螺内酯对急性前壁心肌梗死后左室重构的影响

近年来临床研究显示：醛固酮受体拮抗剂可明显降低慢性心力衰竭和急性心肌梗死（AMI）后心力衰竭患者的病死率；本研究旨在通过观察急性前壁心肌梗死后超声心动图变化来评价应用螺内酯是否能减轻和逆转AMI后左室重构。     

小剂量螺内酯抑制急性前壁心肌梗死患者的左室重构

目的 探讨小剂量螺内酯对急性前壁心肌梗死患者血清脑利钠肽（BNP）水平和左室重构的影响.方法 选择急性前壁心肌梗死患者90例,在常规治疗基础上,随机分为3组：常规治疗组30例,接受转换酶抑制剂、β受体阻滞剂、抗血小板、调脂药物等常规处理;小剂量螺内酯组30例,在上述治疗基础上每日给予螺内酯20 mg;中剂量螺内酯组30例,在上述治疗基础上每日给予螺内酯40 mg.结果 6个月时小剂量螺内酯组、中剂量螺内酯组和常规治疗组左室射血分数显著升高（P＜0.05）.治疗后常规治疗组BNP水平显著下降（P＜0.05）,小剂量螺内酯组和中剂量螺内酯组BNP水平下降更显著（P＜0.01）;小剂量螺内酯组与中剂量螺内酯组比较差异无统计学意义.结论 小剂量螺内酯抑制急性前壁心肌梗死患者的左室重构,血清BNP水平下降.     

急性心肌梗死后螺内酯干预对左室重构的影响

目的　探讨急性心肌梗死(AMI)患者应用螺内酯干预对于左室重构(LVRM)的影响。方法　4家医院共入选AMI患者88例,采用多中心、随机、对照的方法,对46例AMI患者在常规治疗的基础上加用螺内酯40mg/d(螺内酯组),对照组(n=42)常规治疗。在6个月干预期内检测两组血清Ⅲ型前胶原氨基端肽(PⅢNP)、脑钠肽(BNP)及超声心动图,以评价左室纤维化、左室功能和左室容积。结果　88例中,急性前壁心肌梗死患者43例,螺内酯组23例、对照组20例;急性下壁心肌梗死患者45例,螺内酯组23例、对照组22例。急性前壁心肌梗死组在治疗3、6个月时螺内酯组与对照组相比,血清PⅢNP和BNP明显降低[PⅢNP分别为( 260 .2±59. 9 )ng/L比( 328 .0±70 .3 )ng/L, P=0 .001, ( 197 .1±46 .3 )ng/L比( 266. 7±52 .4 )ng/L, P<0. 001 ,BNP分别为( 347 .4±84 .0)ng/L比(430 .1±62 .9)ng/L, P<0 .001, (243 .7±79. 7)ng/L比(334. 6±62. 8)ng/L, P<0. 001]。治疗6个月时螺内酯组较对照组左室舒张末期内径、左室收缩末期内径明显降低[分别为(51. 0±5 .5)mm比(55. 6±4 .5)mm, P=0 .005, (35 .7±4 .6)mm比(39 .1±5 .6)mm, P=0 .046]。急性下壁心肌梗死组在治疗6个月时螺内酯组与对照组相比血清PⅢNP、BNP水平无统计学意义,(P>0 05),并且左     

急性ST段抬高性心肌梗死后立即使用螺内酯对左室重构的影响

目的评价醛固酮拮抗剂螺内酯对急性ST段抬高型心肌梗死（STEMI）后左室重构和心功能的影响。方法连续入选160例STEMI患者,随机分为两组。在发病24h内,以目前最佳常规药物治疗做对照组（79例）,在常规治疗基础上加用螺内酯做螺内酯组（81例）。两组患者均在STEMI后24h内做多功能超声心动图检查,测定并计算左室收缩末期容积指数（LVESVI）、左室舒张末期容积指数（LVEDVI）、室壁运动积分指数（WMSI）,左室射血分数（LVEF）,1月后由专人复查。结果两组基线临床特征及各项超声心动学指标无显著差异,治疗1月后,两组各项超声心动学指标均有明显改善（P<0.05）,但螺内酯组各项指标的改善又显著优于对照组（P<0.05）。结论在STEMI发病后常规治疗基础上立即加用螺内酯可进一步加强抗左室重构的作用,进一步改善心脏功能。     

螺内酯联合贝那普利治疗急性前壁心肌梗死患者的临床疗效

目的:探讨螺内酯联合贝那普利治疗急性前壁心肌梗死患者的临床疗效及对左心室重构的影响。方法:选择本院收治的100例急性前壁心肌梗死患者为研究对象,按照不同治疗方案分为贝那普利组(50例)和联合治疗组(50例,螺内酯和贝那普利联合治疗),治疗6个月,对两组疗效、左心室重构及不良反应情况进行对比。结果:与治疗前比较,治疗6个月后,两组心率变异性(HRV)各指标和左室射血分数(LVEF)均明显提高,左室收缩末期内径(LVESd)和左室舒张末期内径(LVEDd)均明显缩小(P<0.05或<0.01);且与贝那普利组比较,治疗后联合治疗组HRV各指标,LVEF[(52.45±8.65)%比(57.85±9.70)%]明显提高,LVESd[(36.25±2.13)mm比(30.10±2.06)mm]和LVEDd[(58.60±6.41)mm比(51.29±6.20)mm]明显缩小(P均<0.01);两组治疗后总不良反应率无明显差异(P=1.000)。结论:联合螺内酯和贝那普利治疗急性前壁心肌梗死患者能明显改善患者心率变异性心功能,抑制左心室重构,且不良反应少。     

螺内酯对急性心肌梗死患者胶原代谢标志物和左室重构的影响

目的:观察螺内酯对急性心肌梗死(AMI)患者胶原代谢标志物及左室重构的影响。方法:将60例AMI患者分为常规治疗组与螺内酯治疗组,应用放射免疫法测定血浆Ⅲ型前胶原氨基末端肽(PⅢNP)、血清透明质酸(HA)含量,用超声心动图测量左室结构及舒缩功能参数。结果:常规治疗组与螺内酯治疗组AMI后第2天血浆PⅢNP分别为(5.24±1.09)、(5.14±1.21)μg/L与正常组[(5.01±1.18)μg/L]相比差异无统计学意义(均P>0.01)。螺内酯治疗组第4周、第12周血浆PⅢNP含量分别为(7.25±1.97)、(6.82±1.98)μg/L较常规治疗组同时间点含量[(10.23±2.25)、(8.36±2.11)μg/L]均显著下降(均P<0.01)。第4周、第12周螺内酯治疗组血清HA含量[(136.4±28.7)、(109.2±30.5)ng/L]与常规治疗组[(167.5±31.5)、(134.5±36.1)ng/L]比较均显著下降(P<0.01)。螺内酯治疗组第12周左室舒张期末容积指数[(57.2±5.8)ml/m2]和收缩期末容积指数[(29.2±5.3)ml/m2]与常规治疗组[(65.9±6.3),(35.7±6.8)]相比均显著降低(P<0.01);二尖瓣血流舒张早期流速(VE)与心房收缩期流速(VA)比值(VE/VA)与常规治疗组相比均显著增加(P<0.01),射血分数虽有增加,但无明显变化(P>0.05)。结论:螺内酯可降低AMI患者血浆PⅢNP、HA含量,阻抑左室重构,改善左室功能。     

急性心肌梗死后左室重构相关因素探讨

急性心肌梗死后左室重构相关因素探讨徐默玲（江苏省无锡市第二人民医院心内科２１４００２）关键词心肌梗死左室重构急性心肌梗死（ＡＭＩ）后可发生早期左室重构，左室重构又可导致心衰、心律紊乱、心脏破裂和血栓形成。故左室重构是晚近国内外关注的课题，其相关因素和...     

急性前壁心肌梗死后梗死相关血管延迟开通对晚期左室重构的影响

目的　探讨急性前壁心肌梗死(AMI)后延迟经皮冠状动脉介入治疗(PCI)使梗死相关动脉(IRA)开通对AMI晚期左室重构的影响。方法　选择64例急性前壁、前间壁及广泛前壁Q波性AMI后病情稳定,发病2~14天,平均(9 .1±2 .3)天冠状动脉造影证实左前降支完全闭塞者,依据是否成功行PCI,分为成功PCI组和对照组,分别于急性期、术后2个月和6个月应用超声心动图随访左室大小、左室功能和室壁活动异常情况,并观察6个月期间心力衰竭事件的发生情况。结果　AMI后2个月两组左室射血分数、左室收缩末期容积指数、左室舒张末期容积指数和室壁活动异常积分与急性期相比差异无统计学意义,急性期和2个月时两组上述各指标之间差异也无统计学意义。6个月时两组左室射血分数和室壁活动异常积分与急性期和2个月相比差异无统计学意义,但对照组左室舒张末期容积指数和左室收缩末期容积指数较急性期明显增大(P<0 .01, P<0. 05 ),且与成功PCI组相比差异有统计学意义(P<0 .01, P<0 .05)。6个月随访期间心力衰竭事件发生率对照组为19%,成功PCI组为2%,但差异无统计学意义。结论　急性前壁AMI后IRA延迟开通能明显减少AMI后晚期的左室重构,而对AMI后早期左室重构的影响不大。延迟PCI可能有利于减少AMI后远期心力衰竭事件的发生。     

螺内酯对急性心肌梗死患者早期心室重塑的影响

目的观察螺内酯对急性心肌梗死（AMI）后尚无心力衰竭症状患者心室重塑的影响及安全性。方法选择67例AMI患者,随机分为对照组32例（采用基础治疗）和治疗组35例（基础治疗＋螺内酯治疗）,治疗前后检测血压、心率、超声心功能指标、血生化指标等,观察两组治疗后心功能改善情况。结果治疗组超声学及生化学心功能指标改善明显,与对照组比较有统计学差异（P〈0．05）。结论AMI患者早期在常规治疗基础上给予小剂量螺内酯,可进一步抑制左室扩张和纤维化,防止左室重构的发生。     

骨髓干细胞动员对急性心肌梗死后左室重构影响的临床研究

目的 :观察骨髓干细胞动员对急性心肌梗死 (AMI)患者左室重构的影响。方法 :4 8例AMI患者随机分为动员组 (2 5例 )和对照组 (2 3例 ) ,动员组连续 3d给予粒细胞集落刺激因子 (G CSF) 30 0 μg/d ,用2 0 1Tl静息—再分布心肌显像比较两组第 6d、 30d的梗死面积 ,超声心动图观察 72h内和 3个月的左室舒张末期容积指数 (LVEDVI)、收缩末期容积指数 (LVESVI)、室壁运动指数 (WMSI)、射血分数(LVEF)。结果 :动员组治疗后心肌梗死面积明显减少 (0 383± 0 0 77vs 0 5 6 1± 0 0 96 ,P <0 0 1) ,LVESVI减少 [(2 7 4 7± 7 86 )ml/m2 vs (34 5 0± 8 0 8)ml/m2 ,P <0 0 5 ],WMSI减少 (1 10± 0 11vs 2 2 6±0 14 ,P <0 0 1) ,LVEF增加 (0 5 9± 0 0 7vs 0 4 8± 0 0 7,P <0 0 1)。结论 :应用G CSF动员AMI患者自身骨髓干细胞可明显缩小心肌梗死面积及有效防治左室重构     

Relation of circulating interleukin-6 to left ventricular remodeling in patients with reperfused anterior myocardial infarction

BACKGROUND: During the remodeling process after myocardial infarction (MI), the expression of proinflammatory cytokines is enhanced in the myocardium. However, only a few clinical studies have been conducted on cytokine involvement in left ventricular (LV) remodeling after MI. HYPOTHESIS: Circulating proinflammatory cytokines may be involved in LV remodeling in patients with reperfused MI. METHODS: We studied 25 patients with acute anterior MI who had undergone coronary reperfusion therapy, and 10 normal control subjects with no cardiac disease. In all patients, LV ejection fraction, end-diastolic volume index (EDVI), and end-systolic volume index (ESVI) were determined using left ventriculography at the acute phase and 6 months after onset. The delta EDVI and delta ESVI were calculated as the value of LV volume reduction, suggesting LV reverse remodeling. Serum levels of interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha were measured using enzyme-linked immunosorbent assay. RESULTS: Serum levels of IL-6 and TNF-alpha at the acute phase were significantly higher in patients with MI than in control subjects (both p < 0.05). The IL-6 levels correlated well negatively with delta EDVI (r = 0.779, p = 0.039), whereas no correlation was found for TNF-alpha. According to multivariate analysis, IL-6 at the acute phase was a significant independent predictor for LV remodeling after reperfused MI (p = 0.007). CONCLUSIONS: Circulating IL-6 levels correlated closely with LV geometric changes during the remodeling process in patients with reperfused MI. Our study addresses the usefulness of another marker for LV remodeling after MI.     

肝细胞生长因子对急性心肌梗死后左室重构的预测作用

目的: 探讨血清肝细胞生成因子(HGF)对急性心肌梗死(AMI)后早期左室重构的预测价值。方法: 36例AMI患者入院时及发病7 d测定血清HGF水平;AMI其中的26例分别于发病后7~10 d及发病后3个月行超声心动图检查,3个月时左室舒张末期容积指数（LVEDVI）与7~10 d时比增加≥5 ml/m2定义为左室重构组(n=11),对两组血清HGF值进行比较。结果: AMI患者入院时血清HGF浓度较对照组明显升高［(809±288)ng/L vs.(620±162)ng/L,P<0.01］,7 d时升高更显著［(1 607±1 355)ng/L,P<0.01］。发病7 d时血清HGF浓度在左室重构组较非左室重构组升高［(2 216±1 522)ng/L vs.(1 176±593)ng/L,P<0.05］,而入院时两组浓度则无显著差异。结论: AMI时血清HGF浓度升高,AMI后7 d时增高的血清HGF可能预示心室重构。     

急性心肌梗死患者早期血浆脑钠素与左室重塑的关系

目的　探讨急性心肌梗死 (AMI)早期血浆脑钠素与左室重塑的关系。方法　 44例AMI患者分为依那普利组及常规治疗组 ,采用放射免疫法测定入院后 14d内血浆脑钠素水平 ;超声心动图测定同期及 3个月左室舒张末容积指数 (LVEDVI)、左室收缩末容积指数 (LVESVI)及左室射血分数 (LVEF)。结果　常规治疗组入院后即刻血浆脑钠素水平较健康对照组明显升高 (P <0 .0 1) ,5、14d较入院即刻进一步升高 (P <0 .0 5 )。AMI患者 5、14d血浆脑钠素水平与同期及 3个月LVEDVI、LVESVI正相关 (P <0 .0 5 ,0 .0 1)。与常规治疗组相比 ,依那普利组脑钠素与心室容积指数一致性下降。结论　AMI后早期血浆脑钠素升高与左室重塑密切相关。     

Effect of hepatocyte growth factor on left ventricular remodeling after acute myocardial infarction in canine

Background and objectives To investigate the effect of hepatocyte growth factor (HGF) on left ventricular (LV) remodeling after acute myocardial infarction (AMI). Methods AMI was produced by ligation of proximal left anterior descending coronary artery(LAD) in 12 mongrel canines. These animals were randomized into 2 groups. In HGF group (n=6), canines were injected with pcDNA3-HGF lml (about 300ug) at the margin of infarcted myocardium; in control group (n=6) canines were injected with equal volume of normal saline. Cardiac function and left ventricular remodeling were evaluated with echocardiography at 1, 4, 8 weeks after MI. LV myocardium specimens were obtained at 8 weeks and stained with hematoxylin and eosin for histological examination or with sirius red to assess the collagen content. Results Compared with control group, LVEF in HGF group was significantly higher at 4 weeks (49.61+6.66 vs 39.84+6.39; P＜0.05) and at 8 weeks (51.57+8.53 vs 40.61+7.67; P＜0.05) after AMI, while LVESV was significantly lower in HGF group than that in control group at 8 weeks after AMI (18.98+3.47 vs 25.66+5.86; P＜0.05). Posterior left ventricular wall thickness decreased significantly from 1 wk to 8 wks after AMI in control group, while remained unchanged in HGF group. Compared with control group, histological examination showed more neovascularization and less scar, and sirius red staining indicated higher volume of type Ⅲ collagen (7.10&#177;4.06% vs 3.77&#177;1.09%; P＜0.05) and lower collagen Ⅰ/Ⅲ ratio value (1.11&#177;0.52 vs 2.94&#177;2.48; P＜0.05)in HGF group. Conclusion HGF gene transfer might improve cardiac function and LV remodeling after acute myocardial infarction by stimulating angiogenesis, reducing fibrosis, and reducing myocardial scarring.     

急性心肌梗死后左室重构临床研究

目的　探讨溶栓治疗对急性心肌梗死后左室结构和功能的影响。方法　对 36例首发急性心肌梗死患者于梗死后 4周和 12周进行超声心动图观察。分别测定左室舒张末期容积指数 (LVEDVI)、左室收缩末期容积指数 (LVESVI)、射血分数 (EF) ,作为反映左室结构和功能变化的指标。结果　急性心肌梗死后LVEDVI、LVESVI均明显增高 (分别为P <0 0 1,P <0 0 5 )。 4周和 12周检查发现 ,溶栓组LVEDVI、LVESVI无明显差异 (分别P>0 0 5 ,P >0 0 5 ) ,EF值明显增大 (P <0 0 5 ) ;未溶栓组LVEDVI、LVESVI明显增大 (分别为P <0 0 5 ,P <0 0 5 ) ,EF值无明显变化 (P >0 0 5 ) ;对 4周和 12周的检查结果作组间比较发现 ,溶栓组LVEDVI、LVESVI均小于未溶栓组 (P <0 0 5 ) ,EF值溶栓组高于未溶栓组 (P <0 0 5 )。结论　溶栓治疗能有效地抑制急性心肌梗死后左室重构 ,改善心功能。     

Early mitral regurgitation after acute myocardial infarction does not contribute to subsequent left ventricular remodeling

BACKGROUND: It is well known that mitral regurgitation may lead to left ventricular dilation; however, the relationship between progressive left ventricular dilation after acute myocardial infarction (MI) and mitral regurgitation has not yet been clarified. HYPOTHESIS: This study tested the hypothesis that early mitral regurgitation contributes to left ventricular remodeling after acute MI. METHODS: We prospectively evaluated 131 consecutive patients by serial two-dimensional and Doppler echocardiography on Days 1, 2, 3, and 7, after 3 and 6 weeks, 3 and 6 months, and 1 year following acute MI. Patients were divided into two groups: those with mitral regurgitation in the first week after acute MI (Group 1, n = 34) and those without mitral regurgitation (Group 2, n = 81). RESULTS: Over 1 year, a significant increase in end-diastolic volume index (from 62.1 +/- 12.9 to 70.5 +/- 23.6 ml/m2, p = 0.001) with a strong linear trend (F = 15.1, p < 0.001) was noted. Initial end-diastolic volume index was higher in Group 1 (65.6 +/- 13.3 vs. 60.4 +/- 12.5 ml/m2, p = 0.047), but this difference remained constant throughout the study (F = 1.76, p = NS). Therefore, the pattern of end-diastolic volume changes was similar in both groups during the period of observation. CONCLUSIONS: These data indicate that early mitral regurgitation after acute MI does not contribute to subsequent left ventricular remodeling in the first year after myocardial infarction.     

EflFect of hepatocyte growth factor on left ventricular remodeling after acute myocardial infarction in canine

Background and objectives To investigate the effect of hepatocyte growth factor (HGF) on left ventricular (LV) remodeling after acute myocardial infarction (AMI). Methods AMI was produced by ligation of proximal left anterior descending coronary artery (LAD) in 12 mongrel canines. These animals were randomized into 2 groups. In HGF group (n=6), canines were injected with pc-DNA3-HGF 1 ml (about 300ug) at the margin of infarcted myocardium; in control group (n=6) canines were injected with equal volume of normal saline. Cardiac function and left ventricular remodeling were evaluated with echocardiography at 1,4, 8 weeks after MI. LV myocardium specimens were obtained at 8 weeks and stained with hematoxylin and eosin for histological examination or with sirius red to assess the collagen content. Results Compared with control group, LVEF in HGF group was significantly higher at 4 weeks (49.61 6.66 vs 39.84 6.39; P<0.05) and at 8 weeks (51.57 8.53 vs 40.61 7.67; P<0.05) after AMI, while LVESV was significantly lower in HGF group than that in control group at 8 weeks after AMI (18.98 3.47 vs 25.66 5.86; P<0.05). Posterior left ventricular wall thickness decreased significantly from 1 wk to 8 wks after AMI in control group, while remained unchanged in HGF group.Compared with control group, histological examination showed more neovascularization and less scar, and sirius red staining indicated higher volume of typeⅢcollagen (7.10±4.06% vs 3.77±1.09%; P<0.05) and lower collagenⅠ/Ⅲratio value (1.11±0.52 vs 2.94±2.48; P<0.05) in HGF group. Conclusion HGF gene transfer might improve cardiac function and LV remodeling after acute myocardial infarction by stimulating angiogenesis, reducing fibrosis, and reducing myocardial scarring.     

急性心肌梗死与左室重构

急性心肌梗死(AMI)后左室发生细胞学,分子学及细胞间质的变化,进而引起左室在大小、形态、组织结构和功能状态的改变,此即目前许多研究所提及的AMI后的左室重构.AMI后左室的重构贯穿于整个病程的始终,成为影响AMI患者近远期预后的主要原因之一.     

Spontaneous recovery of left ventricular function following acute anterior myocardial infarction

Four patients with acute anterior wall myocardial infarction showing spontaneous and marked improvement in systolic left ventricular function are described. All 4 patients showed abnormal Q waves and severe wall motion abnormalities soon after acute infarction. In all 4 patients, at least some regeneration of R-wave forces occurred and the regional wall motion in the involved area of the left ventricle improved dramatically without coronary angioplasty or surgical revascularization during the intervening period. The improvement in left ventricular function was attributed to spontaneous increase in nutrient flow to the involved area. It is concluded that Q waves and severe wall motion abnormalities do not necessarily indicate irreversible scar formation.