急性心肌梗塞室壁瘤形成的时相性变化及PCI联合rhBNP治疗的逆转效应
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摘要
急性心肌梗死(acute myocardial infarction, AMI)后心室的早期扩展主要发生于梗死相关动脉(infarct related artery,IRA)所支配的区域;如果IRA未及时开通,失去收缩张力的梗死区与非梗死区间发生非同步或矛盾舒缩运动,而形成急性室壁瘤(acute ventricular aneurysm,AVA)。AVA将进一步增加对梗死边缘带心肌的牵张负荷,导致进行性左室重构,加重心肌缺血,促进室壁瘤(left ventricular aneurysm, LVA)扩展与心衰恶化,明显增加AMI后主要恶性心脏事件(major adverse events, MACE)的发生。AVA于AMI后早期即可发生,但目前对于LVA的研究多局限在慢性LVA上,临床上仅在心电图上ST段持续抬高超过半个月时才考虑LVA的诊断,而此时已有肉芽组织长入梗死灶内,形成纤维瘢痕组织已发展至解剖性LVA。一般认为,AMI早期重构发生在心肌梗死后72小时,而对于此阶段急性LVA的形成及其时相演变过程尚不清楚。研究表明,有急性LVA形成的患者死亡率在AMI患者中最高,即使患者的射血分数相似,有LVA的患者病死率,也比无LVA患者高6倍以上。因此早期诊断LVA的形成对于早期进一步强化逆转左室重构的治疗、降低死亡率至关重要。
虽然连续心脏超声检查发现AMI发病后3小时内左心室腔即开始扩大。但目前关于AVA最早何时发生尚缺乏详实报导。AMI后即刻行导管法左室造影(left ventriculography, LVG)检查可直观地了解AMI后心室形态、结构、舒缩功能及血流动力学的变化。对于LVA的形成做出准确判断。而血浆B型钠尿肽(B-type natriuretic peptide, BNP)是属于钠尿肽家族中的一员,它是对容量和压力过负荷的反应性产物,其分泌水平与心室内容量和/或压力负荷状态成正相关,并在血流动力学容积和压力调节的保护性代偿机制中起重要作用。BNP作为反应心脏血流动力学及左室重构的标记物已有共识,它在AMI演变过程的水平变化对于LVA的形成有无预测价值及心肌梗死后LVA形成的时相过程与血浆BNP水平关系亦不清楚。PCI是急性心梗有效的治疗方法,但对于LVA的治疗和逆转作用尚不清楚,尤其是心肌梗死后LVA患者能否长期获益尚不清楚。本研究通过对连续入选的AMI患者行LVG直接获得急性室壁活动的形态与功能参数,明确LVA形成的时相过程。结合平衡法核素心室造影相位分析进一步明确不同时段PCI对于急性LVA患者心室运动的同步性、心功能及心室重塑的影响。
近几年来随着BNP在诊断评价急性冠脉综合症(acute coronary syndrome, ACS)/AMI以及心力衰竭(heart failure,HF)的预后方面上得到多方认可,其在临床治疗领域方面的应用也取得了重大进展, rhBNP临床应用的安全性、改善血流动力学的有效性已在一些急性失代偿HF的试验中得到证实。本研究通过导管法LVG并结合心脏超声和平衡法核素心室造影相位分析,探讨PCI术后常规治疗的基础上联合应用rhBNP对AMI-LVA患者左心功能和收缩同步性的影响。
本研究内容及结果如下:
第一部分急性心肌梗死后室壁瘤形成的时相性变化
目的:通过对连续AMI患者行导管法左室造影,分析AMI后LVA形成的时相性变化及影响LVA形成的相关危险因素,对比AMI后心室容积、压力及形态变化的时相过程,探讨血浆BNP峰值水平与LVA形成的关系。
方法:2004年6月-2008年6月我科连续收治的首次AMI患者678例,其中男性563例,女性115例,年龄58±11岁。根据行左室造影(LVG)距AMI发病的时间分为A组(<3小时,120例)、B组(3-6小时,150例)、C组(6-24小时,228例)、D组(24-72小时,180例)。所有入选患者,均于冠脉造影同时行LVG检查,测定左心室舒张末期压力(LVEDP)、左心室舒张末期容积指数(LVEDVI)、左心室收缩末期容积指数(LVESVI)、左室射血分数(LVEF)、室壁运动积分(LVWMS)。并按LVG室壁运动情况分为有LVA组和无LVA组,比较两者患者的临床资料、冠脉造影资料、血浆BNP水平变化及住院期间主要恶性心脏事件(MACE,包括再梗死、梗死后心绞痛、充血性心衰、恶性心律失常、死亡)的发生率。
结果: 1.各组患者在年龄、性别、危险因素(包括高血压、糖尿病、高脂血症、吸烟史)等方面均无显著性差异。四组间CAG结果显示,IRA病变位置、多支病变率、病变阻塞程度均无显著性差异(P >0.05)。2. LVA累积发生率:3小时以内为10%;6小时以内为15.5%;24小时以内为23.3%、72小时内为30.38%。A、B、C三组LVEDVI、LVWMS明显低于D组,而LVEF明显高于D组(P均<0.05);在A组中,LVESVI亦明显低于D组,LVEDVI、LVWMS较C组降低(P均<0.05)。A、B组比较无显著性差异;B、C组比较无统计学差异。3.有LVA组与无LVA组对18个指标进行Logistic单因素分析:年龄、高血压、糖尿病、梗死前心绞痛史、首次心肌梗死病史、前壁心肌梗死、单支病变(LAD, LMA)、侧支循环、血管闭塞部位、血管闭塞时间是AMI后LVA形成的危险因素。Logistic多因素回归分析结果提示前壁心肌梗死、血管闭塞部位、心肌梗塞病史、PCI距离AMI发病的时间是AMI后LVA形成的独立危险因素。4. LVA组LVEF较无LVA组明显降低(45.7±16.1 %vs 49.0±18.2%,P <0.05); LVEDVI、LVESVI及LVEDP均明显高于无LVA组(113.2±25.1 ml/m~2 vs 104.1±26.3 ml/m~2, 63.2±35.1 ml/m~2 vs 54.6±27.2 ml/m~2, 18.8±3.2 mmHg vs 16.1±3.2 mmHg, P均<0.05)。LVA组LVWMS明显高于无LVA组(7.7±2.9 vs 6.8±2.4,P <0.05)。5 LVA组发病后18小时、第5天和第24周血浆BNP浓度均明显高于无LVA组(592.2±145.8 pg/ml vs 374.3±152.2 pg/ml, 378.2±139.7 pg/ml vs 178.3±31.7 pg/ml,106.4±28.4 pg/ml vs 64.2±22.9 pg/ml, P均<0.05)。LVA组血浆BNP峰值浓度明显高于无LVA组(592.2±145.8 pg/ml vs 384.3±152.2 pg/ml,P<0.05)。且峰值时间显著提前(17.2±2.9h vs 19.1±2.8h,P<0.01)。6. LVA组住院期间梗死后心绞痛、再梗死率、死亡率均高于无LVA组(43/206 vs 42/472,24/206 vs 14/472,16/206 vs 9/472,P均<0.05)。
小结:AMI患者早期即可有LVA的形成,3小时之内,LVA的发生可达10%,至AMI发病72小时,LVA的累积发生率可高达30%。LVA形成受多种因素共同影响,前壁心肌梗死(LAD近中段完全或次全闭塞)、心肌梗塞病史、IRA闭塞时间是独立的危险因素。血浆BNP水平的增加是AMI后LVA形成的早期重要标记物。LVA患者的心功能明显受损,住院期间死亡率增高。
第二部分不同时段介入治疗对心肌梗死室壁瘤患者心室重构及心室收缩同步性影响
目的:通过导管法左室造影结合平衡法核素心室造影(ERNA)的方法,对比不同时间段行冠脉介入治疗(PCI)对急性心肌梗死(AMI)后室壁瘤(LVA)患者左室重构、收缩同步性及心功能的影响。
方法:选择2004年1月-2006年12月我院连续收治的首次急性前壁心肌梗死患者及LVG确定合并室壁瘤者共326例,根据自发病至行PCI的时间,分为:A组(<3小时)、B组(3-6小时)、C组(6-12小时)、D组(AMI后1周),四组患者于PCI后即行左心室造影,测定左心室舒张末期压力(LVEDP)、左心室舒张末期容积指数(LVEDVI)、左心室收缩末期容积指数(LVESVI)、左室射血分数(LVEF)、室壁运动积分(LVWMS);AMI后1周时行平衡法核素心室造影,测定左室收缩功能参数:左室射血分数(LVEF)左室峰射血率时间(TPER)左室峰射血率(PER)及舒张功能参数:左室峰充盈率(PFR)左室峰充盈时间(TPFR)和收缩同步性参数即相角程(PS),半高宽(FWHM),峰相位标准差(PSD)及反常室壁容积指数(PVI);并于急性心肌梗死后不同时间段行BNP监测。AMI后6个月随访时重复行心室造影和核素心室造影检查测定上述参数,并随访3年,记录主要恶性心脏事件(MACE)的发生率。
结果:1. PCI时,A、B、C三组LVEDVI、LVWMS明显低于D组,而LVEF明显高于D组(P均<0.05);在A组中,LVESVI亦明显低于D组,LVEDVI、WMS较C组降低(P均<0.05)。B、C组各指标无统计学差异; PCI术后6个月随访,A、B、C、D四组LVESVI、LVEDVI、WMS、LVEDP均较行PCI时减低,而LVEF较前增高(P均<0.05)。其中A组变化最为显著;2 AMI后6个月随访时, A、B、C三组LVEF、PER、PFR较D组明显增高,而TPER、PS、FWHM明显降低(P均<0.05);3.至AMI后6个月时A组反常容积消失病例数明显高于B、C、D组,且A组PVI亦明显低于B、C、D组(12.08±2.07% vs 15.43±2.39% vs 16.49±2.47% vs 20.41±3.68%,P均<0.05);4. D组发病后18小时、第5天和第24周血浆BNP浓度均明显高于A组(615±112 pg/ml vs 492.5±130 pg/ml,473.5±97.5 pg/ml vs 332.5±78 pg/ml,268±71.5 pg/ml vs163.5±56 pg/ml,P均<0.05 );5. A组、B组和C组梗死后心绞痛(6.2% vs 21%,8.9% vs 21%,9.3% vs 21%,P均<0.05)及3年随访时死亡率(3.1% vs 17.1%,5.6% vs 17.1%,7.7% vs 17.1%,P均<0.05)均低于D组,且A组再梗死率和住院期间死亡率亦明显低于D组(3.1% vs 13.1%,0% vs 6.6%,P均<0.05)
小结:对于AMI患者,早期(尤其是3小时之内)施行PCI可以显著降低血浆BNP的水平,有效地抑制并逆转LVA的形成,提高左室功能,改善患者的预后。
第三部分PCI联合静脉应用rhBNP对急性心肌梗死室壁瘤的逆转效应
目的:通过有创血流动力学监测,结合超声心动图和平衡法核素心室造影的方法,评价冠脉介入治疗(PCI)联合重组人脑利钠肽(rhBNP)对急性心肌梗死伴室壁瘤(AMI-LVA)患者心室重构、收缩同步性及心功能的影响。
方法:2007年6月—2008年6月,我院收治24h内发病的前壁AMI-LVA患者46例,随机分为P-B组(PCI+rhBNP)和P-C组(PCI+常规对照治疗)。两组患者均给予急诊PCI治疗,P-B组在PCI治疗的基础上即刻静脉注射rhBNP(成都诺迪康生物制药有限公司),负荷量1.5μg/kg,90秒内匀速注入,继而以0.0075~0.0150μg·kg-1·min-1的速度维持静脉滴注24 h。所有患者分别于用药前后测心率、血压、左室终末压(LVEDP)及氧饱和度的变化;用药前、用药后1周及用药后24周采用二维超声心动图测定舒张末期容积指数(LVEDVI)、收缩末期容积指数(LVESVI )、左室射血分数(LVEF)、左室质量指数(LVMI)、梗死区的局部室壁运动指数(RWMI)。并于用药1周、24周时行ERNA了解心室收缩同步性参数,即相角程(PS),半高宽(FWHM),峰相位标准差(PSD)。记录应用BNP前及治疗后7天两组患者BNP水平的变化,记录住院期间及随访6个月主要不良心脏事件及并发症的发生率。
结果:1基线资料相比,两组患者性别、年龄、冠心病危险因素均无差异。P-B组中CKMB峰值水平低于P-C组(233.6±35.3 IU/L vs 288.5±34.6 IU/L,P<0.05);2两组患者治疗前后相比,两组患者LVEDP均有降低,在P-B组有显著性差异(P均<0.05)。P-B组LVEDP降低程度较P-C组显著(4.6±1.1 mmHg vs 2.0±0.9 mmHg, P<0.05);3 P-B组治疗后1周时LVEF高于P-C组,24周时两组无显著性差异;治疗后1周及治疗后24周时,两组患者的LVESVI、LVEDVI均较同组基线水平显著降低,且P-B组较P-C组同时间点降低更为显著;治疗后1周及治疗后24周时,两组患者的LVWMI均较同组基线水平显著降低,且P-B组患者治疗后24周时,LVWMI明显低于P-C组同时间点;治疗后24周时,两组患者的LVMI较基线水平均有显著性降低,且P-B组较P-C组降低有显著性差异(P均< 0.05),而治疗后1周两组LVMI均较基线水平无明显变化。4治疗后1周时,两组间患者PS、FWHM、PSD均无显著性差异(P均> 0.05);治疗后24周时,两组患者PS、FWHM、PSD均较1周时明显降低;治疗后24周时,P-B组中PS、FWHM均较P-C组同时间点显著降低,差异有统计学意义(P均<0.05)。5 PCI术后7天,两组患者的BNP水平较前均有下降,分别为(560.5±144.6 pg/ml vs 270.2±95.8 pg/ml, 550.2±124.5 pg/ml vs 398.1±91.7 pg/ml, P均< 0.05),且P-B组显著低于P-C组。6随访6个月时,梗死后心绞痛、再梗死率、死亡率及其它主要并发症(主要脏器出血)的发生率两组间均无统计学差异,分别为(20.8% vs 27.3%,8.3% vs 13.6%, 4.2 % vs 13.6%,12.5% vs 18.2%,P均>0.05)。
小结:PCI联合rhBNP在AMI-LVA可以更有效地改善心功能,抑制心室重构,提高心室收缩同步性,改善患者预后。
The expansion of ventricle after acute myocardial infarction (AMI) is one of the initial factors for the development of ventricular aneurysm . The early ventricular expansion mainly appeared in the region dominated by the infarction-related artery (IRA), if IRA is not opened in time, the infarction and non-infarction zones might have asynchronous motion, which might lead to the formation of acute Left ventricular aneurysm (ALVA). ALVA will aggravate stretch load to the myocardium at infarction margin, resulting in the progressive left ventricular remodeling, inducing or aggravating myocardial ischemia, deteriorating LVA and heart failure, and directly increasing the incidence of major adverse cardiac events (MACE). While AVA might occur at the early stage of AMI, the present researches were mainly focused on chronic LVA, which was clinically diagnosed for sustaining ST elevation lasting more than half a month, when granulation tissue grew into the infarction region to form scar tissue and anatomical LVA came into being, while the occurrence and evolution process of AVA within 72 hours after AMI has not been clear. Related researches indicated that mortality in AMI patients was the highest in those that occurred LVA within 48 hours after AMI. The mortality in patients with LVA was 6 times higher than that without LVA even if they had the similar LVEF. So it is most important to early diagnose LVA to intensify the reversing left ventricular remodeling treatment and decrease the mortality incidence.
There was no detail report about the exact time when the earliest LVA occurred. Continuous ultrasound cardiogram detected that the left ventricle cavity begins to enlarge just 3 hours after AMI. Catheter left ventriculography(LVG)is a useful method for the morphological and hemodynamical diagnosis of LVA, which can be used to intuitively observe the changes of left ventricle’s shape, structure, diastolic and systolic function. While brain or B-type natriuretic peptide (BNP ) is a member of the family of genetically distinct natriuretic peptides synthesized and released by cardiomyocytes in response to the overload of stress and volume, the level of BNP was positively related to volume and/or pressure load, which plays an important role in the protective compensate mechanism that adjusts the circulating dynamic volume and pressure. Brain natriuretic peptide (BNP) is synthesized and released by the stimulation of the ischemia of myocardium, overload of ventricular wall tension and pressure after AMI. The level of BNP was related to the intraventricular pressure, infarction area, the degree of heart failure. So BNP is a new biochemical marker to reflect progressive ventricular remodeling after AMI. But until now, the relationship between the plasma level of BNP and the process of left ventricular aneurysm formation was still unclear. In our study, the plasma BNP levels measured at different time after AMI and the location of infarction identified by LVG, were used to analyze the changes of LV function and remodeling characteristic after AMI and investigate the change of plasma BNP level after AMI, so that to find out the relationship between the plasma BNP level and the formation and progress of LVA in the term of neuroendocrine, as well to probe the significance of plasma peak level of BNP in the diagnosis of ventricular aneurysm. Furthermore, although percutaneous coronary intervention (PCI) is a common way to treat AMI, whether PCI can change or reverse the formation of LVA is still a question, and the report about the long term follow-up for this was rare. So the time sequence of the LVA formation in large scale of consecutive AMI patients and the influence of PCI at different time after AMI on the change of systolic synchrony were evaluated by LVG and phase analysis (PA) of ERNA respectively in our study.
On other hand, in recent years, with the authorization of BNP in the way of diagnosis and assessment of ACS/AMI and the prognosis of heart failure, the clinical application of BNP has achieved great progress, the safety and effect of recombinant human brain natriuretic peptide (rhBNP) had also been proved in the treatment of acute decompensated heart failure (ADHF) by some clinical trails (include the ADHF resulted by acute anterior myocardial infarction). But its influence on the LV remodeling was still unclear. In our study, the influence of PCI combined with rhBNP on heart function and LV remodeling in AMI-LVA patients with HF were investigated through the LVG and equilibrium radionuclide angiography (ERNA).
The contents and results of the study were as follows:
PartⅠA study on the the phasic change of LVA formation in AMI
Objective: This study was to evaluate the relationship between BNP peak level and the formation of LVA through the catheter method LVG in consecutive AMI patients, which can be used to analyse the phasic change of LVA formation , detect the risk factors that influence the formation of LVA and contrast the phasic process in changes of left ventricle’s volume, pressure and configuration after AMI.
Method: Total of 678 consecutive AMI patients (male,563cases, mean age 58±11yrs) admitted in our department from June 2004 to June 2008 were enrolled into this study. All patients were divided into four groups according to the duration of LVG to acute myocardial infarction attack: group A: (<3 hours), group B: (3-6hours), group C (6-24hours) and group D (24-72hours). All the AMI patients were performed coronary angiography (CAG) and PCI, the parameters of left ventricular end diastolic volume index (LVEDVI), left ventricular end systolic volume index (LVESVI), left ventricular ejection fraction (LVEF), left ventricular end diastolic pressure (LVEDP) and left ventricular wall motion score (LVWMS) were measured by LVG. The LVA was identified by LVG. And all the patients were divided into two groups (LVA group and non-LVA group) according to left ventricular wall motion. The clinical data and angiographical data of the patients were recorded. The two group patients’disease history, symptom and coronary CAG data were compared with univariate analysis and multivariate regression. Plasma BNP level was monitored at different time after AMI. The incidence of major adverse cardiac events (MACE) during in-hospital, including re-infarction, angina post AMI, congestive heart failure, malignent arrhythmia and death were recorded.
Result:①There was no significant difference between the four groups in clinical characteristics such as age, sex and risk factors (including hypertension, diabetes mellitus, hyperlipidemia and smoking history). Coronary angiography showed that the occlusion site of infarction related artery (IRA), the multivessle lesion rate and the stenosis degree of the lesions were no significant difference among the four groups (P >0.05).②Cumulated incidence of LVA: 10% within 3 hours, 15.5% within 6 hours, 23.3% within 24 hours, 30.38% within 72 hours. The values of LVEDVI and WMS in group A, B and C were obvious lower, while the value of LVEF was obvious higher than that in group D. In group A, the value of LVESVI was also obvious lower than that in group D and the values of LVEDVI and WMS were lowered than those in group C. There was no significant difference of above parameters between group B and C.③Univariate significance analysis of 18 parameters in LVA group and non-LVA group: age, hypertension, angina history pre-AMI, first AMI history, anterior myocardial infarction, single vascular lesion (LAD or LCX), collateral circulation, occlusion site of IRA, time for occlusion of IRA were the risk factors for the formation of LVA after AMI. Logistic multivariate regression analysis indicated that anterior myocardial infarction, occlusion position of IRA, first AMI history, time from attack of AMI were the independent risk factors for the formation of LVA after AMI.④The value of LVEF in LVA group was significantly lowered (45.7±16.1 % vs 49.0±18.2%,P <0.05), while the values of LVEDVI, LVESVI and LVEDP were all obviously higher (113.2±25.1 ml/m~2 vs 104.1±26.3 ml/m~2, 63.2±35.1 ml/m~2 vs 54.6±27.2 ml/m~2, 18.8±3.2 mmHg vs 16.1±3.2 mmHg, P all<0.05), than those in non-LVA group. The disorder of left ventricular wall motion was obvious, and the LVWMS was obvious higher(7.7±2.9 vs 6.8±2.4,P <0.05), in LVA group than that in non-LVA group. ⑤The plasma concentrations of BNP in LVA group were obvious higher than that in non-LVA group 18 hours, the fifth day and 24th week after AMI (592.2±145.8 pg/ml vs 374.3±152.2 pg/ml, 378.2±139.7 pg/ml vs 178.3±31.7 pg/ml,106.4±28.4 pg/ml vs 64.2±22.9 pg/ml, P all<0.05).The peak value of plasma concentration of BNP was significantly higher (592.2±145.8 pg/ml vs 384.3±152.2 pg/ml,P<0.05), and the time for reaching peak value of plasma concentration of BNP was much shorter(17.2±2.9h vs 19.1±2.8h,P<0.01)in LVA group than that in non-LVA group. 6.The incidence of angina post AMI, re-infarction, mortality in hospital was obvious higher in LVA group than that in non-LVA group (43/206 vs 42/472,24/206 vs 14/472,16/206 vs 9/472,P all <0.05).
Conclusion: The formation of LVA might occur in the early stage of AMI, the incidence of which was 10% within 3 hours after AMI, and the cumulated incidence of it was as high as 30% within 72 hours. The formation of LVA was influenced by a lot of factors. Anterior AMI, total or subtotal occlusion of the proximal and middle segment in LAD, occlusion time of IRA were its independent risk factors. The excess secretion of neuroendocrine hormone BNP played a role in the formation process of LVA. The heart function was obviously damaged and in-hospital mortality incidence was significantly increased in AMI patients with LVA.
PartⅡEffect of percutaneous coronary intervention at different time on ventricular aneurysm formation and systolic synchrony in patients with acute myocardial infarction
Objective: This study was to evaluate the time sequence of the formation of LVA through left ventriculography(LVG) in large scale of consecutive AMI patients and assess the effect of PCI at different time after AMI on the LVA formation and its influence on systolic synchrony. The level of BNP was also measured to investigate its relation with LVA.
Methods: From Jan 2004 to Dec 2006, a total of 326 consecutive patients of anterior AMI with LVA were enrolled into this study. LVA was diagnosed by LVG. All patients were divided into 4 groups according to the time of onset to balloon: group A (<3h), group B (3-6h), group C (6-12h) and group D (>1week). At baseline and 6 months after AMI, the parameters of left ventricular end diastolic volume index (LVEDVI), left ventricular end systolic volume index (LVESVI), left ventricular ejection fraction (LVEF), left ventricular end diastolic pressure (LVEDP) and left ventricular wall motion score (LVWMS) were measured by LVG. The paradox volume (PV) image of ventricle movement on the dynamic cine as well as the parameters of left ventricular systolic function (LVSF), left ventricular diastolic function (LVDF) and left ventricular systolic synchrony (LVSS) were measured by ERNA at 1 week and 6 months after AMI. Plasma BNP was measured 18 hours, 5 days and 24 weeks after AMI. The major adverse cardiac events (MACE) were recorded up to 3 years.
Results:①The baseline LVG showed that the LVESVI, LVEDVI, WMS, LVEDP were lower, while LVEF was increased, in group A than that in other groups (P<0.05, respectively). At 6 months after AMI, the LVESVI, LVEDVI, LVEDP and LVWMS in the four groups were decreased, while LVEF was increased, than that at baseline. Those parameters in group A were changed most obviously (P<0.05, respectively).②At 6 months post AMI, LVEF, PER and PFR in group A were increased, while TPER, PS and FWHM were decreased than those in group D (P<0.05, respectively).③At 6th month post AMI, the cases with disappearance on the paradox volume in group A were obviously higher than that in group B, C, and D, and the PVI in group A was lower than that in group B, C, and D (P<0.05, respectively).④18 hours, 5 days and 24 weeks after AMI, the values of BNP in group D were higher than those in group A, B and C. There was no difference between group B and C (P<0.05, respectively).⑤Within the 3 years follow-up, the incidence of angina post-AMI and mortality in group A, B, and C was significantly lower than those in group D (P<0.05, respectively).
Conclusions: The LVA can emerge shortly after AMI. The early, fully and permanently patency of infarction-related artery (IRA) can effectively inhibit the left ventricular remodeling process, prevent LVA formation, and improve LV function and prognosis.
PartⅢClinical effects of percutaneous coronary intervention combined with intravenous recombinant human brain natriuretic peptide on acute myocardial infarction patients with left ventricular aneurysm
Objective To evaluate the influence of PCI combined with rhBNP on ventricular remodeling and heart function in acute myocardial infarction patients with left ventricular aneurysm (AMI-LVA) through invasive hemodynamic monitoring, ultrasonic cardiogram and equilibrium radionuclide ventriculography (ERNA).
Methods Total of 46 patients admitted in our hospital within 24 hours after AMI from June 2007 to June 2008 were randmized into two groups after PCI: group P-B (PCI combined with rhBNP, n=24) and group B (PCI and routine contrast treatment group, n=22). All the patients were underwent emergency PCI, and group A combined with rhBNP treatment: (1.5μg/kg bolus intravenous injection last for 90s with the same velocity followed by 0.0075-0.015μg/kg/min for the following 72 hours). Before, during and after the rhBNP infusion, the heart rate, systolic pressure, LVEDP and oxygen saturation were recorded. Two dimension echocardiography was used to measure the index of left ventricular end-diastolic volume (LVEDVI), the index of left ventricular end-systolic volume (LVESVI), the left ventricular ejection fraction (LVEF), the index of left ventricular mass (LVMI), the movement index of infarcted regional wall (RWMI) before. 1 week and 24 weeks after the administration of rhBNP. And 1 week and 24 weeks after the administration of rhBNP, the ventricular systolic synchrony parameters, that is phase shift (PS),full width at half maximum (FWHM) and peak phase standard deviation (PSD) were evaluated by ERNA. The changes of plasma BNP level were recorded before and 7 days after the administration of rhBNP The major adverse cardiac events (MACE) were followed up for 6 months.
Results:①There was no significant difference between the two groups in clinical characteristics such as age, sex and risk factors. The peak level of CKMB was significantly lower in group P-B than that in group P-C (233.6±35.3 IU/L vs 288.5±34.6 IU/L,P<0.05).②After the administration of rhBNP, LVEDP was decreased and oxygen saturation was increased in both groups than in the baseline, and in group P-B, the extent was significantly higher than that in group B (4.6±1.1 mmHg vs 2.0±0.9 mmHg,5.5±1.2 % vs 2.3±1.2%, P all<0.05, respectively).③The value of LVEF in group P-B was higher than that in group P-C 1 week after treatment, while no signifcant difference between the two group 24 weeks. The values of LVESVI and LVEDVI in the two groups were both obviously decreased compared with those of baseline, which were more significant in group P-B than that in group P-C at each of the same time point. The values of LVWMI 1 week and 24 weeks after treatment were all obviously lowered compared with that of baseline of each group, and the value of LVWMI 24 weeks after treatment in group P-B was much lower than that in group P-C. The values of LVMI 24 weeks after treatment in group P-B were all significantly decreased in both of the two groups compared with that of baseline, which were decreased more in group P-B than that in group P-C, while there was no significant change 1 week after treatment in both of the two groups.④The values of PS, FWHM and PSD were no significant difference between the 2 groups 1 week after treatment, which were significantly lowered 24 weeks after treatment compared with that of 1week after treatment in both of the 2 groups. The values of PS, FWHM 24 weeks after treatment in group P-B were significantly decreased than that in group P-C.⑤The plasma levels BNP 7 days after PCI were both decreased significantly in both of the two groups (group P-B: 560.5±144.6 pg/ml vs 270.2±95.8 pg/ml, group P-C: 550.2±124.5 pg/ml vs 398.1±91.7 pg/ml, P all< 0.05), which were more significant in group P-B than that in group P-C.⑥The incidence of angina post-AMI, re-myocardial infarction, mortality and other major adverse complications(main organs bleeding) were no significant difference between group P-B and group P-C (20.8% vs 27.3%,8.3% vs 13.6%, 4.2 % vs 13.6%,12.5% vs 18.2%,P all >0.05).
Conclusion: PCI combined with transvenous injection of rhBNP based on other routine treatments can further improve the left ventricular function, inhibit the remodeling of left ventricle, enhance the ventricular systolic synchrony and offer better prognosis of the patients.
虽然连续心脏超声检查发现AMI发病后3小时内左心室腔即开始扩大。但目前关于AVA最早何时发生尚缺乏详实报导。AMI后即刻行导管法左室造影(left ventriculography, LVG)检查可直观地了解AMI后心室形态、结构、舒缩功能及血流动力学的变化。对于LVA的形成做出准确判断。而血浆B型钠尿肽(B-type natriuretic peptide, BNP)是属于钠尿肽家族中的一员,它是对容量和压力过负荷的反应性产物,其分泌水平与心室内容量和/或压力负荷状态成正相关,并在血流动力学容积和压力调节的保护性代偿机制中起重要作用。BNP作为反应心脏血流动力学及左室重构的标记物已有共识,它在AMI演变过程的水平变化对于LVA的形成有无预测价值及心肌梗死后LVA形成的时相过程与血浆BNP水平关系亦不清楚。PCI是急性心梗有效的治疗方法,但对于LVA的治疗和逆转作用尚不清楚,尤其是心肌梗死后LVA患者能否长期获益尚不清楚。本研究通过对连续入选的AMI患者行LVG直接获得急性室壁活动的形态与功能参数,明确LVA形成的时相过程。结合平衡法核素心室造影相位分析进一步明确不同时段PCI对于急性LVA患者心室运动的同步性、心功能及心室重塑的影响。
近几年来随着BNP在诊断评价急性冠脉综合症(acute coronary syndrome, ACS)/AMI以及心力衰竭(heart failure,HF)的预后方面上得到多方认可,其在临床治疗领域方面的应用也取得了重大进展, rhBNP临床应用的安全性、改善血流动力学的有效性已在一些急性失代偿HF的试验中得到证实。本研究通过导管法LVG并结合心脏超声和平衡法核素心室造影相位分析,探讨PCI术后常规治疗的基础上联合应用rhBNP对AMI-LVA患者左心功能和收缩同步性的影响。
本研究内容及结果如下:
第一部分急性心肌梗死后室壁瘤形成的时相性变化
目的:通过对连续AMI患者行导管法左室造影,分析AMI后LVA形成的时相性变化及影响LVA形成的相关危险因素,对比AMI后心室容积、压力及形态变化的时相过程,探讨血浆BNP峰值水平与LVA形成的关系。
方法:2004年6月-2008年6月我科连续收治的首次AMI患者678例,其中男性563例,女性115例,年龄58±11岁。根据行左室造影(LVG)距AMI发病的时间分为A组(<3小时,120例)、B组(3-6小时,150例)、C组(6-24小时,228例)、D组(24-72小时,180例)。所有入选患者,均于冠脉造影同时行LVG检查,测定左心室舒张末期压力(LVEDP)、左心室舒张末期容积指数(LVEDVI)、左心室收缩末期容积指数(LVESVI)、左室射血分数(LVEF)、室壁运动积分(LVWMS)。并按LVG室壁运动情况分为有LVA组和无LVA组,比较两者患者的临床资料、冠脉造影资料、血浆BNP水平变化及住院期间主要恶性心脏事件(MACE,包括再梗死、梗死后心绞痛、充血性心衰、恶性心律失常、死亡)的发生率。
结果: 1.各组患者在年龄、性别、危险因素(包括高血压、糖尿病、高脂血症、吸烟史)等方面均无显著性差异。四组间CAG结果显示,IRA病变位置、多支病变率、病变阻塞程度均无显著性差异(P >0.05)。2. LVA累积发生率:3小时以内为10%;6小时以内为15.5%;24小时以内为23.3%、72小时内为30.38%。A、B、C三组LVEDVI、LVWMS明显低于D组,而LVEF明显高于D组(P均<0.05);在A组中,LVESVI亦明显低于D组,LVEDVI、LVWMS较C组降低(P均<0.05)。A、B组比较无显著性差异;B、C组比较无统计学差异。3.有LVA组与无LVA组对18个指标进行Logistic单因素分析:年龄、高血压、糖尿病、梗死前心绞痛史、首次心肌梗死病史、前壁心肌梗死、单支病变(LAD, LMA)、侧支循环、血管闭塞部位、血管闭塞时间是AMI后LVA形成的危险因素。Logistic多因素回归分析结果提示前壁心肌梗死、血管闭塞部位、心肌梗塞病史、PCI距离AMI发病的时间是AMI后LVA形成的独立危险因素。4. LVA组LVEF较无LVA组明显降低(45.7±16.1 %vs 49.0±18.2%,P <0.05); LVEDVI、LVESVI及LVEDP均明显高于无LVA组(113.2±25.1 ml/m~2 vs 104.1±26.3 ml/m~2, 63.2±35.1 ml/m~2 vs 54.6±27.2 ml/m~2, 18.8±3.2 mmHg vs 16.1±3.2 mmHg, P均<0.05)。LVA组LVWMS明显高于无LVA组(7.7±2.9 vs 6.8±2.4,P <0.05)。5 LVA组发病后18小时、第5天和第24周血浆BNP浓度均明显高于无LVA组(592.2±145.8 pg/ml vs 374.3±152.2 pg/ml, 378.2±139.7 pg/ml vs 178.3±31.7 pg/ml,106.4±28.4 pg/ml vs 64.2±22.9 pg/ml, P均<0.05)。LVA组血浆BNP峰值浓度明显高于无LVA组(592.2±145.8 pg/ml vs 384.3±152.2 pg/ml,P<0.05)。且峰值时间显著提前(17.2±2.9h vs 19.1±2.8h,P<0.01)。6. LVA组住院期间梗死后心绞痛、再梗死率、死亡率均高于无LVA组(43/206 vs 42/472,24/206 vs 14/472,16/206 vs 9/472,P均<0.05)。
小结:AMI患者早期即可有LVA的形成,3小时之内,LVA的发生可达10%,至AMI发病72小时,LVA的累积发生率可高达30%。LVA形成受多种因素共同影响,前壁心肌梗死(LAD近中段完全或次全闭塞)、心肌梗塞病史、IRA闭塞时间是独立的危险因素。血浆BNP水平的增加是AMI后LVA形成的早期重要标记物。LVA患者的心功能明显受损,住院期间死亡率增高。
第二部分不同时段介入治疗对心肌梗死室壁瘤患者心室重构及心室收缩同步性影响
目的:通过导管法左室造影结合平衡法核素心室造影(ERNA)的方法,对比不同时间段行冠脉介入治疗(PCI)对急性心肌梗死(AMI)后室壁瘤(LVA)患者左室重构、收缩同步性及心功能的影响。
方法:选择2004年1月-2006年12月我院连续收治的首次急性前壁心肌梗死患者及LVG确定合并室壁瘤者共326例,根据自发病至行PCI的时间,分为:A组(<3小时)、B组(3-6小时)、C组(6-12小时)、D组(AMI后1周),四组患者于PCI后即行左心室造影,测定左心室舒张末期压力(LVEDP)、左心室舒张末期容积指数(LVEDVI)、左心室收缩末期容积指数(LVESVI)、左室射血分数(LVEF)、室壁运动积分(LVWMS);AMI后1周时行平衡法核素心室造影,测定左室收缩功能参数:左室射血分数(LVEF)左室峰射血率时间(TPER)左室峰射血率(PER)及舒张功能参数:左室峰充盈率(PFR)左室峰充盈时间(TPFR)和收缩同步性参数即相角程(PS),半高宽(FWHM),峰相位标准差(PSD)及反常室壁容积指数(PVI);并于急性心肌梗死后不同时间段行BNP监测。AMI后6个月随访时重复行心室造影和核素心室造影检查测定上述参数,并随访3年,记录主要恶性心脏事件(MACE)的发生率。
结果:1. PCI时,A、B、C三组LVEDVI、LVWMS明显低于D组,而LVEF明显高于D组(P均<0.05);在A组中,LVESVI亦明显低于D组,LVEDVI、WMS较C组降低(P均<0.05)。B、C组各指标无统计学差异; PCI术后6个月随访,A、B、C、D四组LVESVI、LVEDVI、WMS、LVEDP均较行PCI时减低,而LVEF较前增高(P均<0.05)。其中A组变化最为显著;2 AMI后6个月随访时, A、B、C三组LVEF、PER、PFR较D组明显增高,而TPER、PS、FWHM明显降低(P均<0.05);3.至AMI后6个月时A组反常容积消失病例数明显高于B、C、D组,且A组PVI亦明显低于B、C、D组(12.08±2.07% vs 15.43±2.39% vs 16.49±2.47% vs 20.41±3.68%,P均<0.05);4. D组发病后18小时、第5天和第24周血浆BNP浓度均明显高于A组(615±112 pg/ml vs 492.5±130 pg/ml,473.5±97.5 pg/ml vs 332.5±78 pg/ml,268±71.5 pg/ml vs163.5±56 pg/ml,P均<0.05 );5. A组、B组和C组梗死后心绞痛(6.2% vs 21%,8.9% vs 21%,9.3% vs 21%,P均<0.05)及3年随访时死亡率(3.1% vs 17.1%,5.6% vs 17.1%,7.7% vs 17.1%,P均<0.05)均低于D组,且A组再梗死率和住院期间死亡率亦明显低于D组(3.1% vs 13.1%,0% vs 6.6%,P均<0.05)
小结:对于AMI患者,早期(尤其是3小时之内)施行PCI可以显著降低血浆BNP的水平,有效地抑制并逆转LVA的形成,提高左室功能,改善患者的预后。
第三部分PCI联合静脉应用rhBNP对急性心肌梗死室壁瘤的逆转效应
目的:通过有创血流动力学监测,结合超声心动图和平衡法核素心室造影的方法,评价冠脉介入治疗(PCI)联合重组人脑利钠肽(rhBNP)对急性心肌梗死伴室壁瘤(AMI-LVA)患者心室重构、收缩同步性及心功能的影响。
方法:2007年6月—2008年6月,我院收治24h内发病的前壁AMI-LVA患者46例,随机分为P-B组(PCI+rhBNP)和P-C组(PCI+常规对照治疗)。两组患者均给予急诊PCI治疗,P-B组在PCI治疗的基础上即刻静脉注射rhBNP(成都诺迪康生物制药有限公司),负荷量1.5μg/kg,90秒内匀速注入,继而以0.0075~0.0150μg·kg-1·min-1的速度维持静脉滴注24 h。所有患者分别于用药前后测心率、血压、左室终末压(LVEDP)及氧饱和度的变化;用药前、用药后1周及用药后24周采用二维超声心动图测定舒张末期容积指数(LVEDVI)、收缩末期容积指数(LVESVI )、左室射血分数(LVEF)、左室质量指数(LVMI)、梗死区的局部室壁运动指数(RWMI)。并于用药1周、24周时行ERNA了解心室收缩同步性参数,即相角程(PS),半高宽(FWHM),峰相位标准差(PSD)。记录应用BNP前及治疗后7天两组患者BNP水平的变化,记录住院期间及随访6个月主要不良心脏事件及并发症的发生率。
结果:1基线资料相比,两组患者性别、年龄、冠心病危险因素均无差异。P-B组中CKMB峰值水平低于P-C组(233.6±35.3 IU/L vs 288.5±34.6 IU/L,P<0.05);2两组患者治疗前后相比,两组患者LVEDP均有降低,在P-B组有显著性差异(P均<0.05)。P-B组LVEDP降低程度较P-C组显著(4.6±1.1 mmHg vs 2.0±0.9 mmHg, P<0.05);3 P-B组治疗后1周时LVEF高于P-C组,24周时两组无显著性差异;治疗后1周及治疗后24周时,两组患者的LVESVI、LVEDVI均较同组基线水平显著降低,且P-B组较P-C组同时间点降低更为显著;治疗后1周及治疗后24周时,两组患者的LVWMI均较同组基线水平显著降低,且P-B组患者治疗后24周时,LVWMI明显低于P-C组同时间点;治疗后24周时,两组患者的LVMI较基线水平均有显著性降低,且P-B组较P-C组降低有显著性差异(P均< 0.05),而治疗后1周两组LVMI均较基线水平无明显变化。4治疗后1周时,两组间患者PS、FWHM、PSD均无显著性差异(P均> 0.05);治疗后24周时,两组患者PS、FWHM、PSD均较1周时明显降低;治疗后24周时,P-B组中PS、FWHM均较P-C组同时间点显著降低,差异有统计学意义(P均<0.05)。5 PCI术后7天,两组患者的BNP水平较前均有下降,分别为(560.5±144.6 pg/ml vs 270.2±95.8 pg/ml, 550.2±124.5 pg/ml vs 398.1±91.7 pg/ml, P均< 0.05),且P-B组显著低于P-C组。6随访6个月时,梗死后心绞痛、再梗死率、死亡率及其它主要并发症(主要脏器出血)的发生率两组间均无统计学差异,分别为(20.8% vs 27.3%,8.3% vs 13.6%, 4.2 % vs 13.6%,12.5% vs 18.2%,P均>0.05)。
小结:PCI联合rhBNP在AMI-LVA可以更有效地改善心功能,抑制心室重构,提高心室收缩同步性,改善患者预后。
The expansion of ventricle after acute myocardial infarction (AMI) is one of the initial factors for the development of ventricular aneurysm . The early ventricular expansion mainly appeared in the region dominated by the infarction-related artery (IRA), if IRA is not opened in time, the infarction and non-infarction zones might have asynchronous motion, which might lead to the formation of acute Left ventricular aneurysm (ALVA). ALVA will aggravate stretch load to the myocardium at infarction margin, resulting in the progressive left ventricular remodeling, inducing or aggravating myocardial ischemia, deteriorating LVA and heart failure, and directly increasing the incidence of major adverse cardiac events (MACE). While AVA might occur at the early stage of AMI, the present researches were mainly focused on chronic LVA, which was clinically diagnosed for sustaining ST elevation lasting more than half a month, when granulation tissue grew into the infarction region to form scar tissue and anatomical LVA came into being, while the occurrence and evolution process of AVA within 72 hours after AMI has not been clear. Related researches indicated that mortality in AMI patients was the highest in those that occurred LVA within 48 hours after AMI. The mortality in patients with LVA was 6 times higher than that without LVA even if they had the similar LVEF. So it is most important to early diagnose LVA to intensify the reversing left ventricular remodeling treatment and decrease the mortality incidence.
There was no detail report about the exact time when the earliest LVA occurred. Continuous ultrasound cardiogram detected that the left ventricle cavity begins to enlarge just 3 hours after AMI. Catheter left ventriculography(LVG)is a useful method for the morphological and hemodynamical diagnosis of LVA, which can be used to intuitively observe the changes of left ventricle’s shape, structure, diastolic and systolic function. While brain or B-type natriuretic peptide (BNP ) is a member of the family of genetically distinct natriuretic peptides synthesized and released by cardiomyocytes in response to the overload of stress and volume, the level of BNP was positively related to volume and/or pressure load, which plays an important role in the protective compensate mechanism that adjusts the circulating dynamic volume and pressure. Brain natriuretic peptide (BNP) is synthesized and released by the stimulation of the ischemia of myocardium, overload of ventricular wall tension and pressure after AMI. The level of BNP was related to the intraventricular pressure, infarction area, the degree of heart failure. So BNP is a new biochemical marker to reflect progressive ventricular remodeling after AMI. But until now, the relationship between the plasma level of BNP and the process of left ventricular aneurysm formation was still unclear. In our study, the plasma BNP levels measured at different time after AMI and the location of infarction identified by LVG, were used to analyze the changes of LV function and remodeling characteristic after AMI and investigate the change of plasma BNP level after AMI, so that to find out the relationship between the plasma BNP level and the formation and progress of LVA in the term of neuroendocrine, as well to probe the significance of plasma peak level of BNP in the diagnosis of ventricular aneurysm. Furthermore, although percutaneous coronary intervention (PCI) is a common way to treat AMI, whether PCI can change or reverse the formation of LVA is still a question, and the report about the long term follow-up for this was rare. So the time sequence of the LVA formation in large scale of consecutive AMI patients and the influence of PCI at different time after AMI on the change of systolic synchrony were evaluated by LVG and phase analysis (PA) of ERNA respectively in our study.
On other hand, in recent years, with the authorization of BNP in the way of diagnosis and assessment of ACS/AMI and the prognosis of heart failure, the clinical application of BNP has achieved great progress, the safety and effect of recombinant human brain natriuretic peptide (rhBNP) had also been proved in the treatment of acute decompensated heart failure (ADHF) by some clinical trails (include the ADHF resulted by acute anterior myocardial infarction). But its influence on the LV remodeling was still unclear. In our study, the influence of PCI combined with rhBNP on heart function and LV remodeling in AMI-LVA patients with HF were investigated through the LVG and equilibrium radionuclide angiography (ERNA).
The contents and results of the study were as follows:
PartⅠA study on the the phasic change of LVA formation in AMI
Objective: This study was to evaluate the relationship between BNP peak level and the formation of LVA through the catheter method LVG in consecutive AMI patients, which can be used to analyse the phasic change of LVA formation , detect the risk factors that influence the formation of LVA and contrast the phasic process in changes of left ventricle’s volume, pressure and configuration after AMI.
Method: Total of 678 consecutive AMI patients (male,563cases, mean age 58±11yrs) admitted in our department from June 2004 to June 2008 were enrolled into this study. All patients were divided into four groups according to the duration of LVG to acute myocardial infarction attack: group A: (<3 hours), group B: (3-6hours), group C (6-24hours) and group D (24-72hours). All the AMI patients were performed coronary angiography (CAG) and PCI, the parameters of left ventricular end diastolic volume index (LVEDVI), left ventricular end systolic volume index (LVESVI), left ventricular ejection fraction (LVEF), left ventricular end diastolic pressure (LVEDP) and left ventricular wall motion score (LVWMS) were measured by LVG. The LVA was identified by LVG. And all the patients were divided into two groups (LVA group and non-LVA group) according to left ventricular wall motion. The clinical data and angiographical data of the patients were recorded. The two group patients’disease history, symptom and coronary CAG data were compared with univariate analysis and multivariate regression. Plasma BNP level was monitored at different time after AMI. The incidence of major adverse cardiac events (MACE) during in-hospital, including re-infarction, angina post AMI, congestive heart failure, malignent arrhythmia and death were recorded.
Result:①There was no significant difference between the four groups in clinical characteristics such as age, sex and risk factors (including hypertension, diabetes mellitus, hyperlipidemia and smoking history). Coronary angiography showed that the occlusion site of infarction related artery (IRA), the multivessle lesion rate and the stenosis degree of the lesions were no significant difference among the four groups (P >0.05).②Cumulated incidence of LVA: 10% within 3 hours, 15.5% within 6 hours, 23.3% within 24 hours, 30.38% within 72 hours. The values of LVEDVI and WMS in group A, B and C were obvious lower, while the value of LVEF was obvious higher than that in group D. In group A, the value of LVESVI was also obvious lower than that in group D and the values of LVEDVI and WMS were lowered than those in group C. There was no significant difference of above parameters between group B and C.③Univariate significance analysis of 18 parameters in LVA group and non-LVA group: age, hypertension, angina history pre-AMI, first AMI history, anterior myocardial infarction, single vascular lesion (LAD or LCX), collateral circulation, occlusion site of IRA, time for occlusion of IRA were the risk factors for the formation of LVA after AMI. Logistic multivariate regression analysis indicated that anterior myocardial infarction, occlusion position of IRA, first AMI history, time from attack of AMI were the independent risk factors for the formation of LVA after AMI.④The value of LVEF in LVA group was significantly lowered (45.7±16.1 % vs 49.0±18.2%,P <0.05), while the values of LVEDVI, LVESVI and LVEDP were all obviously higher (113.2±25.1 ml/m~2 vs 104.1±26.3 ml/m~2, 63.2±35.1 ml/m~2 vs 54.6±27.2 ml/m~2, 18.8±3.2 mmHg vs 16.1±3.2 mmHg, P all<0.05), than those in non-LVA group. The disorder of left ventricular wall motion was obvious, and the LVWMS was obvious higher(7.7±2.9 vs 6.8±2.4,P <0.05), in LVA group than that in non-LVA group. ⑤The plasma concentrations of BNP in LVA group were obvious higher than that in non-LVA group 18 hours, the fifth day and 24th week after AMI (592.2±145.8 pg/ml vs 374.3±152.2 pg/ml, 378.2±139.7 pg/ml vs 178.3±31.7 pg/ml,106.4±28.4 pg/ml vs 64.2±22.9 pg/ml, P all<0.05).The peak value of plasma concentration of BNP was significantly higher (592.2±145.8 pg/ml vs 384.3±152.2 pg/ml,P<0.05), and the time for reaching peak value of plasma concentration of BNP was much shorter(17.2±2.9h vs 19.1±2.8h,P<0.01)in LVA group than that in non-LVA group. 6.The incidence of angina post AMI, re-infarction, mortality in hospital was obvious higher in LVA group than that in non-LVA group (43/206 vs 42/472,24/206 vs 14/472,16/206 vs 9/472,P all <0.05).
Conclusion: The formation of LVA might occur in the early stage of AMI, the incidence of which was 10% within 3 hours after AMI, and the cumulated incidence of it was as high as 30% within 72 hours. The formation of LVA was influenced by a lot of factors. Anterior AMI, total or subtotal occlusion of the proximal and middle segment in LAD, occlusion time of IRA were its independent risk factors. The excess secretion of neuroendocrine hormone BNP played a role in the formation process of LVA. The heart function was obviously damaged and in-hospital mortality incidence was significantly increased in AMI patients with LVA.
PartⅡEffect of percutaneous coronary intervention at different time on ventricular aneurysm formation and systolic synchrony in patients with acute myocardial infarction
Objective: This study was to evaluate the time sequence of the formation of LVA through left ventriculography(LVG) in large scale of consecutive AMI patients and assess the effect of PCI at different time after AMI on the LVA formation and its influence on systolic synchrony. The level of BNP was also measured to investigate its relation with LVA.
Methods: From Jan 2004 to Dec 2006, a total of 326 consecutive patients of anterior AMI with LVA were enrolled into this study. LVA was diagnosed by LVG. All patients were divided into 4 groups according to the time of onset to balloon: group A (<3h), group B (3-6h), group C (6-12h) and group D (>1week). At baseline and 6 months after AMI, the parameters of left ventricular end diastolic volume index (LVEDVI), left ventricular end systolic volume index (LVESVI), left ventricular ejection fraction (LVEF), left ventricular end diastolic pressure (LVEDP) and left ventricular wall motion score (LVWMS) were measured by LVG. The paradox volume (PV) image of ventricle movement on the dynamic cine as well as the parameters of left ventricular systolic function (LVSF), left ventricular diastolic function (LVDF) and left ventricular systolic synchrony (LVSS) were measured by ERNA at 1 week and 6 months after AMI. Plasma BNP was measured 18 hours, 5 days and 24 weeks after AMI. The major adverse cardiac events (MACE) were recorded up to 3 years.
Results:①The baseline LVG showed that the LVESVI, LVEDVI, WMS, LVEDP were lower, while LVEF was increased, in group A than that in other groups (P<0.05, respectively). At 6 months after AMI, the LVESVI, LVEDVI, LVEDP and LVWMS in the four groups were decreased, while LVEF was increased, than that at baseline. Those parameters in group A were changed most obviously (P<0.05, respectively).②At 6 months post AMI, LVEF, PER and PFR in group A were increased, while TPER, PS and FWHM were decreased than those in group D (P<0.05, respectively).③At 6th month post AMI, the cases with disappearance on the paradox volume in group A were obviously higher than that in group B, C, and D, and the PVI in group A was lower than that in group B, C, and D (P<0.05, respectively).④18 hours, 5 days and 24 weeks after AMI, the values of BNP in group D were higher than those in group A, B and C. There was no difference between group B and C (P<0.05, respectively).⑤Within the 3 years follow-up, the incidence of angina post-AMI and mortality in group A, B, and C was significantly lower than those in group D (P<0.05, respectively).
Conclusions: The LVA can emerge shortly after AMI. The early, fully and permanently patency of infarction-related artery (IRA) can effectively inhibit the left ventricular remodeling process, prevent LVA formation, and improve LV function and prognosis.
PartⅢClinical effects of percutaneous coronary intervention combined with intravenous recombinant human brain natriuretic peptide on acute myocardial infarction patients with left ventricular aneurysm
Objective To evaluate the influence of PCI combined with rhBNP on ventricular remodeling and heart function in acute myocardial infarction patients with left ventricular aneurysm (AMI-LVA) through invasive hemodynamic monitoring, ultrasonic cardiogram and equilibrium radionuclide ventriculography (ERNA).
Methods Total of 46 patients admitted in our hospital within 24 hours after AMI from June 2007 to June 2008 were randmized into two groups after PCI: group P-B (PCI combined with rhBNP, n=24) and group B (PCI and routine contrast treatment group, n=22). All the patients were underwent emergency PCI, and group A combined with rhBNP treatment: (1.5μg/kg bolus intravenous injection last for 90s with the same velocity followed by 0.0075-0.015μg/kg/min for the following 72 hours). Before, during and after the rhBNP infusion, the heart rate, systolic pressure, LVEDP and oxygen saturation were recorded. Two dimension echocardiography was used to measure the index of left ventricular end-diastolic volume (LVEDVI), the index of left ventricular end-systolic volume (LVESVI), the left ventricular ejection fraction (LVEF), the index of left ventricular mass (LVMI), the movement index of infarcted regional wall (RWMI) before. 1 week and 24 weeks after the administration of rhBNP. And 1 week and 24 weeks after the administration of rhBNP, the ventricular systolic synchrony parameters, that is phase shift (PS),full width at half maximum (FWHM) and peak phase standard deviation (PSD) were evaluated by ERNA. The changes of plasma BNP level were recorded before and 7 days after the administration of rhBNP The major adverse cardiac events (MACE) were followed up for 6 months.
Results:①There was no significant difference between the two groups in clinical characteristics such as age, sex and risk factors. The peak level of CKMB was significantly lower in group P-B than that in group P-C (233.6±35.3 IU/L vs 288.5±34.6 IU/L,P<0.05).②After the administration of rhBNP, LVEDP was decreased and oxygen saturation was increased in both groups than in the baseline, and in group P-B, the extent was significantly higher than that in group B (4.6±1.1 mmHg vs 2.0±0.9 mmHg,5.5±1.2 % vs 2.3±1.2%, P all<0.05, respectively).③The value of LVEF in group P-B was higher than that in group P-C 1 week after treatment, while no signifcant difference between the two group 24 weeks. The values of LVESVI and LVEDVI in the two groups were both obviously decreased compared with those of baseline, which were more significant in group P-B than that in group P-C at each of the same time point. The values of LVWMI 1 week and 24 weeks after treatment were all obviously lowered compared with that of baseline of each group, and the value of LVWMI 24 weeks after treatment in group P-B was much lower than that in group P-C. The values of LVMI 24 weeks after treatment in group P-B were all significantly decreased in both of the two groups compared with that of baseline, which were decreased more in group P-B than that in group P-C, while there was no significant change 1 week after treatment in both of the two groups.④The values of PS, FWHM and PSD were no significant difference between the 2 groups 1 week after treatment, which were significantly lowered 24 weeks after treatment compared with that of 1week after treatment in both of the 2 groups. The values of PS, FWHM 24 weeks after treatment in group P-B were significantly decreased than that in group P-C.⑤The plasma levels BNP 7 days after PCI were both decreased significantly in both of the two groups (group P-B: 560.5±144.6 pg/ml vs 270.2±95.8 pg/ml, group P-C: 550.2±124.5 pg/ml vs 398.1±91.7 pg/ml, P all< 0.05), which were more significant in group P-B than that in group P-C.⑥The incidence of angina post-AMI, re-myocardial infarction, mortality and other major adverse complications(main organs bleeding) were no significant difference between group P-B and group P-C (20.8% vs 27.3%,8.3% vs 13.6%, 4.2 % vs 13.6%,12.5% vs 18.2%,P all >0.05).
Conclusion: PCI combined with transvenous injection of rhBNP based on other routine treatments can further improve the left ventricular function, inhibit the remodeling of left ventricle, enhance the ventricular systolic synchrony and offer better prognosis of the patients.
引文
1 Udelson J, Patten RD, Konstam MA. New concepts in post-infarction ventricular remodeling. Rev Cardiovasc Med, 2003, 4 (Suppl 3): S3~12
2 Gorlin R, Klein MD, Sullivan JM. Prospective correlative study of ventricular aneurysm. mechanistic concept and clinical recongnition. Am J Med, 1967, 42(4): 512-531
3 Savoye C, Equine O, Tricot O, et al. Left ventricular remodeling after anterior wall acute myocardial infarction in modern clinical practice (from the REmodelage VEntriculaire [REVE] study group). Am J Cardiol. 2006, 98(9):1144~1149
4 Moustakidis P, Maniar HS, Cupps BP,et al. Altered left ventricular geometry changes the border zone temporal distribution of stress in an experimental model of left ventricular aneurysm: a finite element model study. Circulation,2002,106(12 Suppl 1):1168~1175
5 Sakuma T, Okada T, Hayashi Y, et al. Optimal time for predicting left ventricular remodeling after successful primary coronary angioplasty in acute myocardial infarction using serial myocardial contrast echocardiography and magnetic resonance imaging. Circulation J, 2002, 66 (7): 685~690
6陈在嘉,徐义枢,孔华宇主编.临床冠心病学[M].北京:人民军医出版社,1994,508-511
7陈在嘉,高润霖.冠心病{M}第1版北京人民卫生出版社,2002,1048-1058
8 Dubnow MH, Burchell HB, Titus JL. Post infarction ventricular aneurysm: clinicomorphologic and echocardiographic study of 80 case. Am Heart J,1995,70:753~760
9 Hillock RJ, Frampton CM, Yandle TG, et al. B-type natriuretic peptide infusions in acute myocardial infarction. Heart, 2008, 94(5): 617~622
10 Hirayama A, Kusuoka H, Yamamoto H, et al. Usefulness of plasma brain natriuretic peptide concentration for predicting subsequent leftventricular remodeling after coronary angioplasty in patients with acute myocardial infarction, Am J Cardiol, 2006, 98(4): 453~457
11 The TIMI Study Group. The thrombolysis in myocardial infarction(TIMI) trail: phase I findings. N Engl J Med, 1985, 312(14): 932~936
12 Faxon DP, Ryan TJ, Davis KB, et al. Prognostic significance of angiographically documented left ventricular aneurysm: The Coronary Artery Surgery Study(CASS). Am J Cardiol, 1982, 50(1): 157~164
13 Meizlish JL, Berger MJ, Plankey M, et al. Functional left ventricular aneurysm formation after acute anterior transmural myocardial infarction: Incidence, natural history and prognostic implications. N Engl J Med, 1984, 311(16): 1001~1006
14 Cortina A, Amborose JA, Prieto-Granada FJ, et al. Left ventricular function after myocardial infarction, Clinical and angiographic correlation. J Am Coll Cardiol, 1985, 5(3): 619~624
15 Ogeser M, Jacob K. B-type natriuretic peptide (BNP) validation of an immediate response assay. Clin Lab, 2001, 47(1-2): 29~33
16 Sheihan I, Fragasso G, Lu G, et al. Influence of treatment delay on long-left ventricular function in the patients with acute myocardial infarction successfully treated with primary angioplasty. Am Heart J, 2001, 141(4): 603~609
17 Sutton MG, Sharpe N. Left ventricular remodeling after myocardial infarction pathophysiology and therapy. Circulation, 2000; 101(25): 2981~ 2988
18 Moustakidis P, Maniar HS, Cupps BP, et al. Altered left ventricular geometry changes the border zone temporal distribution of stress in an experimental model of left ventricular aneurysm: a finite element model study. Circulation, 2002, 106(12 Suppl 1): 1168~1175
19 Baltabaeva A, Marciniak M, Bijnens B, et al. Regional left ventricular deformation and geometry analysis provides insights in myocardial remodelling in mild to moderate hypertension. Eur J Echocardiogr. 2008;9(4):501-508
20 de Marchi SF, Oswald P, Windecker SReciprocal relationship between left ventricular filling pressure and the recruitable human coronary collateral circulation. Eur Heart J. 2005;26(6):558-566
21 Colonna P, Cadeddu C, Montisci R, et al. Reduced microvascular and myocardial damage in patients with acute myocardial infarction and preinfarction angina. Am Heart J. 2002 Nov;144(5):796-803
22 Hirai T, Fujita M, Nakajima H, et al. Determinants of left ventricular aneurysm formation after acute anterior myocardial infarction A clinical and angiographic study. Circulation, 1999, 99: 791~796
23 Tatli E, Surucu H, Oztekin E, et al. Effects of coronary collateral vessels in left ventricular segmental motions and myocardial viability using color kinesis dobutamine stress echocardiography. Saudi Med J. 2006 Oct;27(10):1468~1472
24 Sakuma T, Okada T, Hayashi Y, et al. Optimal time for predicting left ventricular remodeling after successful primary coronary angioplasty in acute myocardial infarction using serial myocardial contrast echocardiography and magnetic resonance imaging. Circulation J, 2002, 66 (7): 685~690
25 Tikiz H , Balbay Y, Atak R , et al . The effect of t hrombolytic therapy on left vent ricular aneurysm formation in acute myocardial infarction : relationship to successful reperfusion and vessel patency. Clin Cardiol , 2001, 24 (10):656-662
26 Tikiz H, Atak R, Balbay Y. Left ventricular aneurysm formation after anterior myocardial infarction: clinical and angiographic determinants in 809 patients. Int J Cardiol. 2002 ;82(1):7-14
27 Brzezińska B, Loboz-GrudzieńK, Sokalski L. Patterns of post-MI left ventricular volume changes - clinical implications. Kardiol Pol, 2007, 65(10): 1190~1198
28 Korosoglou G, Haars A, Humpert P, et al. Evaluation of myocardial perfusion and deformation in patients with acute myocardial infarction treated with primary angioplasty and stent placement. Coronary ArteryDisease, 2008, 19(7), 497~506
29 O'Brien RJ, Squire IB, Demme B, et al. Pre-discharge, but not admission, levels of NT-proBNP predict adverse prognosis following acute LVF. Eur J Heart Fail, 2003; 5(4): 499~506
30 Morita E, Yasue H, Yoshimura M, et al. Increased plasma levels of brain natriuretic peptide in patients with myocardial infarction. Circulation , 1993,88:82~90
31 Mair J, Artner-Sworzak E, Lchleitner P, et al. Early diagnosis of actue myocardial infarction by a newly developed rapid immunoturbidimetric assay for myoglobin. Br Heart J, 1992, 68:462~468
32 Parodi G, Memisha G, Carrabba N, et al. Prevalence, predictors, time course, and long-term clinical implications of left ventricular functional recovery after mechanical reperfusion for acute myocardial infarction. Am J Cardiol, 2007, 100(12):1718~1722
1 Udelson J, Patten RD, Konstam MA. New concepts in post-infarction ventricular remodeling. Rev Cardiovasc Med, 2003, 4 (Suppl 3): S3~12
2 Moustakidis P, Maniar HS, Cupps BP, et al. Altered left ventricular geometry changes the border zone temporal distribution of stress in an experimental model of left ventricular aneurysm: a finite element model study. Circulation, 2002, 106(12 Suppl 1): 1168~1175
3 Sakuma T, Okada T, Hayashi Y, et al. Optimal time for predicting left ventricular remodeling after successful primary coronary angioplasty in acute myocardial infarction using serial myocardial contrast echocardiography and magnetic resonance imaging. Circulation J, 2002, 66 (7): 685~690
4 Brzezińska B, Loboz-GrudzieńK, Sokalski L. Patterns of post-MI left ventricular volume changes - clinical implications. Kardiol Pol, 2007,65(10): 1190~1198
5 Korosoglou G, Haars A, Humpert P, et al. Evaluation of myocardial perfusion and deformation in patients with acute myocardial infarction treated with primary angioplasty and stent placement. Coronary Artery Disease, 2008, 19(7), 497~506
6 O'Brien RJ, Squire IB, Demme B, et al. Pre-discharge, but not admission, levels of NT-proBNP predict adverse prognosis following acute LVF. Eur J Heart Fail, 2003; 5(4): 499~506
7 Inoue T, Sakuma M, Yaguchi I, et al. Early recanalization and plasma brain natriuretic peptide as an indicator of left ventricular function after acute myocardial infarction. Am Heart J, 2002, 143(5): 790~796
8 The TIMI Study Group. The thrombolysis in myocardial infarction(TIMI) trail: phase I findings. N Engl J Med, 1985, 312(14): 932~936
9 Faxon DP, Ryan TJ, Davis KB, et al. Prognostic significance of angiographically documented left ventricular aneurysm: The Coronary Artery Surgery Study(CASS). Am J Cardiol, 1982, 50(1): 157~164
10 Meizlish JL, Berger MJ, Plankey M, et al. Functional left ventricular aneurysm formation after acute anterior transmural myocardial infarction: Incidence, natural history and prognostic implications. N Engl J Med, 1984, 311(16):1001~1006
11 Cortina A, Amborose JA, Prieto-Granada FJ, et al. Left ventricular function after myocardial infarction, Clinical and angiographic correlation. J Am Coll Cardiol, 1985, 5(3): 619~624
12 Sutton MG, Sharpe N. Left ventricular remodeling after myocardial infarction pathophysiology and therapy. Circulation, 2000; 101(25): 2981~ 2988
13 Mazzadi AN, André-Fou?t X, Costes N, et al. Mechanisms leading to reversible mechanical dysfunction in severe CAD: alternatives to myocardial stunning. Am J Physiol Heart Circ Physiol, 2006 , 291(6): 2570~2582
14 Parodi G, Memisha G, Carrabba N, et al. Prevalence, predictors, timecourse, and long-term clinical implications of left ventricular functional recovery after mechanical reperfusion for acute myocardial infarction. Am J Cardiol, 2007, 100(12):1718~1722
15 Bisi G, Sciagra R, Santoro GM, et al. Rest technetium-99m Sestamibi tomography in combination with short-term administration of nitrates: Feasibility and reliability for prediction of post-revascularization outcome of asynergic territories. J Am Coll Cardiol, 1994, 24(5): 1282~1289
16 Sciagra R, Bolognese L, Roval D, et al. Detecting myocardial salvage after primary PTCA: early myocardial contrast echocardiography versus delayed sestamibi perfusion imaging. J Nucl Med, 1999, 40(3): 363~370
17 Ohtaki Y, Chikamori T, Igarashi Y, et al. Differential effects comparing exercise and pharmacologic stress on left ventricular function using gated Tc-99m sestamibi SPECT. Ann Nucl Med, 2008, 22(3): 185~190
18 Sciagra R, Parodi G, Sotgia B, et al. Determinants of final infarct size and incidence of aborted infarction in patients treated with primary coronary intervention and adjunctive abciximab therapy. Nuklearmedizin, 2008; 47(1): 56~61
19 Moustakidis P, Maniar HS, Cupps BP, et al. Altered left ventricular geometry changes the border zone temporal distribution of stress in an experimental model of left ventricular aneurysm: a finite element model study. Circulation, 2002, 106(12 Suppl 1):1168~1175
20 Hillock RJ, Frampton CM, Yandle TG, et al. B-type natriuretic peptide infusions in acute myocardial infarction. Heart, 2008, 94(5): 617~622
21 Hirayama A, Kusuoka H, Yamamoto H, et al. Usefulness of plasma brain natriuretic peptide concentration for predicting subsequent left ventricular remodeling after coronary angioplasty in patients with acute myocardial infarction, Am J Cardiol, 2006, 98(4): 453~457
22 Tani S, Nagao K, Watanabe I, et al. Increasingly well-preserved left ventricular function in hospital survivors with acute myocardial infarction: effect of early and complete reperfusion strategy on left ventricular remodeling. Circ J, 2007, 71(2):180~185
23 Sakuma T, Okada T, Hayashi Y, et al. Optimal time for predicting left ventricular remodeling after successful primary coronary angioplasty in acute myocardial infarction using serial myocardial contrast echocardiography and magnetic resonance imaging. Circulation, 2002, 66(7): 685~690
24 Araszkiewicz A, Lesiak M, Grajek S, et al. Relationship between tissue reperfusion and postinfarction left ventricular remodelling in patients with anterior wall myocardial infarction treated with primary coronary angioplasty. Kardiol Pol, 2006, 64(4):383~388
25 Sheihan I, Fragasso G, Lu G, et al. Influence of treatment delay on long-left ventricular function in the patients with acute myocardial infarction successfully treated with primary angioplasty. Am Heart J, 2001, 141(4): 603~609
1 Mattichak SJ, Harjai KJ, Dutcher JR,et al. Left ventricular remodeling and systolic deterioration in acute myocardial infarction: findings from the Stent-PAMI Study. J Interv Cardiol. 2005; 18(4): 255~260
2 Brodie BR, Stuckey TD, Muncy DB, et al. Importance of time-to-reperfusion in patients with acute myocardial infarction with and without cardiogenic shock treated with primary percutaneous coronary intervention. Am Heart J. 2003;145(4):708~715
3 Morishima I, Sone T, Okumura K, et al. Angiographic noreflow phenomenon as a predictor of adverse longterm outcome in patients treated with percutaneous transluminal coronary angioplasty for first acute myocardial infarction. J Am Coll Cardiol , 2000, 36(4): 1202 ~1209
4 Savoye C, Equine O, Tricot O, et al. Left ventricular remodeling after anterior wall acute myocardial infarction in modern clinical practice (from the REmodelage VEntriculaire [REVE] study group). Am J Cardiol, 2006,98(9):1144~1149
5 Korosoglou G, Haars A, Humpert P, et al. Evaluation of myocardial perfusion and deformation in patients with acute myocardial infarction treated with primary angioplasty and stent placement. Coronary Artery Disease, 2008, 19(7), 497~506
6 D'Souza SP, Yellon DM, Martin CM, et al. B-type natriuretic peptide limits infarct size in rat isolated hearts via KATP channel opening. Am J Physiol Heart Circ Physiol, 2003, 284(5): H1592~1600
7 Suzuki S, Yoshimura M, Nakayama M, et al. Plasma level of B-type natriuretic peptide as a prognostic marker after acute myocardial infarction:a long-term follow-up analysis.Circulation. 2004; 110(11): 1387~1391
8 Morita E, Yasue H, Yoshimura M, et al. Increased plasma levels of brain natriuretic peptide in patients with myocardial infarction. Circulation , 1993, 88(1): 82~91
9 Colucci WS, Elkayam U, Horton DP, et al, for the Nesiritide Study Group. Intravenous nesiritide, a natriuretic peptide, in thetreatment of decompensated congestive heart failure. N Engl J Med 2000; 343: 246-253
10 Elkayam U, Akhter MW, Singh H, et al. Comparison of effects on left ventricular filling pressure of intravenous nesiritide and high-dose nitroglycerin in patients with decompensated heart failure. Am J Cardiol 2004; 93: 237-240
11李世强,傅向华,刘君,等.静脉注射重组人脑利钠肽对急性心肌梗死伴心功能不全患者的急性血流动力学效应的研究.中华心血管病杂志,2006,34(1):23~27
12 Suzuki T, YamazakiT, Yazaki Y. The role of the natriuretic peptide in the cardiovascular system. Cardiovasc Res, 2001, 51(3): 489 ~ 494
13 The TIMI Study Group. The thrombolysis in myocardial infarction(TIMI) trail: phase I findings. N Engl J Med, 1985, 312(14): 932~936
14 Hunt SA, Baker OW, Chin MH, et al. ACC-AHA Guidelines for evaluation and management of ch ronic heart failure in the adult: executive summary. Circulation, 2001, 104 (24) : 2996~3007
15 Faxon DP, Ryan TJ, Davis KB, et al. Prognostic significance of angiographically documented left ventricular aneurysm: The Coronary Artery Surgery Study(CASS). Am J Cardiol, 1982, 50(1): 157~164
16 Meizlish JL, Berger MJ, Plankey M, et al. Functional left ventricular aneurysm formation after acute anterior transmural myocardial infarction: Incidence, natural history and prognostic implications. N Engl J Med, 1984, 311(16):1001~1006
17 Devereux RB, Lutas EM, Casale PN, et al. Standardization of M-mode echocardiographic left ventricular anatomic measurements. J Am Coll Cardiol. 1984; 4(6):1222~1230
18 Milo-Cotter O, Cotter G, Kaluski E, et al. Rapid Clinical Assessment of Patients with Acute Heart Failure: First Blood Pressure and Oxygen Saturation - Is That All We Need? Cardiology. 2009 Apr 17;114(1):75-82.
19 Robert Feil, Suzanne M Lohmann, Hugo de Jonge, et al. Cyclic GMP-dependent protein kinases and the cardiovascular system: insights from genetically modified mice. Circulation Research, 2003, 93(10): 907~916
20 D'Souza SP, Yellon DM, Martin C, et al. B-type natriuretic peptide limits infarct size in rat isolated hearts via KATP channel opening. Am J Physiol Heart Circ Physiol. 2003; 284(5): H1592~H1600
21 Michaels AD, Klein A, Madden JA, et al. Effects of intravenous nesiritide on human coronary vasomotor regulation and myocardial oxygen uptake. Circulation, 2003, 107(21): 2697~2701
22 Okumura K, Yasue H, Fujii H, et al. Effects of brain (B-type) natriuretic peptide on coronary artery diameter and coronary hemodynamic variables in human:comparison with effects on systemic hemodynamic variables. J Am Coll Cardiol, 1995, 25(2): 342~348
23 Sudoh T, Kangawa K, Minamino N,et al. A new natriuretic peptide in porcine brain. Nature. 1988; 332 (6159):78~81
24 Kapoun AM, Liang F, O'Young G, et al. B-type natriuretic peptide exerts broad functional opposition to transforming growth factor-beta in primary human cardiac fibroblasts: fibrosis, myofibroblast conversion, proliferation, and inflammation. Circ Res. 2004; 94(4): 453~461
25陶则伟,黄元伟.联合应用血管紧张素转换酶抑制剂与血管紧张素Ⅱ1型受体阻滞剂对心力衰竭的作用,临床心血管病杂志, 2003, 19(2) : 186 ~ 188
26 Ito H, Maruyama A, Iwakura K, et al. Clinical implications of the noreflow phenomenon: a predicator of complication and left ventricular remodeling in reperfused anterior wall myocardial infarction. Circulation, 1996, 93(2); 223~228
27 Wu KC, Zerhouni EA, Judd RM, et al. prognostic significance ofmicrovascular obstruction by magnetic resonance imaging in patients with acute myocardial infarction. Circulation, 1998, 97(8): 765~772
28 Bisi G, Sciagra R, Santoro GM, et al. Rest technetium-99m Sestamibi tomography in combination with short-term administration of nitrates: Feasibility and reliability for prediction of post-revascularization outcome of asynergic territories. J Am Coll Cardiol, 1994, 24(5): 1282~1286
29 Sciagra R, Bolognese L, Roval D, et al. Detecting myocardial salvage after primary PTCA: early myocardial contrast echocardiography versus delayed sestamibi perfusion imaging. J Nucl Med, 1999, 40(3): 363~370
30 Ohtaki Y, Chikamori T, Igarashi Y, et al. Differential effects comparing exercise and pharmacologic stress on left ventricular function using gated Tc~99m sestamibi SPECT. Ann Nucl Med, 2008, 22(3): 185~190
31 Sciagra R, Parodi G, Sotgia B, et al. Determinants of final infarct size and incidence of aborted infarction in patients treated with primary coronary intervention and adjunctive abciximab therapy. Nuklearmedizin, 2008; 47(5): 56~61
32 Schiller NB, Shah PM, Crawford M, et al. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. J Am Soc Echocardiogr, 1989, 2(6): 358 ~ 367
33 de Lemos JA, Morrow DA. Brain natriuretic peptide measurement in acute coronary syndromes :Ready for clinical application. Circulation, 2002, 106(23): 2868~2870
34 Arakawa N, Nakamura M, Aoki H, et al. Relationship between plasma level of brain natriuretic peptide and myocardial infarct size. Cardiology, 1994, 85(5): 334~340
35 Omland T, Persson A, Ng L, et al. N-terminal pro-B-type natriuretic peptide and longterm mortality in acute coronary syndromes. Circulation, 2002, 106(23): 2913~2918
36 Troughton RW, Frampton CM, Yandle TG, et al. Treatment of heart failure guided by plasma aminoterminal brain natriuretic peptide(N-BNP) concentrations. The Lancet, 2000, 355(9210): 1126-1130
1 Pfeffer MA, Braunwald E. Ventricular remodeling after myocardial infarction: experimental observations and clinical implications. Circulation. 1990;81(4): 1161~1172
2 Rouleau JL, de Champlain J, Klein M, et al. Activation of neurohumoral systems in postinfarction left ventricular dysfunction. J Am Coll Cardiol. 1993, 22(2): 390~398
3 Savoye C, Equine O, Tricot O, et al. Left ventricular remodeling after anterior wall acute myocardial infarction in modern clinical practice (from the REmodelage VEntriculaire [REVE] study group). Am J Cardiol. 2006, 98(9):1144~1149
4 Moustakidis P, Maniar HS, Cupps BP,et al. Altered left ventricular geometry changes the border zone temporal distribution of stress in an experimental model of left ventricular aneurysm: a finite element model study. Circulation,2002,106(12 Suppl 1):1168~1175
5 Sakuma T, Okada T, Hayashi Y, et al. Optimal time for predicting left ventricular remodeling after successful primary coronary angioplasty in acute myocardial infarction using serial myocardial contrast echocardiography and magnetic resonance imaging. Circulation J, 2002, 66 (7): 685~690
6 Van Gilst WH, Kingma H, Peels KH, et al. Which patient benefits from early angiotensin-converting enzyme inhibition after myocardial infarction? Results of one-year serial-echocardiographic follow-up form the captopril and thrombolysis study(CATS). J Am Coll Cardiol, 1996, 28(1):114~121
7 Sanchis J, Bodi V, Insa L, et al. Predictors of early and late ventricular remodeling after acute myocardial infarction. Clin Cardiol. 1999; 22(9): 581~586
8 Kim ChB, Braunwald E. Potential benefits of late reperfusion of infracted myocardium. The open artery hypothesis. Circulation, 1993, 88(5 Pt 1): 2426~2436
9 Gandron P, Eillles Ch, Kugler I, et al. Progressive left ventricular dysfunction and remodeling after myocardial infarction. Potential mechanisms and early predictors. Circulation,1993, 87(3): 755~763
10 Nijland F, Kamp O, Verheugt FWA, et al. Long-term implications of reocclusion on left ventricular size and function after successful thrombolysis for first anterior myocardial infarction. Circulation, 1997, 95(1): 111~117
11 Shelban I, Fragasso G, Lu C, et al. Influence of treatment delay on long-left ventricular function in patients with acute myocardial infarction successfully treated with primary angioplasty. Am Heart J 2001, 141(4): 603 ~609
12 Roks AJ, van G PP, Pinto YM, et al. A ngiotensin-(1-7) is a modulator of the human rennin - angiotensin system. Hypertension, 1999, 34(2): 296~301
13 Zhu Z, hong J, Zhu s, et al. Angiotensin (1-7) inhibits angiotensionⅡ-indced signal transduction. J Cardiovasc Pharmacol, 2002, 40(5): 693~700
14 Zhong J, Zhu ZM, Yang YJ. Sheng Li Xue Bao,Inhibition of PKC and ERK1/2 in cultured rat vascular smooth muscle cells by angiotensin-(1-7), 2001, 53( 5): 361 ~363
15 Richards AM, N icholls MG, Yandle TG, et al. Neuroendocrine prediction of left ventricular function and heart failure after acute myocardial infarction. The Christchurch Cardioendocrine Research Group. Heart, 1999, 81(2): 114 ~120
16 PeterGaudronMD, InglerMD, Kai Hu MD, et al. Time course of cardiac structural function and electrical changes in asymptomatic patients after myocardial infarction: Their inter-relation and prognostic impact. Journal of the Am Coll of Cardiology, 2001, 38(1): 33~40
17 Elsasser A, Suzuki K, Schaper J. Unresolved issues regarding the role of apoptosis in the pathogenesis of ischemic injury and heart failure. JM ol Cell Cardiol, 2002, 32(5): 711~724
18 Ikeda S, Hamada M, Q u P, et al. Relationship between cardiomyocyte cell death and cardiac function during hypertensive cardiac remodeling in D ah1 rats [ J ]. C lin Sci, 2002, 102 (3) : 329~335
19 Abbate A, B iondi - Zoccai GG, B ussani R, et al. Increased myocardial apoptosis in patients with unfavorable left ventricular remodeling and early symptomatic post - infarction heart failure. J M Coll Cardiol,2003, 41 (5) : 753~760
20 Misao J, Hayakaw a Y, O hno M,et al. Expression of bcl-2 protein, an inhibitor of apoptosis, and Bax, an accelerator of apoptosis, in ventricular myocytes of human hearts with myocardial infarction. Circulation, 1996, 94 ( 7) : 1506~ 1512
21 Maisel A, Cesario D, Baird S, et al. Experimental autoimmune myocarditis produced by adoptive transfer of splenocytes after myocardial infarction. Circ Res,1998, 82(4): 458–463
22陶荣,廖玉华,程翔等.过继转输急性心肌梗死大鼠脾细胞介导心肌损伤.中国免疫学杂志, 2003, 19(9): 642~644
23 Pang H, L iao Y H. Effect of anti - cardiac myosin antibody on prognosis of patients with acute myocardial infarction. J Tong ji Med Univ, 2000, 20(1): 46~48
24 Uehare K, Nakaya M, Ozaki Y, et al. High-sensitivity C–reactive protein and left ventricular remodeling in patients with acute myocardial infarction. Heart Vessels, 2003, 18(2): 67~74
25 Takahashi T, Anzai Y, Yoshikaw a T, et al. Serum C - reactive protein elevation in left ventricular remodeling after acute myocardial infarction- role of neurohormones and cytokines. Int J Cardiol, 2003, 88(2): 257~265
26 Maedaw a Y, Anzai T, Yoshikawa T, et al. Prognostic T, et al. Prognostic significance of peripheral monocytosis after reperfused acute myocardial infarction: a possible role for left ventricular remodeling. J Am Coll Cardiol, 2002, 39(2): 241~246
27 Hojo Y, Ikeda U, Ueno S, et al. Expression of matrix metalloproteinases in patients with acute myocardial infarction. Jpn Circ J, 2001,65(2): 71~75
28 Askari AT, B rennan ML, Zhou X, et al. Myeloperoxidose and plasm inogen activator inhibitor 1 play a central role in ventricular remodeling after myocardial infarction. J Exp M ed, 2003, 197 (5) : 615~ 624
29 Colucci WS. Molecular and cellular mechanics of myocardial failuer. Am J Cardiol, 1997, 80 (Supp l): 15L~25L
30 Remodino A, Rosenblatt V elin N, M ontessuit C, Tardy I, et al. Altered expression of proteins of metabolic regulation during remodeling of the left ventricle after myocardial infarction. J M bl Cell Caediol, 2000, 32 (11) : 025~034
31胡琴,吴强,耿昭华等.心肌梗死后大鼠心肌脂肪酸基因表达下调.中国动脉硬化杂志, 2003, 11(2): 143 ~ 146
32 Desvergne B,W ahliW. Peroxisome proliferators-activated receptors: nuclear control of metabolism. Endocr Rev, 1999, 20 (1) : 649~688
33 Morrow DA , de Lemos JA , Sabatine MS , et al . Evaluation of B-type natriuretic peptide for risk assessment in unstable angina/ non-ST elevation myocardial infarction : B-type natriuretic peptide and prognosis in TACTICS TIMI 18 . J Am Coll Cardiol, 2003, 41(8): 1264~1272
34 Kohno M, Horio T, Yokokawak, et al. Brain natriuretic peptide as a cardiac hormone in essential hypertention. Am J Med, 1992, 92(1): 29~34
35 Omland T, Persson A, NgL, et al. N-terminal pro-B-type natriuretic peptide and long-term mortality in acute coronary syndromes. Circulation , 2002 , 106(23): 2913~2918
36 Nagaya N, Toshikimi T, Goto Y, et al. Plasma brain natriuretic peptide is a biochemical marker for the prediction of progressive ventricular remodeling after acute myocardial infarction. Am Heart J, 1998, 135(1): 21~28
37 Charron F, Paradis P, Bronchain O, et al. Cooperative interaction between GATA-4 and GATA-6 regulates myocardial gene expression. Mol Cell Biol. 1999; 19(6): 4355~4365
38 Richards AM, Nicholls MG, Yandle TG, et al . Neuroendocrine prediction of left ventricular function and heart failure after acute myocardialinfarction. The Christchurch Cardio endocrine Research Group. Heart , 1999, 81(2): 114~120
39 Talwar S ,Squire IB ,Downie PF ,et al. Plasma N terminal pro-brain natriuretic peptide and cardiotrophin 1 are raised in unstable angina. Heart, 2000, 84(4): 421~424
40 Stein BC, Levin RI. Natriuretic peptides: physiology, therapeutic potential , and risk stratification in ischemic heart disease. Am Heart J, 1998, 135(5 Pt 1): 914~923
41 Abdulla J, Barlera S, Latini R, et al. A systematic review: effect of angiotensin converting enzyme inhibition on left ventricular volumes and ejection fraction in patients with a myocardial infarction and in patients with left ventricular dysfunction. Eur J Heart Fail. 2007; 9(2): 129~135
42 Nguyen Q, Colombo F, Clement R, et al. AT I receptor antagonist therapy preferentially ameliorated ventricular function and phenotype during the early phase of remodeling post-MI. Br J Pharmacol, 2003, 138(8): 1485~1494
43 Onodera H, Matsunaga T, Tamura Y, et al. Enalapril suppresses ventricular remodeling more effectively than losartan in patients with acute myocardial infarction.Am Heart J. 2005 Oct; 150(4): 689~691
44 Solomon SD, Skali H, Anavekar NS,et al. Changes in ventricular size and function in patients treated with valsartan, captopril, or both after myocardial infarction. Circulation, 2005, Jun; 111(25)3411~3419
45 Ricci R,Coletta C,Ceci V, et al. Effect of early treatment with captopril and metoprolol singly and together on post-infarction left ventricular remodeling. Am Heart J. 2001;142(4):E5
46 Doughty RN,Whalley GA,Walsh HA, et al. Effects of carvedilol on left ventricular remodeling after acute myocardial infarction: the CAPRICORN Echo Substudy. Circulation. 2004; 109(2): 201~206
47 Aros F, Loma-Osorio A, Vila J,et al. Effect of combined beta-blocker and angiotensin-converting enzyme inhibitor treatment on 1-year survival afteracute myocardial infarction: findings of the PRIAMHO-II registry. Rev Esp Cardiol. 2006; 59(4): 313~320
48 Katada J, Meguro T, Saito H,et al.Persistent cardiac aldosterone synthesis in angiotensin II type 1A receptor-knockout mice after myocardial infarction. Circulation. 2005; 111(17): 2157~2164
49 Ramires FJ, Salemi VM, Ianni BM, et al.Aldosterone antagonism in an inflammatory state: evidence for myocardial protection.J Renin Angiotensin Aldosterone Syst. 2006; 7(3): 162~167
50 Pitt B, RemmeWL, Zannad F, et al. Ep lerenone, a selective aldosterone blocker in patients with left ventricular dysfunction after myocardial infarction. N Engl J Med, 2003, 348(14):1309~1321
51 Hong YJ, Jeong MH, Hwang SH,et al. Effect of combination therapy with simvastatin and carvedilol in patients with left ventricular dysfunction complicated with acute myocardial infarction who underwent percutaneous coronary intervention.Circ J. 2006; 70(10): 1269~1274
52 Feil R, Lohmann SM, de Jonge H, et al . Cyclic GMP-dependent protein kinases and the cardiovascular system: insights from genetically modified mice. Circulation Research, 2003, 93(10): 907~916
53 Hillock RJ, Frampton CM, Yandle TG, et al. B-type natriuretic peptide infusions in acute myocardial infarction. Heart, 2008, 94(5): 617~622
54 Kapoun AM, Liang F, O'Young G, et al. B-type natriuretic peptide exerts broad functional opposition to transforming growth factor-beta in primary human cardiac fibroblasts: fibrosis, myofibroblast conversion, proliferation, and inflammation.Criculation Research, 2004, 94(4): 453~461
55 Murakami M, Takaki A, Nishida M, et al. Chronic stage left ventricular aneurysm and thrombus after myocardial infarction. Blood coagul firionlysis, 2006; 17(6):489-490
56 Link MS, Wang PJ, VanderBrink BA, et al. Selective activation of the KATP channel is mechanism by which sudden death is produced by low energy chest wall impact. Circulation, 1999;100:413-418
57 Tanoue Y, Anodo H. Ventricular energetics in endoventricular circularpatch plasty for dyskinetic anterior left ventricular aneurysm. Am Thorac Surg, 2003; 75:1205-1208
1 Brunner-La Rocca H, KayeDM, Woods RL, et al. Effects of intravenous BNP on regional sympathetic Activity in patients with chronic heart Failure.J Am Coll Cardiol.2001; 37(5): 1221~1227
2 Sudoh T, Kangawa K, Minamino N, et al. A new natriuretic peptide in porcine brain. Nature. 1988; 332(6159):78~81
3 Kambayashi Y, Nakao K, Kimura H, et al. Biological characterization of human brain natriuretic peptide (BNP) and rat BNP: species-specific actions of BNP. Biochem Biophys Res Commun. 1990;173(2): 599~605
4 M air J , Friedl W, Thomas S, et al. Natriuretic peptides in assessment of left ventricular dysfunction. Scand J Clin Lab Invest, 1999, 59 ( supple 230) :132~142
5 ValliN, Gobinet A, Bo rdenave L. Review of 10 years of the clinical use of brain natriuretic peptide in cardiology. J Lab Clin Med, 1999, 134 (5): 437~444
6 Cowie MR, Mendez GF. BNP and congestive heart failure. Prog Cardiovasc Dis, 2002, 44(4): 293 ~321
7 de Lemos JA, Morrow DA. Brain natriuretic peptide measurement in acute coronary syndromes: Ready for clinical application. Circulation, 2002, 106(23): 2868~2870
8 Sagnella GA. Measurement and significance of circulating natriuretic peptides in cardiovascular disease. Clin Sci(Lond), 1998, 95(5): 519~529
9 Tamura N, Ogawa Y, Chusho H, et al. Cardiac fibrosis in mice lacking brain natriuretic peptide, Proc Natl Acad Sci USA, 2000, 97(8): 4239 ~4244
10 Stockand JD, Sanson SC. Regulation of filtration rate by glomerular mesangial cells in health and diabetic renal disease. Am J Kidney Dis , 1997, 29(6): 971~981
11 Yoshimura M , Yasue H , Okumura K, et al . Different secretion patterns of atrial natriuretic peptide and brain natriuretic peptide in patients with congestive heart failure. Circulation , 1991, 87(2): 464~469
12 Maisel A, B - type natriuretic peptide in the diagnosis and management of congestive heart failure. Cardiol Clin, 2001, 19(4): 557~571
13 Nagaya N, Toshikimi T, Goto Y, et al. Plasma brain natriuretic peptide is a biochemical marker for the prediction of progressive ventricular remodeling after acute myocardial infarction. Am Heart J, 1998, 135(1): 21~28
14 RichardsA M, NichollsM G, Yamdle T G, et al. Neuroendocrine prediction of left ventricular function and heart failure after acute myocardial infarction ,Heat1 1999, 81(2): 114~120
15 Mega JL, Morrow DA, De Lemos JA, et al. B-type natriuretic peptide at presentation and prognosis in patients with ST-segment elevation myocardial infarction: an ENTIRE-TIMI-23 substudy. J Am Coll cardiol,2004, 44 (2): 335~339
16 de Lemos JA, Morrow DA. Brain natriuretic peptide measurement in acute coronary syndromes: Ready for clinical application. Circulation, 2002, 106(23): 2868~2870
17 Talwar S, Squire IB, Downie PF, et al. Plasma N terminal pro-brain natriuretic peptide and cardiotrophin 1 are raised in unstable angina. Heart, 2000, 84(4): 421~424
18 Arakawa N, Nakamura M, Aoki H,et al. Relationship between plasma level of brain natriuretic peptide and myocardial infarct size. Cardiology , 1994, 85(5): 334~340
19 Mair J, Friedl W, Thomas S, et al. Natriuretic peptides in assessment of left-ventricular dysfunction. Scand J Clin Lab Invest Suppl. 1999; 230(1): 132~142
20 Kelly R, Struthers AD. Are natriuretic peptides clinically useful as markers of heart failure? Ann Clin Biochem, 2001; 38(Pt 2): 94~102
21 De Lemos JA, Morrow DA, Bentley JH, et al. The prognostic value of B-type natriuretic peptide in patients with acute coronary syndromes, N EngL J Med, 2001, 345(14): 1014~1021
22 Tapanainen JM, Lindgren KS, Makikallio TH,et al. Natriuretic peptides as predictors of non - sudden cardiac death after acute myocardial infarction in the beta - blocking era, J Am Coll Cardiol, 2004, 43(5); 757~763
23邵乐文,朝阳,王战坤.床边即时脑利钠肽检测对呼吸困难的诊断价值.中华心血管病杂志, 2004, 32(12): 1123~1125
24 Nagaya N , Go to Y, Yo sh imura M , et al. Increased plasma levels of brain natriuretic peptide levels associated with progressive ventricular remodeling after acute myocardial infarction. Clin Sci, 1999, 96 (2) : 129~136
25张军,黄占东,肖占森.脑钠肽在心力衰竭患者治疗中的浓度变化.北京医学, 2006, 28(6): 378~379
26 Bettencourt P, Ferreira A , Pardal O, et al. Clinical significance of brain natriuretic peptide in patients with post myocardial infarction. Clin Cardio l,2000, 23 (12) : 921~927
27 Nilsson JC, Groenning BA , Nielsen G, et al. Left ventricular remodeling in the first year after acute myocardial pro-brain natriuretic peptide. Am Heart J, 2002, 143(6): 696~702
28 de Lemos JA, Morrow DA. Brain natriuretic peptide measurement in acute coronary syndromes: ready for clinical application. Circulation, 2002, 106 (23) : 2868~2869
29 Nagaya N, Goto Y, Nishikimi T, et al. Sustained elevation of plasma brain natriuretic peptide levels associated with progressive ventricular romodeling after acute myocardial infarction. Clinical Science, 1999, 96(2): 129~136
30 Nakagawa O , Ogawa Y, Itoh H, et al. Rapid transcriptional activation and early mRNA turnover of brain natriuretic peptide in cardiocyte hypertrophy. Evidence for brain natriuretic peptide as an emergency cardiac hormone against ventricular overload. J Clin Invest, 1995, 96(3): 1280~1287
31 Grilley JG, Farrer M. Left ventricular remodeling and brain natriuretic peptide after first myocardial infarction. Heart, 2001, 86(6) : 638~642
32 delemos JA, Marrow DA, Bentley JH, et al. The prognostic value of B~type natriuretic peptide in patients with acute coronary syndrome. N Engl J Med, 2001, 345(14): 1014~1021
33 Morrow DA, delemos JA, Sabatine MS, et al. Evaluation of B-type natriuretic peptide for risk assessment in unstable angina non~ST elevation myocardial infarction: B-type natriuretic peptide and prognosis in TACT ICS2T IM I 18. J Am Coll Cardiol, 2003(8), 41: 1264~1272
34刘梅林,李继敏,胡大一,等.心绞痛患者血浆NproBNP水平的变化及其临床意义.中华心血管病杂志, 2004, 32(6): 497~500
35 Tamura N, Ogawa Y, Chusho H, et al. Cardiac fibrosis in mice lacking brain natriuretic peptide. Proc Natl Acad Sci USA, 2000, 97(8): 4239~4244
36 Bettencourt P, F rioes F,A zevedo A , et al. Prognotic information provided by serial measurements of brain natriuretic peptide in heart failure[J ]. Int J Cardio l, 2004, 93 (1) : 45~48
37刘东,张晓雪,马丽雅,等.高血压病左心室肥厚患者血浆脑钠素水平。高血压杂志, 2004, 5(5): 396~398
38 Ogawa Y, Itoh H, Nakao K. Molecular biology and biochemistry of natriuretic peptide family. Clin ExpPhamacol Physiol, 1995, 22(1): 49~53
39 Wei CM, Heublein DM, Perrella MA, et al . Natriuretic peptide system in human heart failure. Circulation, 1993, 88(3 ) : 1004~1009
40 Lang CC, Choy AM, Struthers AD. Atrial and brain Natriuretic peptides: adual natriuretic peptide system potentially involved in circulatory homeostasis. Clin Sci, 1992, 83 (5): 519~527
41 Omland T,Aakvaag A, Bonarjee VV, et al. Plasma brain natriuretic peptide as an indicator of left ventricular systolic function and long-term survival after acute myocardial infarction.Comparison with plasma atrial natriuretic peptide and N~terminal proatrial natriuretic peptide. Circulation. 1996; 93 (11):1963~1969
42 Paelinck BP,Vrints CJ,Bax JJ,et al.Relation of B-type natriuretic peptide early after acute myocardial infarction to left ventricular diastolic function and extent of myocardial damage determined by magnetic resonance imaging.Am J Cardiol. 2006; 97(8): 1146~1150
43 Mukoyama A ,Nakao K, Hosoda K, et al . Brain natriuretic peptides as a novel cardiac hormone in humans : Evidence for an exquisite kual natriuretic peptide system , atrial natriuretic peptide and brain natriuretic peptide. J Clin Invest , 1991 , 87(4):1402~1412
44 Selvais PL ,Donckier J E , Robert A , et al . Cardiac natriuretic peptides for diagnosis and risk stratification in heart failure : influences of left ventricular dysfunction and coronary artery disease on cardiac hormonal activation. Eur J Clin Investigation, 1998, 28(8): 636~642
45 Lin Jie , Zhang Delin , Li Tingfu. Correlations between plasma concentration of brain natriuretic peptide and cardiac function in patients with heart failure. J Clin Cardiol (China), 2001, 17(10): 454~455
46李静宇,王宇航,杨志新.放免法测定血浆脑钠素水平诊断无症状性心力衰竭.中国卫生检验杂志, 2000, 10 (4): 454~455
47 Nagaya N, Nishikimi T, Goto Y, et al. Sustained elevation if plasma brain natriuretic peptide is a biochemical marker for the prediction of progressive ventricular remodeling after acute myocardial infarction. Am Heart J ,1998 ,135(1): 21~28
48 Nagaya N, Nishikimi T, Uematsu M , et al . Plasma brain natriuretic peptide as a prognostic indicator in patients with primary pulmonary hypertension. Circulation, 2000, 102 ( 8): 865~867
49 Wallen T, Landahl S, Hedner T, et al. Brain natriuretic peptide predicts mortality in the elderly. Heart, 1997, 77 ( 3): 264~267
50 Corti R, Burnett JC, Rouleau JL, et al . Vasopeptidase inhibitors , a new therapeutic concept in cardiovascular disease. Circulation, 2001, 104(15): 1856~1862
51 Tsutamoto T, Matsumoto T, Wada A, et al . Plasma BNP level as a biochemical marker of morbidity and mortality in patients with asymptomatic or minimally symptomatic LVD : comparison with plasma AngⅡand ET-1 . Eur Heart J, 1999, 20(24):1799~1807
52 Bettencourt P. Brain Natriuretic Peptide in the treatment of heart failure. Cardiovase Daug Rev, 2002, 20 (1): 20~37
53 Hobbs RE, Miller LW, Silverman CB, et al . Hemodynamic effects of asingle intravenous injection of synthetic human brain natriureticpeptide in patients with heart failure secondary to ischemic ordialated cardiomyopathy. Am J Cardiol , 1996 , 78(8): 896~901
54 Troughton RW, Frampton CM , Yandle TG, et al . Treatment of heart failure guided by plasma aminoterminal brain natriuretic peptide (N-BNP) concentrations. Lancet, 2000, 355 (9210): 1216~1230
55 Clarkson PBM, Wheeldon NM, MacFadyen RJ, et al . Effects of brain natriuretic peptide on exercise hemodynamics and neurohormones in isolated diastolic heart failure. Circulation, 1996, 93(11): 2037~2042
56 Yanue KH, Yoshimura M. Suppression of hyperventilation induced attracts with infusion of brain natriuretic peptide in patients with variant angina. Am Heart J ,1994 ,128 (6pt 1) : 1098~1101
57 Mega JL,Morrow DA,De Lemos JA,et al.B-type natriuretic peptide at presentation and prognosis in patients with ST-segment elevation myocardial infarction: an ENTIRE-TIMI-23 substudy.J Am Coll Cardiol.2004; 44(2): 335~339
58 Tapanainen JM,Lindgren KS,Makikallio TH,et al.Natriuretic peptides as predictors of non~sudden and sudden cardiac death after acute myocardial infarction in the beta~blocking era.J Am Coll Cardiol. 2004; 43(5): 757~763
59 Okumura K, Yasue H , Fujii H ,et al . Effects of brain (B-type)natriuretic peptide on coronary artery diameter and coronary hemodynamic variables in human :comparison with effects on syetemic hemodynamic variables. A m Coll Cardiol, 1995, 25(2): 342~348
60 Matsumura T, Kugiyama K, Sugiyama S, et al. Neutral endopeptidase
24.11 in neutrophils modulates protectives effects of natriuretic peptides against neutrophils~induced endothelial cytotoxity. J Clin Invest, 1996, 97 (10): 2192~2203
61 Peacock WFⅣ, Emerman CL, young J. Nesiritide in congestive heart failure associated with acute coronary syndromes: a pilot study of safety and efficacy. J Card Fail. 2004; 10(2): 120~125
62李世强,傅向华,刘君,等.静脉注射重组人脑利钠肽对急性心肌梗死伴心功能不全患者的急性血流动力学效应的研究.中华心血管病杂志, 2006, 34(1):23~27
63 Hunt SA, Baker OW, Chin MH, et al. ACC-AHA Guidelines for evaluation and management of chronic heart failure in the adult: executive summary. Circulation, 2001, 104 (24): 2996~3007
64 Go to T, Takase H, To riyama T, et al. Circulating concentrations of cardiac proteins indicate the severity of congestive heart failure. Heart, 2003, 89(11): 1303~1307
2 Gorlin R, Klein MD, Sullivan JM. Prospective correlative study of ventricular aneurysm. mechanistic concept and clinical recongnition. Am J Med, 1967, 42(4): 512-531
3 Savoye C, Equine O, Tricot O, et al. Left ventricular remodeling after anterior wall acute myocardial infarction in modern clinical practice (from the REmodelage VEntriculaire [REVE] study group). Am J Cardiol. 2006, 98(9):1144~1149
4 Moustakidis P, Maniar HS, Cupps BP,et al. Altered left ventricular geometry changes the border zone temporal distribution of stress in an experimental model of left ventricular aneurysm: a finite element model study. Circulation,2002,106(12 Suppl 1):1168~1175
5 Sakuma T, Okada T, Hayashi Y, et al. Optimal time for predicting left ventricular remodeling after successful primary coronary angioplasty in acute myocardial infarction using serial myocardial contrast echocardiography and magnetic resonance imaging. Circulation J, 2002, 66 (7): 685~690
6陈在嘉,徐义枢,孔华宇主编.临床冠心病学[M].北京:人民军医出版社,1994,508-511
7陈在嘉,高润霖.冠心病{M}第1版北京人民卫生出版社,2002,1048-1058
8 Dubnow MH, Burchell HB, Titus JL. Post infarction ventricular aneurysm: clinicomorphologic and echocardiographic study of 80 case. Am Heart J,1995,70:753~760
9 Hillock RJ, Frampton CM, Yandle TG, et al. B-type natriuretic peptide infusions in acute myocardial infarction. Heart, 2008, 94(5): 617~622
10 Hirayama A, Kusuoka H, Yamamoto H, et al. Usefulness of plasma brain natriuretic peptide concentration for predicting subsequent leftventricular remodeling after coronary angioplasty in patients with acute myocardial infarction, Am J Cardiol, 2006, 98(4): 453~457
11 The TIMI Study Group. The thrombolysis in myocardial infarction(TIMI) trail: phase I findings. N Engl J Med, 1985, 312(14): 932~936
12 Faxon DP, Ryan TJ, Davis KB, et al. Prognostic significance of angiographically documented left ventricular aneurysm: The Coronary Artery Surgery Study(CASS). Am J Cardiol, 1982, 50(1): 157~164
13 Meizlish JL, Berger MJ, Plankey M, et al. Functional left ventricular aneurysm formation after acute anterior transmural myocardial infarction: Incidence, natural history and prognostic implications. N Engl J Med, 1984, 311(16): 1001~1006
14 Cortina A, Amborose JA, Prieto-Granada FJ, et al. Left ventricular function after myocardial infarction, Clinical and angiographic correlation. J Am Coll Cardiol, 1985, 5(3): 619~624
15 Ogeser M, Jacob K. B-type natriuretic peptide (BNP) validation of an immediate response assay. Clin Lab, 2001, 47(1-2): 29~33
16 Sheihan I, Fragasso G, Lu G, et al. Influence of treatment delay on long-left ventricular function in the patients with acute myocardial infarction successfully treated with primary angioplasty. Am Heart J, 2001, 141(4): 603~609
17 Sutton MG, Sharpe N. Left ventricular remodeling after myocardial infarction pathophysiology and therapy. Circulation, 2000; 101(25): 2981~ 2988
18 Moustakidis P, Maniar HS, Cupps BP, et al. Altered left ventricular geometry changes the border zone temporal distribution of stress in an experimental model of left ventricular aneurysm: a finite element model study. Circulation, 2002, 106(12 Suppl 1): 1168~1175
19 Baltabaeva A, Marciniak M, Bijnens B, et al. Regional left ventricular deformation and geometry analysis provides insights in myocardial remodelling in mild to moderate hypertension. Eur J Echocardiogr. 2008;9(4):501-508
20 de Marchi SF, Oswald P, Windecker SReciprocal relationship between left ventricular filling pressure and the recruitable human coronary collateral circulation. Eur Heart J. 2005;26(6):558-566
21 Colonna P, Cadeddu C, Montisci R, et al. Reduced microvascular and myocardial damage in patients with acute myocardial infarction and preinfarction angina. Am Heart J. 2002 Nov;144(5):796-803
22 Hirai T, Fujita M, Nakajima H, et al. Determinants of left ventricular aneurysm formation after acute anterior myocardial infarction A clinical and angiographic study. Circulation, 1999, 99: 791~796
23 Tatli E, Surucu H, Oztekin E, et al. Effects of coronary collateral vessels in left ventricular segmental motions and myocardial viability using color kinesis dobutamine stress echocardiography. Saudi Med J. 2006 Oct;27(10):1468~1472
24 Sakuma T, Okada T, Hayashi Y, et al. Optimal time for predicting left ventricular remodeling after successful primary coronary angioplasty in acute myocardial infarction using serial myocardial contrast echocardiography and magnetic resonance imaging. Circulation J, 2002, 66 (7): 685~690
25 Tikiz H , Balbay Y, Atak R , et al . The effect of t hrombolytic therapy on left vent ricular aneurysm formation in acute myocardial infarction : relationship to successful reperfusion and vessel patency. Clin Cardiol , 2001, 24 (10):656-662
26 Tikiz H, Atak R, Balbay Y. Left ventricular aneurysm formation after anterior myocardial infarction: clinical and angiographic determinants in 809 patients. Int J Cardiol. 2002 ;82(1):7-14
27 Brzezińska B, Loboz-GrudzieńK, Sokalski L. Patterns of post-MI left ventricular volume changes - clinical implications. Kardiol Pol, 2007, 65(10): 1190~1198
28 Korosoglou G, Haars A, Humpert P, et al. Evaluation of myocardial perfusion and deformation in patients with acute myocardial infarction treated with primary angioplasty and stent placement. Coronary ArteryDisease, 2008, 19(7), 497~506
29 O'Brien RJ, Squire IB, Demme B, et al. Pre-discharge, but not admission, levels of NT-proBNP predict adverse prognosis following acute LVF. Eur J Heart Fail, 2003; 5(4): 499~506
30 Morita E, Yasue H, Yoshimura M, et al. Increased plasma levels of brain natriuretic peptide in patients with myocardial infarction. Circulation , 1993,88:82~90
31 Mair J, Artner-Sworzak E, Lchleitner P, et al. Early diagnosis of actue myocardial infarction by a newly developed rapid immunoturbidimetric assay for myoglobin. Br Heart J, 1992, 68:462~468
32 Parodi G, Memisha G, Carrabba N, et al. Prevalence, predictors, time course, and long-term clinical implications of left ventricular functional recovery after mechanical reperfusion for acute myocardial infarction. Am J Cardiol, 2007, 100(12):1718~1722
1 Udelson J, Patten RD, Konstam MA. New concepts in post-infarction ventricular remodeling. Rev Cardiovasc Med, 2003, 4 (Suppl 3): S3~12
2 Moustakidis P, Maniar HS, Cupps BP, et al. Altered left ventricular geometry changes the border zone temporal distribution of stress in an experimental model of left ventricular aneurysm: a finite element model study. Circulation, 2002, 106(12 Suppl 1): 1168~1175
3 Sakuma T, Okada T, Hayashi Y, et al. Optimal time for predicting left ventricular remodeling after successful primary coronary angioplasty in acute myocardial infarction using serial myocardial contrast echocardiography and magnetic resonance imaging. Circulation J, 2002, 66 (7): 685~690
4 Brzezińska B, Loboz-GrudzieńK, Sokalski L. Patterns of post-MI left ventricular volume changes - clinical implications. Kardiol Pol, 2007,65(10): 1190~1198
5 Korosoglou G, Haars A, Humpert P, et al. Evaluation of myocardial perfusion and deformation in patients with acute myocardial infarction treated with primary angioplasty and stent placement. Coronary Artery Disease, 2008, 19(7), 497~506
6 O'Brien RJ, Squire IB, Demme B, et al. Pre-discharge, but not admission, levels of NT-proBNP predict adverse prognosis following acute LVF. Eur J Heart Fail, 2003; 5(4): 499~506
7 Inoue T, Sakuma M, Yaguchi I, et al. Early recanalization and plasma brain natriuretic peptide as an indicator of left ventricular function after acute myocardial infarction. Am Heart J, 2002, 143(5): 790~796
8 The TIMI Study Group. The thrombolysis in myocardial infarction(TIMI) trail: phase I findings. N Engl J Med, 1985, 312(14): 932~936
9 Faxon DP, Ryan TJ, Davis KB, et al. Prognostic significance of angiographically documented left ventricular aneurysm: The Coronary Artery Surgery Study(CASS). Am J Cardiol, 1982, 50(1): 157~164
10 Meizlish JL, Berger MJ, Plankey M, et al. Functional left ventricular aneurysm formation after acute anterior transmural myocardial infarction: Incidence, natural history and prognostic implications. N Engl J Med, 1984, 311(16):1001~1006
11 Cortina A, Amborose JA, Prieto-Granada FJ, et al. Left ventricular function after myocardial infarction, Clinical and angiographic correlation. J Am Coll Cardiol, 1985, 5(3): 619~624
12 Sutton MG, Sharpe N. Left ventricular remodeling after myocardial infarction pathophysiology and therapy. Circulation, 2000; 101(25): 2981~ 2988
13 Mazzadi AN, André-Fou?t X, Costes N, et al. Mechanisms leading to reversible mechanical dysfunction in severe CAD: alternatives to myocardial stunning. Am J Physiol Heart Circ Physiol, 2006 , 291(6): 2570~2582
14 Parodi G, Memisha G, Carrabba N, et al. Prevalence, predictors, timecourse, and long-term clinical implications of left ventricular functional recovery after mechanical reperfusion for acute myocardial infarction. Am J Cardiol, 2007, 100(12):1718~1722
15 Bisi G, Sciagra R, Santoro GM, et al. Rest technetium-99m Sestamibi tomography in combination with short-term administration of nitrates: Feasibility and reliability for prediction of post-revascularization outcome of asynergic territories. J Am Coll Cardiol, 1994, 24(5): 1282~1289
16 Sciagra R, Bolognese L, Roval D, et al. Detecting myocardial salvage after primary PTCA: early myocardial contrast echocardiography versus delayed sestamibi perfusion imaging. J Nucl Med, 1999, 40(3): 363~370
17 Ohtaki Y, Chikamori T, Igarashi Y, et al. Differential effects comparing exercise and pharmacologic stress on left ventricular function using gated Tc-99m sestamibi SPECT. Ann Nucl Med, 2008, 22(3): 185~190
18 Sciagra R, Parodi G, Sotgia B, et al. Determinants of final infarct size and incidence of aborted infarction in patients treated with primary coronary intervention and adjunctive abciximab therapy. Nuklearmedizin, 2008; 47(1): 56~61
19 Moustakidis P, Maniar HS, Cupps BP, et al. Altered left ventricular geometry changes the border zone temporal distribution of stress in an experimental model of left ventricular aneurysm: a finite element model study. Circulation, 2002, 106(12 Suppl 1):1168~1175
20 Hillock RJ, Frampton CM, Yandle TG, et al. B-type natriuretic peptide infusions in acute myocardial infarction. Heart, 2008, 94(5): 617~622
21 Hirayama A, Kusuoka H, Yamamoto H, et al. Usefulness of plasma brain natriuretic peptide concentration for predicting subsequent left ventricular remodeling after coronary angioplasty in patients with acute myocardial infarction, Am J Cardiol, 2006, 98(4): 453~457
22 Tani S, Nagao K, Watanabe I, et al. Increasingly well-preserved left ventricular function in hospital survivors with acute myocardial infarction: effect of early and complete reperfusion strategy on left ventricular remodeling. Circ J, 2007, 71(2):180~185
23 Sakuma T, Okada T, Hayashi Y, et al. Optimal time for predicting left ventricular remodeling after successful primary coronary angioplasty in acute myocardial infarction using serial myocardial contrast echocardiography and magnetic resonance imaging. Circulation, 2002, 66(7): 685~690
24 Araszkiewicz A, Lesiak M, Grajek S, et al. Relationship between tissue reperfusion and postinfarction left ventricular remodelling in patients with anterior wall myocardial infarction treated with primary coronary angioplasty. Kardiol Pol, 2006, 64(4):383~388
25 Sheihan I, Fragasso G, Lu G, et al. Influence of treatment delay on long-left ventricular function in the patients with acute myocardial infarction successfully treated with primary angioplasty. Am Heart J, 2001, 141(4): 603~609
1 Mattichak SJ, Harjai KJ, Dutcher JR,et al. Left ventricular remodeling and systolic deterioration in acute myocardial infarction: findings from the Stent-PAMI Study. J Interv Cardiol. 2005; 18(4): 255~260
2 Brodie BR, Stuckey TD, Muncy DB, et al. Importance of time-to-reperfusion in patients with acute myocardial infarction with and without cardiogenic shock treated with primary percutaneous coronary intervention. Am Heart J. 2003;145(4):708~715
3 Morishima I, Sone T, Okumura K, et al. Angiographic noreflow phenomenon as a predictor of adverse longterm outcome in patients treated with percutaneous transluminal coronary angioplasty for first acute myocardial infarction. J Am Coll Cardiol , 2000, 36(4): 1202 ~1209
4 Savoye C, Equine O, Tricot O, et al. Left ventricular remodeling after anterior wall acute myocardial infarction in modern clinical practice (from the REmodelage VEntriculaire [REVE] study group). Am J Cardiol, 2006,98(9):1144~1149
5 Korosoglou G, Haars A, Humpert P, et al. Evaluation of myocardial perfusion and deformation in patients with acute myocardial infarction treated with primary angioplasty and stent placement. Coronary Artery Disease, 2008, 19(7), 497~506
6 D'Souza SP, Yellon DM, Martin CM, et al. B-type natriuretic peptide limits infarct size in rat isolated hearts via KATP channel opening. Am J Physiol Heart Circ Physiol, 2003, 284(5): H1592~1600
7 Suzuki S, Yoshimura M, Nakayama M, et al. Plasma level of B-type natriuretic peptide as a prognostic marker after acute myocardial infarction:a long-term follow-up analysis.Circulation. 2004; 110(11): 1387~1391
8 Morita E, Yasue H, Yoshimura M, et al. Increased plasma levels of brain natriuretic peptide in patients with myocardial infarction. Circulation , 1993, 88(1): 82~91
9 Colucci WS, Elkayam U, Horton DP, et al, for the Nesiritide Study Group. Intravenous nesiritide, a natriuretic peptide, in thetreatment of decompensated congestive heart failure. N Engl J Med 2000; 343: 246-253
10 Elkayam U, Akhter MW, Singh H, et al. Comparison of effects on left ventricular filling pressure of intravenous nesiritide and high-dose nitroglycerin in patients with decompensated heart failure. Am J Cardiol 2004; 93: 237-240
11李世强,傅向华,刘君,等.静脉注射重组人脑利钠肽对急性心肌梗死伴心功能不全患者的急性血流动力学效应的研究.中华心血管病杂志,2006,34(1):23~27
12 Suzuki T, YamazakiT, Yazaki Y. The role of the natriuretic peptide in the cardiovascular system. Cardiovasc Res, 2001, 51(3): 489 ~ 494
13 The TIMI Study Group. The thrombolysis in myocardial infarction(TIMI) trail: phase I findings. N Engl J Med, 1985, 312(14): 932~936
14 Hunt SA, Baker OW, Chin MH, et al. ACC-AHA Guidelines for evaluation and management of ch ronic heart failure in the adult: executive summary. Circulation, 2001, 104 (24) : 2996~3007
15 Faxon DP, Ryan TJ, Davis KB, et al. Prognostic significance of angiographically documented left ventricular aneurysm: The Coronary Artery Surgery Study(CASS). Am J Cardiol, 1982, 50(1): 157~164
16 Meizlish JL, Berger MJ, Plankey M, et al. Functional left ventricular aneurysm formation after acute anterior transmural myocardial infarction: Incidence, natural history and prognostic implications. N Engl J Med, 1984, 311(16):1001~1006
17 Devereux RB, Lutas EM, Casale PN, et al. Standardization of M-mode echocardiographic left ventricular anatomic measurements. J Am Coll Cardiol. 1984; 4(6):1222~1230
18 Milo-Cotter O, Cotter G, Kaluski E, et al. Rapid Clinical Assessment of Patients with Acute Heart Failure: First Blood Pressure and Oxygen Saturation - Is That All We Need? Cardiology. 2009 Apr 17;114(1):75-82.
19 Robert Feil, Suzanne M Lohmann, Hugo de Jonge, et al. Cyclic GMP-dependent protein kinases and the cardiovascular system: insights from genetically modified mice. Circulation Research, 2003, 93(10): 907~916
20 D'Souza SP, Yellon DM, Martin C, et al. B-type natriuretic peptide limits infarct size in rat isolated hearts via KATP channel opening. Am J Physiol Heart Circ Physiol. 2003; 284(5): H1592~H1600
21 Michaels AD, Klein A, Madden JA, et al. Effects of intravenous nesiritide on human coronary vasomotor regulation and myocardial oxygen uptake. Circulation, 2003, 107(21): 2697~2701
22 Okumura K, Yasue H, Fujii H, et al. Effects of brain (B-type) natriuretic peptide on coronary artery diameter and coronary hemodynamic variables in human:comparison with effects on systemic hemodynamic variables. J Am Coll Cardiol, 1995, 25(2): 342~348
23 Sudoh T, Kangawa K, Minamino N,et al. A new natriuretic peptide in porcine brain. Nature. 1988; 332 (6159):78~81
24 Kapoun AM, Liang F, O'Young G, et al. B-type natriuretic peptide exerts broad functional opposition to transforming growth factor-beta in primary human cardiac fibroblasts: fibrosis, myofibroblast conversion, proliferation, and inflammation. Circ Res. 2004; 94(4): 453~461
25陶则伟,黄元伟.联合应用血管紧张素转换酶抑制剂与血管紧张素Ⅱ1型受体阻滞剂对心力衰竭的作用,临床心血管病杂志, 2003, 19(2) : 186 ~ 188
26 Ito H, Maruyama A, Iwakura K, et al. Clinical implications of the noreflow phenomenon: a predicator of complication and left ventricular remodeling in reperfused anterior wall myocardial infarction. Circulation, 1996, 93(2); 223~228
27 Wu KC, Zerhouni EA, Judd RM, et al. prognostic significance ofmicrovascular obstruction by magnetic resonance imaging in patients with acute myocardial infarction. Circulation, 1998, 97(8): 765~772
28 Bisi G, Sciagra R, Santoro GM, et al. Rest technetium-99m Sestamibi tomography in combination with short-term administration of nitrates: Feasibility and reliability for prediction of post-revascularization outcome of asynergic territories. J Am Coll Cardiol, 1994, 24(5): 1282~1286
29 Sciagra R, Bolognese L, Roval D, et al. Detecting myocardial salvage after primary PTCA: early myocardial contrast echocardiography versus delayed sestamibi perfusion imaging. J Nucl Med, 1999, 40(3): 363~370
30 Ohtaki Y, Chikamori T, Igarashi Y, et al. Differential effects comparing exercise and pharmacologic stress on left ventricular function using gated Tc~99m sestamibi SPECT. Ann Nucl Med, 2008, 22(3): 185~190
31 Sciagra R, Parodi G, Sotgia B, et al. Determinants of final infarct size and incidence of aborted infarction in patients treated with primary coronary intervention and adjunctive abciximab therapy. Nuklearmedizin, 2008; 47(5): 56~61
32 Schiller NB, Shah PM, Crawford M, et al. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. J Am Soc Echocardiogr, 1989, 2(6): 358 ~ 367
33 de Lemos JA, Morrow DA. Brain natriuretic peptide measurement in acute coronary syndromes :Ready for clinical application. Circulation, 2002, 106(23): 2868~2870
34 Arakawa N, Nakamura M, Aoki H, et al. Relationship between plasma level of brain natriuretic peptide and myocardial infarct size. Cardiology, 1994, 85(5): 334~340
35 Omland T, Persson A, Ng L, et al. N-terminal pro-B-type natriuretic peptide and longterm mortality in acute coronary syndromes. Circulation, 2002, 106(23): 2913~2918
36 Troughton RW, Frampton CM, Yandle TG, et al. Treatment of heart failure guided by plasma aminoterminal brain natriuretic peptide(N-BNP) concentrations. The Lancet, 2000, 355(9210): 1126-1130
1 Pfeffer MA, Braunwald E. Ventricular remodeling after myocardial infarction: experimental observations and clinical implications. Circulation. 1990;81(4): 1161~1172
2 Rouleau JL, de Champlain J, Klein M, et al. Activation of neurohumoral systems in postinfarction left ventricular dysfunction. J Am Coll Cardiol. 1993, 22(2): 390~398
3 Savoye C, Equine O, Tricot O, et al. Left ventricular remodeling after anterior wall acute myocardial infarction in modern clinical practice (from the REmodelage VEntriculaire [REVE] study group). Am J Cardiol. 2006, 98(9):1144~1149
4 Moustakidis P, Maniar HS, Cupps BP,et al. Altered left ventricular geometry changes the border zone temporal distribution of stress in an experimental model of left ventricular aneurysm: a finite element model study. Circulation,2002,106(12 Suppl 1):1168~1175
5 Sakuma T, Okada T, Hayashi Y, et al. Optimal time for predicting left ventricular remodeling after successful primary coronary angioplasty in acute myocardial infarction using serial myocardial contrast echocardiography and magnetic resonance imaging. Circulation J, 2002, 66 (7): 685~690
6 Van Gilst WH, Kingma H, Peels KH, et al. Which patient benefits from early angiotensin-converting enzyme inhibition after myocardial infarction? Results of one-year serial-echocardiographic follow-up form the captopril and thrombolysis study(CATS). J Am Coll Cardiol, 1996, 28(1):114~121
7 Sanchis J, Bodi V, Insa L, et al. Predictors of early and late ventricular remodeling after acute myocardial infarction. Clin Cardiol. 1999; 22(9): 581~586
8 Kim ChB, Braunwald E. Potential benefits of late reperfusion of infracted myocardium. The open artery hypothesis. Circulation, 1993, 88(5 Pt 1): 2426~2436
9 Gandron P, Eillles Ch, Kugler I, et al. Progressive left ventricular dysfunction and remodeling after myocardial infarction. Potential mechanisms and early predictors. Circulation,1993, 87(3): 755~763
10 Nijland F, Kamp O, Verheugt FWA, et al. Long-term implications of reocclusion on left ventricular size and function after successful thrombolysis for first anterior myocardial infarction. Circulation, 1997, 95(1): 111~117
11 Shelban I, Fragasso G, Lu C, et al. Influence of treatment delay on long-left ventricular function in patients with acute myocardial infarction successfully treated with primary angioplasty. Am Heart J 2001, 141(4): 603 ~609
12 Roks AJ, van G PP, Pinto YM, et al. A ngiotensin-(1-7) is a modulator of the human rennin - angiotensin system. Hypertension, 1999, 34(2): 296~301
13 Zhu Z, hong J, Zhu s, et al. Angiotensin (1-7) inhibits angiotensionⅡ-indced signal transduction. J Cardiovasc Pharmacol, 2002, 40(5): 693~700
14 Zhong J, Zhu ZM, Yang YJ. Sheng Li Xue Bao,Inhibition of PKC and ERK1/2 in cultured rat vascular smooth muscle cells by angiotensin-(1-7), 2001, 53( 5): 361 ~363
15 Richards AM, N icholls MG, Yandle TG, et al. Neuroendocrine prediction of left ventricular function and heart failure after acute myocardial infarction. The Christchurch Cardioendocrine Research Group. Heart, 1999, 81(2): 114 ~120
16 PeterGaudronMD, InglerMD, Kai Hu MD, et al. Time course of cardiac structural function and electrical changes in asymptomatic patients after myocardial infarction: Their inter-relation and prognostic impact. Journal of the Am Coll of Cardiology, 2001, 38(1): 33~40
17 Elsasser A, Suzuki K, Schaper J. Unresolved issues regarding the role of apoptosis in the pathogenesis of ischemic injury and heart failure. JM ol Cell Cardiol, 2002, 32(5): 711~724
18 Ikeda S, Hamada M, Q u P, et al. Relationship between cardiomyocyte cell death and cardiac function during hypertensive cardiac remodeling in D ah1 rats [ J ]. C lin Sci, 2002, 102 (3) : 329~335
19 Abbate A, B iondi - Zoccai GG, B ussani R, et al. Increased myocardial apoptosis in patients with unfavorable left ventricular remodeling and early symptomatic post - infarction heart failure. J M Coll Cardiol,2003, 41 (5) : 753~760
20 Misao J, Hayakaw a Y, O hno M,et al. Expression of bcl-2 protein, an inhibitor of apoptosis, and Bax, an accelerator of apoptosis, in ventricular myocytes of human hearts with myocardial infarction. Circulation, 1996, 94 ( 7) : 1506~ 1512
21 Maisel A, Cesario D, Baird S, et al. Experimental autoimmune myocarditis produced by adoptive transfer of splenocytes after myocardial infarction. Circ Res,1998, 82(4): 458–463
22陶荣,廖玉华,程翔等.过继转输急性心肌梗死大鼠脾细胞介导心肌损伤.中国免疫学杂志, 2003, 19(9): 642~644
23 Pang H, L iao Y H. Effect of anti - cardiac myosin antibody on prognosis of patients with acute myocardial infarction. J Tong ji Med Univ, 2000, 20(1): 46~48
24 Uehare K, Nakaya M, Ozaki Y, et al. High-sensitivity C–reactive protein and left ventricular remodeling in patients with acute myocardial infarction. Heart Vessels, 2003, 18(2): 67~74
25 Takahashi T, Anzai Y, Yoshikaw a T, et al. Serum C - reactive protein elevation in left ventricular remodeling after acute myocardial infarction- role of neurohormones and cytokines. Int J Cardiol, 2003, 88(2): 257~265
26 Maedaw a Y, Anzai T, Yoshikawa T, et al. Prognostic T, et al. Prognostic significance of peripheral monocytosis after reperfused acute myocardial infarction: a possible role for left ventricular remodeling. J Am Coll Cardiol, 2002, 39(2): 241~246
27 Hojo Y, Ikeda U, Ueno S, et al. Expression of matrix metalloproteinases in patients with acute myocardial infarction. Jpn Circ J, 2001,65(2): 71~75
28 Askari AT, B rennan ML, Zhou X, et al. Myeloperoxidose and plasm inogen activator inhibitor 1 play a central role in ventricular remodeling after myocardial infarction. J Exp M ed, 2003, 197 (5) : 615~ 624
29 Colucci WS. Molecular and cellular mechanics of myocardial failuer. Am J Cardiol, 1997, 80 (Supp l): 15L~25L
30 Remodino A, Rosenblatt V elin N, M ontessuit C, Tardy I, et al. Altered expression of proteins of metabolic regulation during remodeling of the left ventricle after myocardial infarction. J M bl Cell Caediol, 2000, 32 (11) : 025~034
31胡琴,吴强,耿昭华等.心肌梗死后大鼠心肌脂肪酸基因表达下调.中国动脉硬化杂志, 2003, 11(2): 143 ~ 146
32 Desvergne B,W ahliW. Peroxisome proliferators-activated receptors: nuclear control of metabolism. Endocr Rev, 1999, 20 (1) : 649~688
33 Morrow DA , de Lemos JA , Sabatine MS , et al . Evaluation of B-type natriuretic peptide for risk assessment in unstable angina/ non-ST elevation myocardial infarction : B-type natriuretic peptide and prognosis in TACTICS TIMI 18 . J Am Coll Cardiol, 2003, 41(8): 1264~1272
34 Kohno M, Horio T, Yokokawak, et al. Brain natriuretic peptide as a cardiac hormone in essential hypertention. Am J Med, 1992, 92(1): 29~34
35 Omland T, Persson A, NgL, et al. N-terminal pro-B-type natriuretic peptide and long-term mortality in acute coronary syndromes. Circulation , 2002 , 106(23): 2913~2918
36 Nagaya N, Toshikimi T, Goto Y, et al. Plasma brain natriuretic peptide is a biochemical marker for the prediction of progressive ventricular remodeling after acute myocardial infarction. Am Heart J, 1998, 135(1): 21~28
37 Charron F, Paradis P, Bronchain O, et al. Cooperative interaction between GATA-4 and GATA-6 regulates myocardial gene expression. Mol Cell Biol. 1999; 19(6): 4355~4365
38 Richards AM, Nicholls MG, Yandle TG, et al . Neuroendocrine prediction of left ventricular function and heart failure after acute myocardialinfarction. The Christchurch Cardio endocrine Research Group. Heart , 1999, 81(2): 114~120
39 Talwar S ,Squire IB ,Downie PF ,et al. Plasma N terminal pro-brain natriuretic peptide and cardiotrophin 1 are raised in unstable angina. Heart, 2000, 84(4): 421~424
40 Stein BC, Levin RI. Natriuretic peptides: physiology, therapeutic potential , and risk stratification in ischemic heart disease. Am Heart J, 1998, 135(5 Pt 1): 914~923
41 Abdulla J, Barlera S, Latini R, et al. A systematic review: effect of angiotensin converting enzyme inhibition on left ventricular volumes and ejection fraction in patients with a myocardial infarction and in patients with left ventricular dysfunction. Eur J Heart Fail. 2007; 9(2): 129~135
42 Nguyen Q, Colombo F, Clement R, et al. AT I receptor antagonist therapy preferentially ameliorated ventricular function and phenotype during the early phase of remodeling post-MI. Br J Pharmacol, 2003, 138(8): 1485~1494
43 Onodera H, Matsunaga T, Tamura Y, et al. Enalapril suppresses ventricular remodeling more effectively than losartan in patients with acute myocardial infarction.Am Heart J. 2005 Oct; 150(4): 689~691
44 Solomon SD, Skali H, Anavekar NS,et al. Changes in ventricular size and function in patients treated with valsartan, captopril, or both after myocardial infarction. Circulation, 2005, Jun; 111(25)3411~3419
45 Ricci R,Coletta C,Ceci V, et al. Effect of early treatment with captopril and metoprolol singly and together on post-infarction left ventricular remodeling. Am Heart J. 2001;142(4):E5
46 Doughty RN,Whalley GA,Walsh HA, et al. Effects of carvedilol on left ventricular remodeling after acute myocardial infarction: the CAPRICORN Echo Substudy. Circulation. 2004; 109(2): 201~206
47 Aros F, Loma-Osorio A, Vila J,et al. Effect of combined beta-blocker and angiotensin-converting enzyme inhibitor treatment on 1-year survival afteracute myocardial infarction: findings of the PRIAMHO-II registry. Rev Esp Cardiol. 2006; 59(4): 313~320
48 Katada J, Meguro T, Saito H,et al.Persistent cardiac aldosterone synthesis in angiotensin II type 1A receptor-knockout mice after myocardial infarction. Circulation. 2005; 111(17): 2157~2164
49 Ramires FJ, Salemi VM, Ianni BM, et al.Aldosterone antagonism in an inflammatory state: evidence for myocardial protection.J Renin Angiotensin Aldosterone Syst. 2006; 7(3): 162~167
50 Pitt B, RemmeWL, Zannad F, et al. Ep lerenone, a selective aldosterone blocker in patients with left ventricular dysfunction after myocardial infarction. N Engl J Med, 2003, 348(14):1309~1321
51 Hong YJ, Jeong MH, Hwang SH,et al. Effect of combination therapy with simvastatin and carvedilol in patients with left ventricular dysfunction complicated with acute myocardial infarction who underwent percutaneous coronary intervention.Circ J. 2006; 70(10): 1269~1274
52 Feil R, Lohmann SM, de Jonge H, et al . Cyclic GMP-dependent protein kinases and the cardiovascular system: insights from genetically modified mice. Circulation Research, 2003, 93(10): 907~916
53 Hillock RJ, Frampton CM, Yandle TG, et al. B-type natriuretic peptide infusions in acute myocardial infarction. Heart, 2008, 94(5): 617~622
54 Kapoun AM, Liang F, O'Young G, et al. B-type natriuretic peptide exerts broad functional opposition to transforming growth factor-beta in primary human cardiac fibroblasts: fibrosis, myofibroblast conversion, proliferation, and inflammation.Criculation Research, 2004, 94(4): 453~461
55 Murakami M, Takaki A, Nishida M, et al. Chronic stage left ventricular aneurysm and thrombus after myocardial infarction. Blood coagul firionlysis, 2006; 17(6):489-490
56 Link MS, Wang PJ, VanderBrink BA, et al. Selective activation of the KATP channel is mechanism by which sudden death is produced by low energy chest wall impact. Circulation, 1999;100:413-418
57 Tanoue Y, Anodo H. Ventricular energetics in endoventricular circularpatch plasty for dyskinetic anterior left ventricular aneurysm. Am Thorac Surg, 2003; 75:1205-1208
1 Brunner-La Rocca H, KayeDM, Woods RL, et al. Effects of intravenous BNP on regional sympathetic Activity in patients with chronic heart Failure.J Am Coll Cardiol.2001; 37(5): 1221~1227
2 Sudoh T, Kangawa K, Minamino N, et al. A new natriuretic peptide in porcine brain. Nature. 1988; 332(6159):78~81
3 Kambayashi Y, Nakao K, Kimura H, et al. Biological characterization of human brain natriuretic peptide (BNP) and rat BNP: species-specific actions of BNP. Biochem Biophys Res Commun. 1990;173(2): 599~605
4 M air J , Friedl W, Thomas S, et al. Natriuretic peptides in assessment of left ventricular dysfunction. Scand J Clin Lab Invest, 1999, 59 ( supple 230) :132~142
5 ValliN, Gobinet A, Bo rdenave L. Review of 10 years of the clinical use of brain natriuretic peptide in cardiology. J Lab Clin Med, 1999, 134 (5): 437~444
6 Cowie MR, Mendez GF. BNP and congestive heart failure. Prog Cardiovasc Dis, 2002, 44(4): 293 ~321
7 de Lemos JA, Morrow DA. Brain natriuretic peptide measurement in acute coronary syndromes: Ready for clinical application. Circulation, 2002, 106(23): 2868~2870
8 Sagnella GA. Measurement and significance of circulating natriuretic peptides in cardiovascular disease. Clin Sci(Lond), 1998, 95(5): 519~529
9 Tamura N, Ogawa Y, Chusho H, et al. Cardiac fibrosis in mice lacking brain natriuretic peptide, Proc Natl Acad Sci USA, 2000, 97(8): 4239 ~4244
10 Stockand JD, Sanson SC. Regulation of filtration rate by glomerular mesangial cells in health and diabetic renal disease. Am J Kidney Dis , 1997, 29(6): 971~981
11 Yoshimura M , Yasue H , Okumura K, et al . Different secretion patterns of atrial natriuretic peptide and brain natriuretic peptide in patients with congestive heart failure. Circulation , 1991, 87(2): 464~469
12 Maisel A, B - type natriuretic peptide in the diagnosis and management of congestive heart failure. Cardiol Clin, 2001, 19(4): 557~571
13 Nagaya N, Toshikimi T, Goto Y, et al. Plasma brain natriuretic peptide is a biochemical marker for the prediction of progressive ventricular remodeling after acute myocardial infarction. Am Heart J, 1998, 135(1): 21~28
14 RichardsA M, NichollsM G, Yamdle T G, et al. Neuroendocrine prediction of left ventricular function and heart failure after acute myocardial infarction ,Heat1 1999, 81(2): 114~120
15 Mega JL, Morrow DA, De Lemos JA, et al. B-type natriuretic peptide at presentation and prognosis in patients with ST-segment elevation myocardial infarction: an ENTIRE-TIMI-23 substudy. J Am Coll cardiol,2004, 44 (2): 335~339
16 de Lemos JA, Morrow DA. Brain natriuretic peptide measurement in acute coronary syndromes: Ready for clinical application. Circulation, 2002, 106(23): 2868~2870
17 Talwar S, Squire IB, Downie PF, et al. Plasma N terminal pro-brain natriuretic peptide and cardiotrophin 1 are raised in unstable angina. Heart, 2000, 84(4): 421~424
18 Arakawa N, Nakamura M, Aoki H,et al. Relationship between plasma level of brain natriuretic peptide and myocardial infarct size. Cardiology , 1994, 85(5): 334~340
19 Mair J, Friedl W, Thomas S, et al. Natriuretic peptides in assessment of left-ventricular dysfunction. Scand J Clin Lab Invest Suppl. 1999; 230(1): 132~142
20 Kelly R, Struthers AD. Are natriuretic peptides clinically useful as markers of heart failure? Ann Clin Biochem, 2001; 38(Pt 2): 94~102
21 De Lemos JA, Morrow DA, Bentley JH, et al. The prognostic value of B-type natriuretic peptide in patients with acute coronary syndromes, N EngL J Med, 2001, 345(14): 1014~1021
22 Tapanainen JM, Lindgren KS, Makikallio TH,et al. Natriuretic peptides as predictors of non - sudden cardiac death after acute myocardial infarction in the beta - blocking era, J Am Coll Cardiol, 2004, 43(5); 757~763
23邵乐文,朝阳,王战坤.床边即时脑利钠肽检测对呼吸困难的诊断价值.中华心血管病杂志, 2004, 32(12): 1123~1125
24 Nagaya N , Go to Y, Yo sh imura M , et al. Increased plasma levels of brain natriuretic peptide levels associated with progressive ventricular remodeling after acute myocardial infarction. Clin Sci, 1999, 96 (2) : 129~136
25张军,黄占东,肖占森.脑钠肽在心力衰竭患者治疗中的浓度变化.北京医学, 2006, 28(6): 378~379
26 Bettencourt P, Ferreira A , Pardal O, et al. Clinical significance of brain natriuretic peptide in patients with post myocardial infarction. Clin Cardio l,2000, 23 (12) : 921~927
27 Nilsson JC, Groenning BA , Nielsen G, et al. Left ventricular remodeling in the first year after acute myocardial pro-brain natriuretic peptide. Am Heart J, 2002, 143(6): 696~702
28 de Lemos JA, Morrow DA. Brain natriuretic peptide measurement in acute coronary syndromes: ready for clinical application. Circulation, 2002, 106 (23) : 2868~2869
29 Nagaya N, Goto Y, Nishikimi T, et al. Sustained elevation of plasma brain natriuretic peptide levels associated with progressive ventricular romodeling after acute myocardial infarction. Clinical Science, 1999, 96(2): 129~136
30 Nakagawa O , Ogawa Y, Itoh H, et al. Rapid transcriptional activation and early mRNA turnover of brain natriuretic peptide in cardiocyte hypertrophy. Evidence for brain natriuretic peptide as an emergency cardiac hormone against ventricular overload. J Clin Invest, 1995, 96(3): 1280~1287
31 Grilley JG, Farrer M. Left ventricular remodeling and brain natriuretic peptide after first myocardial infarction. Heart, 2001, 86(6) : 638~642
32 delemos JA, Marrow DA, Bentley JH, et al. The prognostic value of B~type natriuretic peptide in patients with acute coronary syndrome. N Engl J Med, 2001, 345(14): 1014~1021
33 Morrow DA, delemos JA, Sabatine MS, et al. Evaluation of B-type natriuretic peptide for risk assessment in unstable angina non~ST elevation myocardial infarction: B-type natriuretic peptide and prognosis in TACT ICS2T IM I 18. J Am Coll Cardiol, 2003(8), 41: 1264~1272
34刘梅林,李继敏,胡大一,等.心绞痛患者血浆NproBNP水平的变化及其临床意义.中华心血管病杂志, 2004, 32(6): 497~500
35 Tamura N, Ogawa Y, Chusho H, et al. Cardiac fibrosis in mice lacking brain natriuretic peptide. Proc Natl Acad Sci USA, 2000, 97(8): 4239~4244
36 Bettencourt P, F rioes F,A zevedo A , et al. Prognotic information provided by serial measurements of brain natriuretic peptide in heart failure[J ]. Int J Cardio l, 2004, 93 (1) : 45~48
37刘东,张晓雪,马丽雅,等.高血压病左心室肥厚患者血浆脑钠素水平。高血压杂志, 2004, 5(5): 396~398
38 Ogawa Y, Itoh H, Nakao K. Molecular biology and biochemistry of natriuretic peptide family. Clin ExpPhamacol Physiol, 1995, 22(1): 49~53
39 Wei CM, Heublein DM, Perrella MA, et al . Natriuretic peptide system in human heart failure. Circulation, 1993, 88(3 ) : 1004~1009
40 Lang CC, Choy AM, Struthers AD. Atrial and brain Natriuretic peptides: adual natriuretic peptide system potentially involved in circulatory homeostasis. Clin Sci, 1992, 83 (5): 519~527
41 Omland T,Aakvaag A, Bonarjee VV, et al. Plasma brain natriuretic peptide as an indicator of left ventricular systolic function and long-term survival after acute myocardial infarction.Comparison with plasma atrial natriuretic peptide and N~terminal proatrial natriuretic peptide. Circulation. 1996; 93 (11):1963~1969
42 Paelinck BP,Vrints CJ,Bax JJ,et al.Relation of B-type natriuretic peptide early after acute myocardial infarction to left ventricular diastolic function and extent of myocardial damage determined by magnetic resonance imaging.Am J Cardiol. 2006; 97(8): 1146~1150
43 Mukoyama A ,Nakao K, Hosoda K, et al . Brain natriuretic peptides as a novel cardiac hormone in humans : Evidence for an exquisite kual natriuretic peptide system , atrial natriuretic peptide and brain natriuretic peptide. J Clin Invest , 1991 , 87(4):1402~1412
44 Selvais PL ,Donckier J E , Robert A , et al . Cardiac natriuretic peptides for diagnosis and risk stratification in heart failure : influences of left ventricular dysfunction and coronary artery disease on cardiac hormonal activation. Eur J Clin Investigation, 1998, 28(8): 636~642
45 Lin Jie , Zhang Delin , Li Tingfu. Correlations between plasma concentration of brain natriuretic peptide and cardiac function in patients with heart failure. J Clin Cardiol (China), 2001, 17(10): 454~455
46李静宇,王宇航,杨志新.放免法测定血浆脑钠素水平诊断无症状性心力衰竭.中国卫生检验杂志, 2000, 10 (4): 454~455
47 Nagaya N, Nishikimi T, Goto Y, et al. Sustained elevation if plasma brain natriuretic peptide is a biochemical marker for the prediction of progressive ventricular remodeling after acute myocardial infarction. Am Heart J ,1998 ,135(1): 21~28
48 Nagaya N, Nishikimi T, Uematsu M , et al . Plasma brain natriuretic peptide as a prognostic indicator in patients with primary pulmonary hypertension. Circulation, 2000, 102 ( 8): 865~867
49 Wallen T, Landahl S, Hedner T, et al. Brain natriuretic peptide predicts mortality in the elderly. Heart, 1997, 77 ( 3): 264~267
50 Corti R, Burnett JC, Rouleau JL, et al . Vasopeptidase inhibitors , a new therapeutic concept in cardiovascular disease. Circulation, 2001, 104(15): 1856~1862
51 Tsutamoto T, Matsumoto T, Wada A, et al . Plasma BNP level as a biochemical marker of morbidity and mortality in patients with asymptomatic or minimally symptomatic LVD : comparison with plasma AngⅡand ET-1 . Eur Heart J, 1999, 20(24):1799~1807
52 Bettencourt P. Brain Natriuretic Peptide in the treatment of heart failure. Cardiovase Daug Rev, 2002, 20 (1): 20~37
53 Hobbs RE, Miller LW, Silverman CB, et al . Hemodynamic effects of asingle intravenous injection of synthetic human brain natriureticpeptide in patients with heart failure secondary to ischemic ordialated cardiomyopathy. Am J Cardiol , 1996 , 78(8): 896~901
54 Troughton RW, Frampton CM , Yandle TG, et al . Treatment of heart failure guided by plasma aminoterminal brain natriuretic peptide (N-BNP) concentrations. Lancet, 2000, 355 (9210): 1216~1230
55 Clarkson PBM, Wheeldon NM, MacFadyen RJ, et al . Effects of brain natriuretic peptide on exercise hemodynamics and neurohormones in isolated diastolic heart failure. Circulation, 1996, 93(11): 2037~2042
56 Yanue KH, Yoshimura M. Suppression of hyperventilation induced attracts with infusion of brain natriuretic peptide in patients with variant angina. Am Heart J ,1994 ,128 (6pt 1) : 1098~1101
57 Mega JL,Morrow DA,De Lemos JA,et al.B-type natriuretic peptide at presentation and prognosis in patients with ST-segment elevation myocardial infarction: an ENTIRE-TIMI-23 substudy.J Am Coll Cardiol.2004; 44(2): 335~339
58 Tapanainen JM,Lindgren KS,Makikallio TH,et al.Natriuretic peptides as predictors of non~sudden and sudden cardiac death after acute myocardial infarction in the beta~blocking era.J Am Coll Cardiol. 2004; 43(5): 757~763
59 Okumura K, Yasue H , Fujii H ,et al . Effects of brain (B-type)natriuretic peptide on coronary artery diameter and coronary hemodynamic variables in human :comparison with effects on syetemic hemodynamic variables. A m Coll Cardiol, 1995, 25(2): 342~348
60 Matsumura T, Kugiyama K, Sugiyama S, et al. Neutral endopeptidase
24.11 in neutrophils modulates protectives effects of natriuretic peptides against neutrophils~induced endothelial cytotoxity. J Clin Invest, 1996, 97 (10): 2192~2203
61 Peacock WFⅣ, Emerman CL, young J. Nesiritide in congestive heart failure associated with acute coronary syndromes: a pilot study of safety and efficacy. J Card Fail. 2004; 10(2): 120~125
62李世强,傅向华,刘君,等.静脉注射重组人脑利钠肽对急性心肌梗死伴心功能不全患者的急性血流动力学效应的研究.中华心血管病杂志, 2006, 34(1):23~27
63 Hunt SA, Baker OW, Chin MH, et al. ACC-AHA Guidelines for evaluation and management of chronic heart failure in the adult: executive summary. Circulation, 2001, 104 (24): 2996~3007
64 Go to T, Takase H, To riyama T, et al. Circulating concentrations of cardiac proteins indicate the severity of congestive heart failure. Heart, 2003, 89(11): 1303~1307