应蛋白等。以酶联免疫吸附法测定血清抵抗素、空腹胰岛素水平,计算定量胰岛素敏感性检测指数 QUICKI,并以胰岛素抵抗的体内稳定状态模式评估法(HOMA-IR)来评价胰岛素抵抗。于出院时和出院后连续8年对所有患者进行临床随访,记录主要心脏不良事件发生情况,包括心绞痛、心肌梗死、心力衰竭、再次血运重建及死亡。结果急性心肌梗死组患者血清抵抗素水平为5.04(1.20~12.45)μg/L,显著高于对照组1.57(0.32~3.55)μg/L(P<0.05)。血清抵抗素水平与白细胞计数、高敏C反应蛋白呈正相关(r分别为0.459和0.344,P均<0.05)。8年随访结果显示,对照组均未发生不良事件;急性心肌梗死患者血清抵抗素水平高于7.4μg/L者,主要心脏不良事件发生率明显高于血清抵抗素水平低于7.4μg/L者(61.5%vs.23.5%,P=0.035)。结论绝经后女性急性心肌梗死患者血清抵抗素水平显著升高。在绝经后女性急性心肌梗死患者中血清抵抗素水平显著升高组患者主要心脏不良事件发生率显著增加。血清抵抗素在急性心肌梗死患者中升高可能与体内炎症激活有关。
目的:研究絕經後女性急性心肌梗死患者血清牴抗素水平的變化,探討血清牴抗素水平與急性心肌梗死髮病和預後的關繫。方法入選2005年3~8月住院的絕經後女性患者67例,其中急性心肌梗死患者30例,非冠心病患者37例。收集所有患者的臨床資料,包括病史、身高、體重、血壓、空腹血糖、血脂、纖維蛋白原、白細胞計數、高敏C反應蛋白等。以酶聯免疫吸附法測定血清牴抗素、空腹胰島素水平,計算定量胰島素敏感性檢測指數 QUICKI,併以胰島素牴抗的體內穩定狀態模式評估法(HOMA-IR)來評價胰島素牴抗。于齣院時和齣院後連續8年對所有患者進行臨床隨訪,記錄主要心髒不良事件髮生情況,包括心絞痛、心肌梗死、心力衰竭、再次血運重建及死亡。結果急性心肌梗死組患者血清牴抗素水平為5.04(1.20~12.45)μg/L,顯著高于對照組1.57(0.32~3.55)μg/L(P<0.05)。血清牴抗素水平與白細胞計數、高敏C反應蛋白呈正相關(r分彆為0.459和0.344,P均<0.05)。8年隨訪結果顯示,對照組均未髮生不良事件;急性心肌梗死患者血清牴抗素水平高于7.4μg/L者,主要心髒不良事件髮生率明顯高于血清牴抗素水平低于7.4μg/L者(61.5%vs.23.5%,P=0.035)。結論絕經後女性急性心肌梗死患者血清牴抗素水平顯著升高。在絕經後女性急性心肌梗死患者中血清牴抗素水平顯著升高組患者主要心髒不良事件髮生率顯著增加。血清牴抗素在急性心肌梗死患者中升高可能與體內炎癥激活有關。
목적:연구절경후녀성급성심기경사환자혈청저항소수평적변화,탐토혈청저항소수평여급성심기경사발병화예후적관계。방법입선2005년3~8월주원적절경후녀성환자67례,기중급성심기경사환자30례,비관심병환자37례。수집소유환자적림상자료,포괄병사、신고、체중、혈압、공복혈당、혈지、섬유단백원、백세포계수、고민C반응단백등。이매련면역흡부법측정혈청저항소、공복이도소수평,계산정량이도소민감성검측지수 QUICKI,병이이도소저항적체내은정상태모식평고법(HOMA-IR)래평개이도소저항。우출원시화출원후련속8년대소유환자진행림상수방,기록주요심장불량사건발생정황,포괄심교통、심기경사、심력쇠갈、재차혈운중건급사망。결과급성심기경사조환자혈청저항소수평위5.04(1.20~12.45)μg/L,현저고우대조조1.57(0.32~3.55)μg/L(P<0.05)。혈청저항소수평여백세포계수、고민C반응단백정정상관(r분별위0.459화0.344,P균<0.05)。8년수방결과현시,대조조균미발생불량사건;급성심기경사환자혈청저항소수평고우7.4μg/L자,주요심장불량사건발생솔명현고우혈청저항소수평저우7.4μg/L자(61.5%vs.23.5%,P=0.035)。결론절경후녀성급성심기경사환자혈청저항소수평현저승고。재절경후녀성급성심기경사환자중혈청저항소수평현저승고조환자주요심장불량사건발생솔현저증가。혈청저항소재급성심기경사환자중승고가능여체내염증격활유관。
Objective To evaluate the correlation between the level of serum resistin and acute myocardial infarction (AMI) in postmenopausal women. Methods Sixty-seven consecutive postmenopausal women patients were admitted in our hospital and were performed coronary angiography (CAG). In all patients resistin, fasting blood glucose, insulin, high sensitive C-reactive protein(hs-CRP), fibrinogen levels and lipid profile were measured. Quantitative insulin sensitivity check index (QUICKI) and Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) were calculated to evaluate insulin resistance. AMI patients were divided into two groups: high resistin group (the blood resistin level was more than 7.4 μg/L, n=13) and low resistin group (the blood resistin level was less than 7.4 μg/L, n=17). These patients were then followed-up for 8 years after hospitalization. General condition, treatment and adverse events including cardiovascular motality, recurrent myocardial infarction or pectoris angina, rehospitalization for heart failure and revascularization procedure were recorded. Results Thirty-seven patients were diagnosed as AMI with the level of serum resistin being 5.04(1.20-12.45)μg/L. Thirty patients with normal coronary artery were diagnosed as non-CHD and the level of resistin was 1.57(0.32-3.55)μg/L (P<0.05). In multiple Logistic regression analysis, resistin level were associated with AMI. Kendall's tau_b correlation analysis reveals a positive correlation between serum resistin level and white blood cell count (r=0.459, P<0.05), hs-CRP (r=0.344, P<0.05). During the follow-up, AMI patients with high serum resistin level had more occurrence rate of clinical events compared with AMI patients with low serum resistin level (61.5% vs. 23.5%, P=0.035). Conclusions Serum resistin level in postmenopausal women was correlated with AMI significantly, and resistin may play an important role in the development of AMI by inflammatory mechanism.