C-Terminal Provasopressin (Copeptin) is Associated With Left Ventricular Dysfunction, Remodeling, and Clinical Heart Failure in Survivors of Myocardial Infarction

C-Terminal Provasopressin (Copeptin) is Associated With Left Ventricular Dysfunction, Remodeling, and Clinical Heart Failure in Survivors of Myocardial Infarction
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DOI:
10.1016/j.cardfail.2008.07.231
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发表时间:
2008-11-01
影响因子:
6
通讯作者:
Ng, Leong L.
Ng, Leong L.
中科院分区:
医学2区
文献类型:
--
作者:
Kelly, Dominic;Squire, Iain B.;Ng, Leong L.

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背景:急性心肌梗死(AMI)与左心室功能障碍和临床心力衰竭有关。精氨酸抗利尿激素在心力衰竭时升高,抗利尿激素c末端(Copeptin)与ami后的不良结果相关。本研究的目的是描述Copeptin与ami后左室功能障碍、容积和重塑以及临床心力衰竭之间的关系。方法与结果:对274例AMI患者进行研究。在充电时测定血浆中的Copeptin,受试者在出院和随访时(中位155天)接受超声心动图检查。研究对象的临床心力衰竭随访时间中位数为381天。通过超声检查之间左室容积的变化(Delta)来评估重塑。Copeptin与壁面运动指数评分(WMIS)正相关,与放电时左室射血分数(LVEF)负相关。r = 0.276, P < 0.001。P = .03)及随访(WMIS)。R = 0.244。P < 0.001: P < 0.05。R = -0.270。P < 0.001)和随访时心室容积(LVEDV, r = 0.215)。P = .002;LVESV, r = 0.299。P < 0.001)。Copeptin与心室重构有关;Delta EDV: r = 0.171, P = 0.015; Delta ESV: r = 0.186, P = 0.008。LVESV升高的受试者Copeptin水平较高(中位数为6.30 vs 5.75 pmol/L)。P = .012)。随访期间临床心力衰竭患者(n = 30)出院前Copeptin较高(中位数为13.55比5.80)。P < 0.001)。在Cox比例风险模型中。Copeptin仍与临床心力衰竭有关。Kaplan-Meier评估显示Copeptin浓度为6.31 pmol/L的受试者风险增加。结论:Copeptin与ami后I-V功能障碍、容量、重构和临床心力衰竭有关。Copeptin的测量可以提供预后信息,AVP系统可能是心肌梗死后左室功能障碍的治疗靶点。(J heart failure 2008:14:739-745)
Background: Acute myocardial infarction (AMI) is associated with left ventricular (LV) dysfunction and clinical heart failure. Arginine vasopressin is elevated in heart failure and the C-terminal of provasopressin (Copeptin) is associated with adverse outcome post-AMI. The aim of this study was to describe the association between Copeptin with LV dysfunction, volumes and remodeling and clinical heart failure post-AMI.Methods and Results: We studied 274 subjects with AMI. Copeptin was measured from plasma at charge and subjects underwent echocardiography at discharge and follow-up (median 155 days). Subjects were followed tor clinical heart failure for a median of 381 days. Remodeling was assessed as the change (Delta) in LV volumes between echo examinations. Copeptin correlated directly with wall motion index score (WMIS) and inversely with LV ejection fraction (LVEF) at discharge (WMIS. r = 0.276, P < .001 LVEF r = -0.188. P = .03) and follow-up (WMIS. r = 0.244. P < .001: LVEF. r = -0.270. P < .001) and with ventricular volumes at follow-up (LVEDV, r = 0.215. P = .002; LVESV, r = 0.299. P < .001). Copeptin was associated with ventricular remodeling; Delta EDV: r = 0.171, P = 0.015, Delta ESV: r = 0.186, P = .008. Subjects with increasing LVESV had higher levels of Copeptin (median 6.30 vs. 5.75 pmol/L. P = .012). Subjects with clinical heart failure (n = 30) during follow-up had higher Copeptin before discharge (median 13.55 vs. 5.80. P < .001). In a Cox proportional hazards model. Copeptin retained association with clinical heart failure. Kaplan-Meier assessment revealed increased risk in subjects With Copeptin >6.31 pmol/L.Conclusions: Copeptin is associated with I-V dysfunction, volumes, and remodeling and clinical heart failure post-AMI. Measurement of Copeptin may provide prognostic information and AVP system may be a therapeutic target in post-MI LV dysfunction. (J Cardiac Fail 2008:14:739-745)