ST段抬高心肌梗死经皮冠状动脉介入治疗后血中肾上腺髓质素研究

目的:探讨ST段抬高心肌梗死(STEMI)直接经皮冠状动脉介入治疗(PCI)后,血液中肾上腺髓质素(AM)2种分子形态在冠状窦-主动脉差值是否有变化。方法:对152例首次发生STEMI患者和53例冠状动脉造影阴性作对照。入选的STEMI患者症状出现后12 h内完成PCI的再灌注治疗。再灌注后取主动脉和冠状窦血,用放免分析的方法测定血浆AM的2种分子形态(AM-m和AM-Gly)。结果:STEMI患者主动脉和冠状窦血浆AM-m、AM-Gly水平明显高于对照组〔(1.8±0.7)比(0.5±0.2)pmol/L,P<0.01〕。STEMI患者血浆AM-m水平的冠状窦-主动脉差值明显高于对照组,而AM-Gly在2组之间无统计学意义(P=0.29)。AM-m的冠状窦-主动脉差值,在伴有左心室(LV)功能障碍的STEMI患者(n=54)明显高于不伴有LV功能障碍的STEMI患者(n=98)。主动脉和冠状窦的血浆AM-m水平与左心室射血分数(LVEF)呈负相关(r=-0.51,r=-0.47,P<0.01)。结论:STEMI再灌注后,尤其伴有严重左心室功能障碍的患者冠状动脉循环血液中有活性的成熟型肾上腺髓质素(AM-m)合成加速。     

重症高血压大鼠左心室肥厚时肾上腺髓质素系统的上调

目的探讨肾上腺髓质素(AM)在重症高血压大鼠左心室心肌肥大中的病理生理作用,包括其配体及酰胺化活性。方法试验分为4组：Wistar-Kyoto大鼠为对照组,有卒中倾向的自然发症高血压大鼠组,用卡托普利治疗8周组,用三氯甲噻嗪治疗8周组。AM前体为无活性的甘氨酸基肾上腺髓质素(AM-Gly),AM-Gly经酰胺化转变为成熟的有活性的AM(AM-m)。通过放射性免疫分析,检测血浆和左心室中AM-m、总AM(AM-m AM-G]y)、心房利钠肽含量,以及AM和心房利钠肽基因水平。结果自然发症高血压大鼠组血压、左心室重量、血浆和左心室中心房利钠肽及其mRNA水平均较对照有所升高。血浆中(AM-m： 31％,总AM： 56％)及心室中(AM-m： 84％,总AM： 31％)的AM-m和总AM均较对照组显升高。在左心室组织中自然发症高血压大鼠组(93．2％)的AM-m／总AM比率明显高于对照组。在左心室中的AM的mRNA水平显高于对照组。卡托普利和三氯甲噻嗪降血压和降低肥大左心室中AM-m、总AM、AM的mRNA含量作用相似。结论此高血压模型的肥大心肌中肾上腺髓质素系统上调。作为一个抗重塑的自分泌和(或)旁分泌因子,AM的上调可能改变左心室肥厚的病理生理过程。     

经胸超声心动图测定无冠状动脉狭窄的糖尿病患者左心室灌注量可行性的观察

目的 探讨常规经胸超声心动图(TTE)评估糖尿病患者左心室整体灌注功能的可行性及其与糖尿病病程的相关性. 方法 选取经冠状动脉造影证实无冠状动脉狭窄的T2DM患者(T2 DM组)60例和健康对照(NC)者60名.采用多普勒和三维超声心动图测量冠状窦血流和左心室质量(LVM).左心室整体灌注量由冠状窦血流量除以LVM计算所得,并分析其与糖尿病病程的相关性.结果 与NC组比较,T2DM组LVM增加[(154.35±19.44)vs(163.00±17.94)g,P＜0.05],静息时左心室灌注量减少[(6.04±4.77)vs(1.72±0.33) ml/(min·g),P＜0.01].静息时左心室整体灌注量与糖尿病病程呈负相关(r=-0.533,P=0.000). 结论 TTE可有效地检测出经冠状动脉造影证实无冠状动脉狭窄的糖尿病患者在静息时存在冠状动脉微血管功能障碍.糖尿病患者的左心室整体灌注量减少,且与其糖尿病病程呈负相关.     

BNP对急性心肌梗死再灌注治疗效果的评价

目的:探讨血浆BNP水平对急性心肌梗死(AMI)再灌注治疗效果的具评价作用。方法:测定88例AMI患者早期血浆BNP水平,比较采用不同治疗方法(包括早期再灌注、择期经皮冠状动脉介入治疗与单纯药物治疗)的患者血浆BNP水平的差异,以及左室重构、心功能改善和远期预后的情况。结果:AMI患者血浆BNP水平明显高于正常人为(325.74±354.11)pg/ml对(21.26±10.01)pg/ml,P<0.01。经治疗后,早期再灌注组BNP水平较另两组明显降低,为(155.12±72.33)pg/ml对(253.01±277.25)pg/ml对(665.01±456.59)pg/ml,(P<0.01),心脏不良事件的发生率亦显著降低(P=0.01),且与出院6个月后左室重构程度呈正相关(r=0.614),与心功能的改善呈负相关(r=-0.504)。结论:血浆BNP水平对急性心肌梗死再灌注治疗的效果具有一定的评价作用。     

急性心肌梗死急诊介入治疗后患者心肌灌注的动态演变

目的:观察急性心肌梗死(AMI)患者梗死相关血管再通达心肌梗死溶栓治疗临床试验(TIMI)3级血流后心肌组织灌注的动态演变,以探讨心肌无复流现象的临床特点及意义。方法:43例AMI患者,急诊冠状动脉介入治疗后梗死相关血管血流达TIMI 3级。分别于冠状动脉介入治疗后即刻、24 h内、2周和3个月时行单光子发射型计算机断层扫描(SPECT)。根据心肌灌注缺损积分,将患者分为无复流组(17例)和复流组(26例)。分析两组心肌灌注缺损积分、左心室射血分数、左心室舒张末期容积(LVEDV)和左心室收缩末期容积(LVESV)的变化规律,并进行组间比较。结果:(1)无复流组在冠状动脉介入治疗后即刻、24 h内、2周和3个月时的心肌灌注缺损积分分别为8．5±1．9, 6．4±2．3、4．6±2．1和4．2±1．7,复流组为4．1±1．0、1．7±1．2、0．5±1．1和0．4±1．0;无复流组和复流组冠状动脉介入治疗后积分在2周内均呈逐渐减低趋势,至2周时趋与稳定,2周和3个月之间比较均无显著差异(P>0．05);两组间同时相点比较,无复流组心肌灌注缺损积分在各点均显著高于复流组(P<0．01)。(2)两组左心室射血分数均呈逐渐增加趋势,但无复流组左心室射血分数较复流组恢复延迟,且在各时点均显著低于复流组。复流组冠状动脉介入治疗后左心室舒张末容积逐渐减小,无复流组则继续增加,2周时达高峰,而后开始减小,3个月时虽低于2周时,但仍显著大于冠状动脉介入治疗后24 h内(P<0．01);无复流组的左心室舒张末容积在各时相点均显著大于复流组。(3)无复流组冠状动脉介入治疗后即刻的灌注缺损积分与同时相点和3个月时的左心室射血分数均呈显著负相关(分别为r=-0．512,P< 0．05和r=-0．498,P<0．05)。结论:AMI血运重建后梗死相关血管血流达TIMI 3级的患者仍存在心肌无复流现象,但心肌无复流现象有随时间改善的趋势,至2周左右趋于稳定;早期的心肌灌注状况与后期的心功能恢复及左心室重构的发生密切相关。     

急性心肌梗死患者血浆肾上腺髓质素浓度与心功能的关系

目的 :探讨急性心肌梗死 (AMI)患者血浆肾上腺髓质素 (AM)浓度与心功能的关系。方法 :用放射免疫法测定 2 0例 AMI患者在发病后第 2 4小时及 15例正常人血浆 AM和心房利钠肽 (ANP)浓度 ,AMI患者还同时用超声心动图测左室射血分数 (L VEF)。结果 :AMI患者血浆 AM浓度无论在心力衰竭组 [(15 .6± 2 .1) pmol/L]或无心力衰竭组 [(7.4± 1.1) pm ol/ L]都显著高于对照组 [(2 .3± 0 .3) pmol/ L,P <0 .0 1,P <0 .0 5 ],而且心力衰竭组显著高于无心力衰竭组 (P <0 .0 5 )。 AMI患者血浆 AM浓度与 ANP浓度 (r =0 .47,P <0 .0 5 )及L VEF(r =- 0 .5 3,P <0 .0 5 )呈相关关系。结论 :血浆 AM参与了 AMI后心功能的调节 ,是对 AMI后心功能下降的一种代偿性反应     

BNP对急性心肌梗死再灌注治疗效果的评价

目的:探讨血浆BNP水平对急性心肌梗死(AMI)再灌注治疗效果的具评价作用. 方法:测定88例AMI患者早期血浆BNP水平,比较采用不同治疗方法(包括早期再灌注、择期经皮冠状动脉介入治疗与单纯药物治疗)的患者血浆BNP水平的差异,以及左室重构、心功能改善和远期预后的情况. 结果:AMI患者血浆BNP水平明显高于正常人为(325.74±354.11)pg/ml对(21.26±1 0.01)pg/ml,P＜0.01.经治疗后,早期再灌注组BNP水平较另两组明显降低,为(155.12±72.33)pg/ml对(253.01±277.25)pg/ml对(665.01±456.59)pg/ml,(P＜0.01),心脏不良事件的发生率亦显著降低(P=0.01),且与出院6个月后左室重构程度呈正相关(r=0.614),与心功能的改善呈负相关(r=-0.504).结论:血浆BNP水平对急性心肌梗死再灌注治疗的效果具有一定的评价作用.     

心绞痛患者冠状静脉-主动脉血浆肾素活性和血管紧张素Ⅱ差值的检测及临床意义

目的　检测心绞痛患者冠状静脉与主动脉血液中血浆肾素活性 (PRA)差值和血管紧张素Ⅱ (AngⅡ )的浓度差值 ,并探讨其在冠心病发生、发展过程中的临床意义。方法　 3 7例心绞痛患者均经选择性冠状动脉造影证实有明显的冠状动脉狭窄 ;18例正常对照组经临床检查和选择性冠状动脉造影排除冠心病。通过测定冠状静脉和主动脉血液中PRA和AngⅡ的浓度 ,分别计算各自在两个部位之间的差值 ,比较不稳定性心绞痛、稳定性心绞痛和正常对照组冠状静脉 主动脉PRA差值和AngⅡ浓度差值间的差异。结果　不稳定性心绞痛患者的冠状静脉 主动脉PRA差值和AngⅡ浓度差值较稳定性心绞痛患者和对照组均明显升高 (P <0 0 1或P <0 0 5) ,稳定性心绞痛患者的上述二种差值均较对照组高 (P <0 0 1或P <0 0 5)。结论　心脏局部存在肾素 血管紧张素系统 (RAS)在冠心病患者该系统明显激活 ,且与病情严重程度相一致     

高血压合并急性心肌梗死早期血压变化及其原因探讨

目的探讨高血压患者发生急性心肌梗死(acute myocardial infarction,AMI)早期血压的动态变化及其相关原因。方法AMI病人分为高血压组、无高血压组各60例,比较两组患者AMI后1个月的血压的动态变化,与原血压水平、左心室肥厚、血浆血管紧张素Ⅱ、β内啡肽、降钙素基因相关肽、心肌酶峰值的关系及对心收缩功能影响。结果发生AMI后,收缩压下降,高血压组71．7％患者下降(37±16)mm Hg (1 mm Hg=0．133 kPa);无高血压组16．7％患者下降(4．3±4．1)mm Hg(P<0．01)。血压下降程度与AMI前血压呈正相关(P<0．05)。左心室肥厚患者AMI后血压下降显著,心功能Ⅲ-Ⅳ级患者较多。高血压组AMI后血压下降患者的血浆血管紧张素、β-内啡肽、降钙素基因相关肽及肌酸激酶、心肌型肌酸激酶活性高于血压未降者(P<0．01);而射血分数、E／A显著低于血压未降者(P<0．05),心功能衰竭发生率高于血压未降者(P<0．05)。结论高血压患者发生急性心肌梗死早期可出现血压下降,血压下降水平与AMI前的血压、是否有左心室肥厚、梗死面积、左心室功能恶化及某些神经内分泌因子相关。     

经皮冠状动脉介入治疗对急性心肌梗死患者血浆脑钠素水平和左心室重塑的影响

研究发现急性心肌梗死(AMI)患者血浆脑钠素(BNP)水平明显升高.BNP水平高低与AMI后左心室重塑(LVRM)密切相关.本文研究了经皮冠状动脉介入治疗(PCI)对AMI患者血浆BNP水平和LVRM的影响,现报告如下.     

Production and clearance sites of two molecular forms of adrenomedullin in human plasma

Human adrenomedullin (AM) precursor is converted to glycine-extended AM (AM-Gly), an inactive intermediate form of AM. Subsequently, AM-Gly is converted to active mature AM (AM-m) by enzymatic amidation. A recent study showed that two molecular forms of adrenomedullin (AM) are present in human plasma. In this study we investigated the production and clearance sites of two molecular forms of adrenomedullin in humans. We measured plasma levels of AM-m and AM-Total (T) (AM-m+AM-Gly) by immunoradiometric assay and calculated plasma levels of AM-Gly in blood samples taken from various sites during cardiac catheterization in patients with ischemic heart disease. Plasma AM-m levels were significantly lower in left-sided sites after passing through pulmonary circulation than in right-sided sites, whereas there were no significant differences in AM-Gly levels between left-sided sites and right-sided sites. These results suggest that AM-m produced in many organs is released into veins and that the main clearance sites of AM-m are the lungs. Considering that AM preferentially dilates pulmonary vessels rather than systemic vessels, a possible role of this peptide is suggested in the regulation of pulmonary vascular tonus.     

Molecular forms of plasma and urinary adrenomedullin in normal, essential hypertension and chronic renal failure

OBJECTIVES: Human adrenomedullin precursor is converted to glycine-extended adrenomedullin (AM-Gly), an intermediate inactive form of adrenomedullin. Subsequently, AM-Gly is converted to active form of mature adrenomedullin (AM-m). The aim of the present study was to investigate (i) whether sex or age influences plasma and urinary AM-m and AM-Gly levels in normal subjects; (ii) the daytime variability of plasma AM-m and AM-Gly levels in normal subjects; (iii) AM-m and AM-Gly levels and its ratio in plasma and urine in normal subjects, individuals with essential hypertension (HT), and chronic renal failure (CRF); and (iv) the ratio of AM-m and AM-total (T) in plasma of various veins and aorta. METHODS: We measured plasma levels and urinary excretions of AM-m, AM-Gly and AM-T (AM-m + AM-Gly) by recently developed immunoradiometric assay in normal subjects (n = 81), HT (n = 28) and CRF (n = 30). We also determined the molecular forms of plasma adrenomedullin taken from various sites during angiography in patients with suspected renovascular hypertension (n = 9). RESULTS: There were no differences in plasma and urinary excretions of two molecular forms of adrenomedullin among sexes or ages in normal subjects. There was no daytime variation of plasma two molecular forms of adrenomedullin in normal subjects. Plasma AM-m, AM-Gly and AM-T levels were increased in patients with HT and CRF compared with normal subjects, whereas urinary AM-m, AM-Gly and AM-T excretions were decreased in patients with HT and CRF compared with normal subjects. Urinary AM-m: AM-T ratios were significantly higher than plasma AM-m: AM-T ratios. Plasma AM-m and AM-T levels taken from various veins were similar, and they were significantly higher than those of aorta, although there were no differences in plasma AM-Gly levels between aorta and veins. CONCLUSIONS: These results suggest that in normal subjects, and individuals with HT and CRF: (i) plasma and urinary excretions of AM-m and AM-Gly are not affected by age or sex; (ii) AM-m in parallel with AM-Gly is increased; (iii) urine contains a higher percentage of active adrenomedullin than plasma; and (iv) plasma AM-m may be partly metabolized in the lung.     

Source of plasma adrenomedullin in patients with pheochromocytoma

Controversy exists as to the origin of plasma adrenomedullin (AM). To elucidate the source of plasma AM, we measured two molecular forms of AM, an active form of mature AM (AM-m) and an intermediate inactive form of glycine-extended AM (AM-Gly), by immunoradiometric assay using specific kits in two female patients with pheochromocytoma before and 3 weeks after surgery. We also measured plasma AM-m, AM-Gly, and AM-T (AM-m + AM-Gly) levels, in addition to plasma epinephrine (E) and norepinephrine (NE) levels, in bilateral adrenal veins of one patient. Although plasma E and NE levels decreased markedly after surgery in these patients, changes in plasma AM appeared to be confined to the normal range. There were no obvious differences in plasma AM-T, AM-m, or AM-Gly levels in adrenal veins between healthy tissue and tumor sides. Furthermore, plasma AM-T, AM-m, or AM-Gly levels in adrenal veins were comparable with those in the infrarenal inferior vena cavae (IVC) or the suprarenal IVC. In contrast, plasma E and NE levels increased in the adrenal vein of the healthy side and increased further in the adrenal vein of the tumor side compared with those in the infrarenal IVC. These results suggest that the origin of plasma E and NE is the adrenal gland and that elevated plasma levels of E and NE in pheochromocytoma are due to excessive production of E and NE in the adrenal gland of the tumor side. In contrast, it is suggested that neither plasma AM levels in the adrenal vein of the healthy side nor those of the tumor side contribute to the systemic levels of plasma AM. The present results appear to be consistent with the hypothesis that the source of circulating AM is systemic vasculature.     

B型钠尿肽对心肌梗死患者心功能评估的研究

目的观察急性心肌梗死（AMI）患者血B型钠尿肽（BNP）水平的变化特点,探讨BNP对评估AMI患者心力衰竭及心肌缺血严重程度的临床意义。方法入选住院AMI患者93例及正常对照组50例进行BNP的床旁快速检测,并行超声心动图测定左心室射血分数（LVEF）和左心室舒张末期内径（LVEDd）,按照心肌梗死Killip心功能分级分为Ⅰ—Ⅳ级,按照梗死部位分为广泛前壁AMI组、前壁和／或前间壁AMI组、下壁和／或后壁AMI组,根据ST段有无抬高分为ST段抬高型心肌梗死（STEMI）和非ST段抬高型心肌梗死（NSTEMI）,计算各组内的BNP值并进行统计学分析。结果随着AMI患者Killip心功能分级的递增,BNP水平不断增高（除KillipⅠ级与对照组BNP浓度比较P〉0．05,其余各组之间BNP差异有统计学意义P〈0．05）,LVEF随着Killip分级递增而减少,与BNP呈中度负相关（r=-0．79,P〈0．05）而LVEDd逐渐增大与BNP呈高度正相关（r=0．96,P〈0．05）。广泛前壁AMI组BNP浓度〉前壁和／或前间壁AMI组〉下壁和／或后壁AMI组。STEMI组和非NSTEMI组BNP水平差异无统计学意义。结论床旁快速测定BNP浓度可作为判定AMI患者心功能状况及心肌缺血严重程度的重要生化指标之一。     

Plasma levels of neuropeptide Y i patients with current myocardial infarction

Neuropeptide Y (NPY) has been recently characterised as one of the strongest circulating vasoconstrictor peptides, its elevated level may cause coronary artery spasm and increase of peripheral vascular resistance. All this contributes to ischemic myocardial damage and decrease of regional and global left ventricular function. The aim of the study was the examination of NPY plasma levels in patients with acute myocardial infarction (AMI) after thrombolytic therapy with or without reperfusion. The survey was made in 82 patients with AMI after thrombolytic therapy: 40 of them without reperfusion and 42 with reperfusion. The control group consisted of 20 healthy persons. Plasma levels of NPY were measured before thrombolysis, then 1, 3 and 5 days after, using a radioimmunologic method. All patients were treated with aspirin, glyceryl trinitrate and thrombolytic therapy (TT) with alteplase (r-TPA). In patients with AMI, NPY plasma levels were normal before and 1 day after TT, and were significant elevated 3 days after TT 5 days after TT, plasma NPY levels were still high in patients without reperfusion, but they decreased in patients with reperfusion. There was significant negative correlation between NPY level and left ventricular ejection fraction measured 5 days after AMI. During 30-days follow up systolic dysfunction of left ventricle with ejection fraction under 40% occurred in 21 patients and in 11 of them clinical symptoms of heart failure were observed. Using the multivariable regression analysis we showed that NPY concentration over 60 pg/ml is the independent factor leading to left ventricle systolic dysfunction. The results of our study suggest the contribution of NPY to the left ventricular remodeling after AMI.     

Upregulation of ligand,receptor system,and amidating activity of adrenomedullin in left ventricular hypertrophy of severely hypertensive rats: effects of angiotensin-converting enzyme inhibitors and diuretic

OBJECT: We investigated the pathophysiological role of the cardiac adrenomedullin (AM) system, including the ligand, receptor and amidating activity in the hypertrophied heart in severe hypertension. METHOD: We studied the following four groups: control Wistar-Kyoto rats (WKY), spontaneously hypertensive stroke-prone rats (SHR-SP), 8 weeks captopril-treated SHR-SP, and 8 weeks trichlormethiazide-treated SHR-SP. AM precursor is converted to inactive glycine-extended AM (AM-Gly) and subsequently AM-Gly is converted to active mature AM (AM-m) by enzymatic amidation. We measured AM-m, AM-total (AM-T; AM-T = AM-m + AM-Gly), and atrial natriuretic peptide (ANP) in the plasma and left ventricle (LV) by immunoradiometric assay. We also measured gene expression of AM and ANP was and gene expression and protein levels of AM receptor system components such as calcitonin receptor-like receptor (CRLR), receptor-activity modifying protein (RAMP) 2 and RAMP3. RESULTS: At 7 weeks old, SHR-SP had higher blood pressure and ANP mRNA levels and lower plasma AM-T compared with WKY, however, there were no differences in other indices between the two groups. At 17 weeks old, SHR-SP had increased blood pressure, LV weight, plasma and LV ANP levels and mRNA levels of ANP compared with WKY. AM-m and AM-T levels in plasma (AM-m: + 31%; AM-T: + 56%) and the LV (AM-m: + 84%; AM-T: + 31%) were significantly higher in SHR-SP than in WKY. The LV tissue AM-m/AM-T ratio was significantly higher in SHR-SP (93.2%) than in WKY. The mRNA levels of AM, CRLR, and RAMP2 in the LV were significantly higher in SHR-SP than in WKY. Captopril and trichlormethiazide similarly decreased blood pressure and LV hypertrophy with the reduction of the LV AM-m and AM-T levels and mRNA abundance of AM and its receptor component. CONCLUSION: These results suggest that cardiac AM system is upregulated in the hypertrophied heart in this hypertension model. Considering that AM acts as an anti-remodeling autocrine and/or paracrine factor, upregulation of the AM system may modulate the pathophysiology in LV hypertrophy.     

Myocardial endothelin-1 release and indices of inflammation during angioplasty for acute myocardial infarction and stable coronary artery disease

Background

Elevations in endothelin-1 (ET-1) and inflammatory cytokines may impair myocardial reperfusion through the induction of microvascular constriction or obstruction; however, the generation of these factors close to the site of lesion rupture is unknown.

Methods and results

Coronary sinus (CS) and aortic blood was sampled during angioplasty for acute myocardial infarction (AMI) or stable angina to assess the local release of ET-1, interleukin-1β, interleukin-6, tumor necrosis factor-α and C-reactive protein following atherosclerotic plaque rupture. Transthoracic echocardiography documented left ventricular function in AMI. ET-1 levels were higher in CS than in aortic blood in AMI (3.0 ± 0.3 pmol/L vs 2.6 ± 0.3 pmol/L, P = .04), but not in stable angina (1.7 ± 0.2 pmol/L vs 1.5 ± 0.3 pmol/L, P = NS). CS ET-1 levels were also higher in AMI than in stable angina (3.0 ± 0.3 pmol/L vs 1.7 ± 0.2 pmol/L, P = .002), and correlated with left ventricular dysfunction (R² = 0.51, P = .02). In contrast, C-reactive protein levels were higher in CS than in aortic blood only in stable angina (2.3 ± 0.4 mg/L vs 1.8 ± 0.3 mg/L, P = .01). Similarly, CS tumor necrosis factor-α was higher in stable angina than in AMI (6.0 ± 1.4 pg/mL vs 2.5 ± 0.9 pg/mL, P = .02).

Conclusions

Local myocardial release of ET-1 is highest in AMI, where it relates to the extent of myocardial dysfunction. Although local inflammation is a component of stable coronary artery disease, it does not appear acutely enhanced in AMI.     

急性心肌梗塞溶栓治疗期间血浆D-二聚体的动态变化及其临床意义

目的 :探讨血浆 D-二聚体对评价溶栓治疗急性心肌梗塞 (AMI)的价值及意义。　　方法 :2 9例 AMI患者分为溶栓组 (n=2 1) ,未溶栓组 (n=8) ;溶栓组根据溶栓治疗后冠状动脉 (冠脉 )是否开通又分为溶栓再通组 (n=12 ) ,溶栓未通组 (n=9) ;采用酶联免疫吸附试验 (EL ISA)法检测血浆 D-二聚体的水平 ,并与正常对照组 (n=2 0 )进行比较。　　结果 :AMI未溶栓组血浆 D-二聚体较正常对照组显著升高 (P<0 .0 5 ) ;溶栓组血浆 D-二聚体较未溶栓组显著升高(P<0 .0 5 ) ,溶栓后血浆 D-二聚体较溶栓前显著升高 (P<0 .0 1) ,于溶栓后 6小时达高峰 ;溶栓再通组血浆 D-二聚体较溶栓未通组显著升高 ,溶栓前及溶栓后 6小时两组比较有极显著统计学意义 (P<0 .0 1)。　　结论 :AMI早期已有纤溶系统亢进 ,应用溶栓药后进一步激活纤溶系统而发挥作用 ,且以溶栓再通组更显著。