血浆脑钠肽和尿微量白蛋白在心力衰竭中浓度变化及相关性
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摘要
研究背景和目的
研究背景：
心力衰竭是各种原因造成的心脏疾病的终末期,早期、及时和正确的诊断、治疗,对于患者的预后具有重要的临床和社会意义。在心力衰竭的诊断中,实验室检查目前有了较大的进展,脑钠肽(N-terminal pro-brain natriuretic pepide, NT-proBNP)是一种心脏神经激素,主要由心室肌合成和分泌,反映心室的功能。NT-proBNP成为诊断心力衰竭的较实用的方法,已经成为国际公认的诊断心力衰竭的血浆标志物。
脑钠肽(brain natriuretic pepide, BNP)是利钠肽(NP)家族中的一员,NT-proBNP是BNP激素原分裂后没有活性的N-末端片段,比BNP半衰期更长、更稳定,更能反映BNP通路的激活。正常人血浆BNP和NT-proBNP的浓度相似。在左室功能障碍时,血浆NT-proBNP的水平超过BNP水平可达4倍。血浆NT-proBNP水平随心衰程度加重而升高,在伴急性冠脉综合证、慢性肺部疾病、肺动脉高压、高血压、心房颤抖(AF)时也会升高。BNP亦有类似改变。NT-proBNP浓度大于450pg/ml诊断心衰的敏感性和特异性分别为93%和95%。NT-proBNP小于300pg/ml排除心力衰竭的阴性预测值为99%,NT-proBNP在100-400pg/ml之间还应考虑其他原因,如肺栓塞、慢性阻塞性肺部疾病。
尿微量白蛋白(microalbuminuria, MAU)最初是在糖尿病病人发生肾脏早期损害时被发现,随后发现MAU也是反映内皮损伤的一个指标,是一般人群发生心血管死亡和心力衰竭危险的预测因子。MAU最早在糖尿病肾病患者中发现对于其诊断治疗具有重要的临床和科研意义。随着研究的深入,现在通常认为MAU是全身血管内皮细胞受损,特别是心血管疾病内皮细胞受损的一个重要标志,在部分心力衰竭患者中,MAU较无心力衰竭患者明显升高,有研究报道心力衰竭患者出现MAU的占研究人群的48%。虽然NT-proBNP和MAU两者都与心力衰竭密切相关但是NT-proBNP和MAU两者的关系很少有研究者报道。因此本研究目的为：
1、血浆NT-proBNP水平随心衰程度加重而升高,NT-proBNP浓度大于450pg/ml诊断心衰的敏感性和特异性分别为93%和95%。观察心力衰竭患者NT-proBNP随心力衰竭加重的变化趋势,
2、MAU是全身血管内皮细胞受损,特别是心血管疾病内皮细胞受损的一个重要标志,在部分心力衰竭患者中,MAU较无心力衰竭患者明显升高,观察MAU随心力衰竭加重的变化趋势。
3、分析与心力衰竭密切相关的NT-proBNP和MAU两者的关系,为简化临床治疗程序、节省医疗费用提供参考。
研究方法：
1、选择于2008年9月至2010年3月在山东大学齐鲁医院就诊的门诊、急诊及住院患者共91,其中男性46例,女性45例,平均(64±9.7)岁。入选标准：①.入选者均符合心力衰竭诊断标准：心力衰竭的临床表现：心功能NYHA分级Ⅰ-Ⅲ级；NT-proBNP>450pg/ml;左心室射血分数(left ventricular ejection fraction, LVEF)< 50%;左心室舒张末期内径(left ventricular end diastolic diameter, LVEDD)>55mm。②.血清肌酐(Scr)<88.4umol/L, MAU>30mg/L。③.发生心力衰竭前无肝脏、肾脏、肺部及风湿系统疾病。所有入选者根据临床表现和实验室检查分为,心功能Ⅰ级21例,心功能Ⅱ级25例,心功能Ⅲ级23例,心功能Ⅳ级22例。各个心功能分级患者之间年龄、性别、原发病、病程无差异(P<0.05)。
2、所有入选者均行肾功能、心脏超声检查。采用HP Sonos 5500型彩色多普勒超声显像仪,探头频率2-4MHz,根据美国超声心动图学会推荐标准,患者取左侧卧位,于左室长轴切面测量,记录LVEF和LVEDD.心脏超声检查与测定NT-proBNP同日进行。入选者入院后立即取外周静脉血2ml,加入含有10%EDTA30ul的塑料试管中,在4℃2000r/min离心5min,将分离的血浆密封储存于-20℃冰箱中,集中后采用电化学发光法(electrochemiluminescence immunoassay, ECMI)在罗氏公司COBAS检测仪上检测NT-proBNP。取入选患者就诊次日晨尿5ml,半小时内送检,采用免疫散射比浊法(immune scattering turbidimetry, ICTM)测定MAU。
结果：
1.随着心力衰竭患者心脏功能的进展恶化,血浆NT-proBNP及MAU呈上升的趋势,且每级NT-proBNP和MAU较前一级差异具有显著性(P<0.05)。
2.心力衰竭患者MAU和LVEF存在负相关(r=-0.733,P<0.001)。MAU与LVEDD之间存在正相关(r=0.704,P<0.001)。心力衰竭患者血浆NT-proBNP和MAU之间存在正相关(r=0.885,P<0.001)。
结论：
1.心力衰竭时血浆NT-proBNP和MAU均出现升高,且随着心力衰竭的进展加重,NT-proBNP和MAU升高出现同步的现象,即NT-proBNP变化趋势和MAU的变化趋势存在正相关(r=0.885,P<0.001),这与随着心力衰竭进展加重,内皮损伤也出现进行性加重,造成MAU排泄增加有关,同时也与心力衰竭患者肾素-血管紧张素系统被高度激活,导致肾小球滤过膜通透性增加、肾小球滤过压升高以及肾小球滤过屏障的孔径增大有关。
2.心力衰竭时,随着疾病加重恶化,NT-proBNP和MAU出现同步升高的现象(r=0.885,P<0.001)提示我们,临床上可以应用检查心力衰竭患者的MAU来一定程度的代替NT-proBNP测定。
Backgrounds and aims:
Measurable B-type natriuretic peptides (BNPs), which are largely produced by the left ventricle, include BNP and N-terminal prohormone BNP (NT-proBNP). These proteins are released from cardiomyocytes in response to wall tension and neurohumoral signals. These proteins are used as the tools for the diagnosis and prognosis of heart failure (HF).
The level of NT-proBNP, a biomarker of cardiac function and heart failure, has become an important diagnostic tool for assessing patients who present acutely with dyspnea, and provides important prognostic information in both acute and chronic heart failure. Also, monitoring NT-proBNP plasma level is expected to improve patient care and outcomes. Secretion and plasma level of NT-proBNP respond to intracardiac distending pressures, with other modulating influences including age, sex, renal function and other aspects of neurohormonal status. Single measurement of NT-proBNP shows promise in diagnosis of heart failure.
Minor increase in urinary albumin excretion (MAU) is known to predict adverse renal and cardiovascular events in diabetic and hypertensive patients. Recent findings show that MAU is an early and sensitive marker of future cardiovascular events even in healthy subjects. Albumin transition is indicative of a disturbance of the barrier function of endothelial cells, and vascular alterations are not confined to the kidney but can also be observed in the myocardium. MAU is now considered to be an atherosclerotic risk factor and predicts future cardiovascular disease risk in diabetic patients, in elderly patients, as well as in the general population. Lowering of MAU using rennin angiosin aldosterone sysyem (RAAS) inhibitors and others drugs appears to lower the risk for heart failure.
Both of the plasm levels of NT-proBNP and MAU increased in patient with heart failure. The costs of monitoring MAU and NT-proBNP are different. Therefore, measurement of MAU instead of NT-proBNP in inpatients and outpatients with heart failure maybe a economic and easy way to monitor the progress of heart failue.
Therefore, the aims of this study are as follows:
1. NT-proBNP at cutpoints of>450 pg/ml was highly sensitive and specific for the diagnosis of heart failure and NT-proBNP level<300 pg/ml was optimal for ruling out acute chronic heart failure(CHF), with a negative predictive value of 99%. To investigate whether is the plasma levels of NT-proBNP increased synchronously in pace with the aggravation of heart failure.
2. MAU is associated with increased heart failure risk. To investigate whether is the plasma levels of MAU increased synchronously in pace with the aggravation of heart failure.
3. To evaluate whether is the plasm levels of NT-proBNP and MAU increased synchronously with the aggravation of heart failure.
Methods:
1. Ninety-one patients enrolled came from in-patient in this study with primary heart failure (NYHA stageⅠ-Ⅳ; NT-proBNP>450pg/ml; LVEF<50%; LVED>55mm), a normal renal function (GFR>90 ml/min/1.73 m2), and MAU (>30mg/L). All enrolled subjects were without diabetic signs, liver dysfunction, other causes of dyspnea and dyslipoproteinemia. All subjects were enrolled without any acute illness.
2. Ninety-one patients with heart failure were devided into different groups according to different stage of heart failure.As per standard guidelines, all patients were processed for measuring left ventricular ejection fraction (LVEF) and left ventricular end diastolic diameter (LVEDD) by Doppler echocardiograph (HP Sonos 7500). Serum creatinine was also determined. Glomerular filtration rate (GFR) was calculated by using the Modification of Diet in Renal Disease (MDRD). Plasma levels of NT-proBNP was determined at baseline by electrochemiluminescence immunoassay in COB AS (sensitivity 10pg/ml) and MAU at baseline by immune scattering turbidimetry (ICTM)(sensitivity 2mg/L).
Results:
1. In all the groups, significant difference in every stage of heart failure was noted from the last baseline values of NT-proBNP and MAU among the subjects with the progress of heart failure (P<0.05).
2. For all enrolled subjects with heart failure, there was a significant negative correlation in MAU and LVEF (r= -0.733, P<0.001). There were all positive correlation for MAU with LVEDD and NT-proBNP. The values of r and P were 0.704, <0.001,0.885,<0.001, respectively.
Conclusions:
1. The plasma levels of NT-proBNP and MAU increased synchronously in pace with the aggravation of heart failure, at the same time there was positive correlation for MAU with NT-proBNP (r=0.885,P<0.001). For all enrolled suhjects, there was a significant negative correlation between MAU and LVEF (r=-0.733, P<0.001).These phenomena indicated that a disturbance of the barrier function of vascular endothelial cells gradually increased with the aggravation of heart failure. Very likely, generalized endothelial dysfunction plays an important role on the mechanisms of the linking MAU and NT-proBNP with end-organ damage.
2. The plasm levels of NT-proBNP and MAU increased synchronously with the aggravation of heart failure. Monitoring MAU might takes the place of monitoring NT-proBNP in patients with heart failure.
研究背景：
心力衰竭是各种原因造成的心脏疾病的终末期,早期、及时和正确的诊断、治疗,对于患者的预后具有重要的临床和社会意义。在心力衰竭的诊断中,实验室检查目前有了较大的进展,脑钠肽(N-terminal pro-brain natriuretic pepide, NT-proBNP)是一种心脏神经激素,主要由心室肌合成和分泌,反映心室的功能。NT-proBNP成为诊断心力衰竭的较实用的方法,已经成为国际公认的诊断心力衰竭的血浆标志物。
脑钠肽(brain natriuretic pepide, BNP)是利钠肽(NP)家族中的一员,NT-proBNP是BNP激素原分裂后没有活性的N-末端片段,比BNP半衰期更长、更稳定,更能反映BNP通路的激活。正常人血浆BNP和NT-proBNP的浓度相似。在左室功能障碍时,血浆NT-proBNP的水平超过BNP水平可达4倍。血浆NT-proBNP水平随心衰程度加重而升高,在伴急性冠脉综合证、慢性肺部疾病、肺动脉高压、高血压、心房颤抖(AF)时也会升高。BNP亦有类似改变。NT-proBNP浓度大于450pg/ml诊断心衰的敏感性和特异性分别为93%和95%。NT-proBNP小于300pg/ml排除心力衰竭的阴性预测值为99%,NT-proBNP在100-400pg/ml之间还应考虑其他原因,如肺栓塞、慢性阻塞性肺部疾病。
尿微量白蛋白(microalbuminuria, MAU)最初是在糖尿病病人发生肾脏早期损害时被发现,随后发现MAU也是反映内皮损伤的一个指标,是一般人群发生心血管死亡和心力衰竭危险的预测因子。MAU最早在糖尿病肾病患者中发现对于其诊断治疗具有重要的临床和科研意义。随着研究的深入,现在通常认为MAU是全身血管内皮细胞受损,特别是心血管疾病内皮细胞受损的一个重要标志,在部分心力衰竭患者中,MAU较无心力衰竭患者明显升高,有研究报道心力衰竭患者出现MAU的占研究人群的48%。虽然NT-proBNP和MAU两者都与心力衰竭密切相关但是NT-proBNP和MAU两者的关系很少有研究者报道。因此本研究目的为：
1、血浆NT-proBNP水平随心衰程度加重而升高,NT-proBNP浓度大于450pg/ml诊断心衰的敏感性和特异性分别为93%和95%。观察心力衰竭患者NT-proBNP随心力衰竭加重的变化趋势,
2、MAU是全身血管内皮细胞受损,特别是心血管疾病内皮细胞受损的一个重要标志,在部分心力衰竭患者中,MAU较无心力衰竭患者明显升高,观察MAU随心力衰竭加重的变化趋势。
3、分析与心力衰竭密切相关的NT-proBNP和MAU两者的关系,为简化临床治疗程序、节省医疗费用提供参考。
研究方法：
1、选择于2008年9月至2010年3月在山东大学齐鲁医院就诊的门诊、急诊及住院患者共91,其中男性46例,女性45例,平均(64±9.7)岁。入选标准：①.入选者均符合心力衰竭诊断标准：心力衰竭的临床表现：心功能NYHA分级Ⅰ-Ⅲ级；NT-proBNP>450pg/ml;左心室射血分数(left ventricular ejection fraction, LVEF)< 50%;左心室舒张末期内径(left ventricular end diastolic diameter, LVEDD)>55mm。②.血清肌酐(Scr)<88.4umol/L, MAU>30mg/L。③.发生心力衰竭前无肝脏、肾脏、肺部及风湿系统疾病。所有入选者根据临床表现和实验室检查分为,心功能Ⅰ级21例,心功能Ⅱ级25例,心功能Ⅲ级23例,心功能Ⅳ级22例。各个心功能分级患者之间年龄、性别、原发病、病程无差异(P<0.05)。
2、所有入选者均行肾功能、心脏超声检查。采用HP Sonos 5500型彩色多普勒超声显像仪,探头频率2-4MHz,根据美国超声心动图学会推荐标准,患者取左侧卧位,于左室长轴切面测量,记录LVEF和LVEDD.心脏超声检查与测定NT-proBNP同日进行。入选者入院后立即取外周静脉血2ml,加入含有10%EDTA30ul的塑料试管中,在4℃2000r/min离心5min,将分离的血浆密封储存于-20℃冰箱中,集中后采用电化学发光法(electrochemiluminescence immunoassay, ECMI)在罗氏公司COBAS检测仪上检测NT-proBNP。取入选患者就诊次日晨尿5ml,半小时内送检,采用免疫散射比浊法(immune scattering turbidimetry, ICTM)测定MAU。
结果：
1.随着心力衰竭患者心脏功能的进展恶化,血浆NT-proBNP及MAU呈上升的趋势,且每级NT-proBNP和MAU较前一级差异具有显著性(P<0.05)。
2.心力衰竭患者MAU和LVEF存在负相关(r=-0.733,P<0.001)。MAU与LVEDD之间存在正相关(r=0.704,P<0.001)。心力衰竭患者血浆NT-proBNP和MAU之间存在正相关(r=0.885,P<0.001)。
结论：
1.心力衰竭时血浆NT-proBNP和MAU均出现升高,且随着心力衰竭的进展加重,NT-proBNP和MAU升高出现同步的现象,即NT-proBNP变化趋势和MAU的变化趋势存在正相关(r=0.885,P<0.001),这与随着心力衰竭进展加重,内皮损伤也出现进行性加重,造成MAU排泄增加有关,同时也与心力衰竭患者肾素-血管紧张素系统被高度激活,导致肾小球滤过膜通透性增加、肾小球滤过压升高以及肾小球滤过屏障的孔径增大有关。
2.心力衰竭时,随着疾病加重恶化,NT-proBNP和MAU出现同步升高的现象(r=0.885,P<0.001)提示我们,临床上可以应用检查心力衰竭患者的MAU来一定程度的代替NT-proBNP测定。
Backgrounds and aims:
Measurable B-type natriuretic peptides (BNPs), which are largely produced by the left ventricle, include BNP and N-terminal prohormone BNP (NT-proBNP). These proteins are released from cardiomyocytes in response to wall tension and neurohumoral signals. These proteins are used as the tools for the diagnosis and prognosis of heart failure (HF).
The level of NT-proBNP, a biomarker of cardiac function and heart failure, has become an important diagnostic tool for assessing patients who present acutely with dyspnea, and provides important prognostic information in both acute and chronic heart failure. Also, monitoring NT-proBNP plasma level is expected to improve patient care and outcomes. Secretion and plasma level of NT-proBNP respond to intracardiac distending pressures, with other modulating influences including age, sex, renal function and other aspects of neurohormonal status. Single measurement of NT-proBNP shows promise in diagnosis of heart failure.
Minor increase in urinary albumin excretion (MAU) is known to predict adverse renal and cardiovascular events in diabetic and hypertensive patients. Recent findings show that MAU is an early and sensitive marker of future cardiovascular events even in healthy subjects. Albumin transition is indicative of a disturbance of the barrier function of endothelial cells, and vascular alterations are not confined to the kidney but can also be observed in the myocardium. MAU is now considered to be an atherosclerotic risk factor and predicts future cardiovascular disease risk in diabetic patients, in elderly patients, as well as in the general population. Lowering of MAU using rennin angiosin aldosterone sysyem (RAAS) inhibitors and others drugs appears to lower the risk for heart failure.
Both of the plasm levels of NT-proBNP and MAU increased in patient with heart failure. The costs of monitoring MAU and NT-proBNP are different. Therefore, measurement of MAU instead of NT-proBNP in inpatients and outpatients with heart failure maybe a economic and easy way to monitor the progress of heart failue.
Therefore, the aims of this study are as follows:
1. NT-proBNP at cutpoints of>450 pg/ml was highly sensitive and specific for the diagnosis of heart failure and NT-proBNP level<300 pg/ml was optimal for ruling out acute chronic heart failure(CHF), with a negative predictive value of 99%. To investigate whether is the plasma levels of NT-proBNP increased synchronously in pace with the aggravation of heart failure.
2. MAU is associated with increased heart failure risk. To investigate whether is the plasma levels of MAU increased synchronously in pace with the aggravation of heart failure.
3. To evaluate whether is the plasm levels of NT-proBNP and MAU increased synchronously with the aggravation of heart failure.
Methods:
1. Ninety-one patients enrolled came from in-patient in this study with primary heart failure (NYHA stageⅠ-Ⅳ; NT-proBNP>450pg/ml; LVEF<50%; LVED>55mm), a normal renal function (GFR>90 ml/min/1.73 m2), and MAU (>30mg/L). All enrolled subjects were without diabetic signs, liver dysfunction, other causes of dyspnea and dyslipoproteinemia. All subjects were enrolled without any acute illness.
2. Ninety-one patients with heart failure were devided into different groups according to different stage of heart failure.As per standard guidelines, all patients were processed for measuring left ventricular ejection fraction (LVEF) and left ventricular end diastolic diameter (LVEDD) by Doppler echocardiograph (HP Sonos 7500). Serum creatinine was also determined. Glomerular filtration rate (GFR) was calculated by using the Modification of Diet in Renal Disease (MDRD). Plasma levels of NT-proBNP was determined at baseline by electrochemiluminescence immunoassay in COB AS (sensitivity 10pg/ml) and MAU at baseline by immune scattering turbidimetry (ICTM)(sensitivity 2mg/L).
Results:
1. In all the groups, significant difference in every stage of heart failure was noted from the last baseline values of NT-proBNP and MAU among the subjects with the progress of heart failure (P<0.05).
2. For all enrolled subjects with heart failure, there was a significant negative correlation in MAU and LVEF (r= -0.733, P<0.001). There were all positive correlation for MAU with LVEDD and NT-proBNP. The values of r and P were 0.704, <0.001,0.885,<0.001, respectively.
Conclusions:
1. The plasma levels of NT-proBNP and MAU increased synchronously in pace with the aggravation of heart failure, at the same time there was positive correlation for MAU with NT-proBNP (r=0.885,P<0.001). For all enrolled suhjects, there was a significant negative correlation between MAU and LVEF (r=-0.733, P<0.001).These phenomena indicated that a disturbance of the barrier function of vascular endothelial cells gradually increased with the aggravation of heart failure. Very likely, generalized endothelial dysfunction plays an important role on the mechanisms of the linking MAU and NT-proBNP with end-organ damage.
2. The plasm levels of NT-proBNP and MAU increased synchronously with the aggravation of heart failure. Monitoring MAU might takes the place of monitoring NT-proBNP in patients with heart failure.
引文
1、中华医学会心血管病学分会,中华心血管病杂志编辑委员会.慢性心力衰竭诊断治疗指南.中华心血管病杂志,2007；35(12)：1076-1095
2、Braunwald E, Bristow MR. Congenstive heart failure:fifty years of progress. Circulation,2000,102(20 Suppl 4):IV 14-23
3、European Society of Cardiology, Heart Failure Association of the ESC (HFA), European Society of Intensive Care Medicine (ESICM), et al. ESC guidelines for the diagnosis and treatment of acute and chronic heart failure 2008:the Task Force for the diagnosis and treatment of acute and chronic heart failure 2008 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association of the ESC (HFA) and endorsed by the European Society of Intensive Care Medicine (ESICM). Eur J Heart Fail.2008 Oct;10(10):933-989.
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