急性心肌梗死溶栓治疗肌钙蛋白T动态变化

目的：观察静脉溶栓治疗急性心肌梗死（ＡＭＩ）患者肌钙蛋白Ｔ（ＴｎＴ）的血清浓度动态变化特点，探讨其对溶栓疗效判定价值。方法：采用全自动酶联免疫吸附测定（ＥＬＩＳＡ）法，测定３９例ＡＭＩ患者肌钙蛋白Ｔ血清浓度变化。结果：１４例ＡＭＩ溶栓再通组的肌钙蛋白Ｔ第１高峰时间（１３．４３±４．０３小时）较１３例溶栓未通组（１８．６２±４．０３小时，Ｐ＜０．０１）及１２例非溶栓组（２４．００±１４．８７小时，Ｐ＜０．０５）明显前移；肌钙蛋白Ｔ发病第１２小时／第７２小时比值，在溶栓再通组（２．４４±１．５２）大于溶栓未通组（１．１２±０．８３）及非溶栓组（１．００±１．０３，Ｐ均＜０．０５）；对ＡＭＩ溶栓再通预测的敏感性、特异性及准确性：在以肌钙蛋白Ｔ第１峰时间≤１４小时为界时分别为７１．４％、８４．６％、７８．０％，在肌钙蛋白Ｔ第１２小时／第７２小时比值≥２．０时为６６．７％、８４．６％及７５．７％。结论：肌钙蛋白Ｔ对ＡＭＩ溶栓疗效具有一定的判定价值。     

急性心肌梗塞溶栓治疗血清肌钙蛋白T检测的临床价值

为了解肌钙蛋白Ｔ（ＴｎＴ）在不同情况下的释放入血情况以及与心功能受损的关系。本研究用链霉亲和素包被的一步夹心法动态测定了６４例急性心肌梗塞（ＡＭⅠ）患者血清ＴｎＴ的浓度，并用超声心动图的方法检查其心功能。结果显示：（１）溶栓组ＴｎＴ释放曲线呈双峰改变；（２）Ⅰ组（溶栓成功组２４例）与Ⅱ组（溶栓失败组１２例）比较，溶栓后２小时内ＴｎＴ上升速度差异有显著性（２．７９±０．９２μｇＬ－１／ｈ对０．５６±０．１２μｇＬ－１／ｈ，Ｐ＜０．０５）；第一峰与第二峰比值差异也有显著性（Ⅰ组１．８７±０．８１对Ⅱ组０．７７±０．２６，Ｐ＜０．０５）；（３）ＴｎＴ平均浓度和持续天数的乘积与１个月左室射血分数呈负相关（ｒ＝－０．８４，Ｐ＜０．０１）。提示：血管再通影响ＴｎＴ的释放动力曲线；血清ＴｎＴ２小时内的上升速度以及第一峰与第二峰的比值可作为溶栓成功的临床参考指标之一；ＴｎＴ释放入血的平均浓度与持续天数的乘积基本能反映心功能受损的情况。     

肌钙蛋白T检测对不稳定性心绞痛患者的预后判断

目的本研究旨在评价血清肌钙蛋白Ｔ（ｃＴｎＴ）定量测定对不稳定性心绞痛患者的预后判断价值。方法对６０例不稳定性心绞痛患者（ＵＡＰ）、１８例稳定心绞痛患者及２０例健康人分别进行血清ｃＴｎＴ、肌酸激酶（ＣＫ）和其同工酶（ＣＫ－ＭＢ）的测定，并观察住院期间的心性事件发生率。结果６０例ＵＡＰ患者中３２例（５３％）ｃＴｎＴ≥０．３μｇ／Ｌ，明显高于余２８例（分别为０．７５±０．２４μｇ／Ｌ和０．１２±０．０４μｇ／Ｌ，Ｐ＜０．００１），但ＣＫ、ＣＫ－ＭＢ差异并无显著性。不稳定心绞痛患者中ｃＴｎＴ升高组３０天内其发生急性心肌梗塞、心脏性猝死、顽固性心绞痛的发生率明显高于ｃＴｎＴ正常值（４３．８％比７．１％，Ｐ＜０．０１）；对上述心脏事件，定量ｃＴｎＴ检测的敏感性为８７．５％，阴性预期值达９２．９％，准确性为６６．７％。结论ｃＴｎＴ是反映心肌细胞损伤的灵敏性、特异性均较好的生化指标；ｃＴｎＴ升高对判断不稳定心绞痛患者预后有较好的预测价值。     

心脏肌钙蛋白T对不稳定性心绞痛危险分层的价值

目的：探讨心脏肌钙蛋白Ｔ（ｃＴｎＴ）对不稳定心绞痛（ＵＡ）危险分层的临床价值。方法：用酶联免疫法测定１１２例ＵＡ患入院即刻、第２、３日血浆ｃＴｎＴ≥０．１ｎｇ／ｍｌ或〈０．１ｎｇ／ｍｌ将患分为ｃＴｎＴ升高组和ｃＴｎＴ正常组;观察住院期间两组急性心肌梗死（ＭＡＩ）、心脏性死亡和难治性心绞痛的发生率。结果：在１１２例ＵＡ患中,ｃＴｎＴ升高４４例（３９％）,ｃＴｎＴ正常６８例（６１％）。住院期间发生ＡＭＩ１２例（１０．７％,死亡５例（４．５％）,非致死性心肌梗死及心脏性死亡１５例（１３．４％）。其中ｃＴｎＴ升高组的死亡率较ｃＴｎＴ正常组有升高趋势,但差异无显性;而ｃＴｎＴ升高组ＡＭＩ、非致死性心肌梗死及心脏性死亡的发生率显高于ｃＴｎＴ正常组（Ｐ〈０．０１）。校正年龄、性别、心绞痛分级、心电图改变等因素后,ｃ     

冠心病患者可溶性肿瘤坏死因子受体的改变与临床意义

目的：观察冠心病患者可溶性肿瘤坏死因子受体（ＳＴＮＦＲ）的改变与临床意义。方法：ＳＴＮＦＲ采用酶联免疫双抗体夹心法测定。结果：血清ＳＴＮＦＲ（ｎｇ／ｍｌ）在急性心肌梗死患者（３．５５±２．０１，ｎ＝２９）和冠心病心肌缺血患者（１．９９±０．６２，ｎ＝２３）中均较正常对照有所升高（０．９３±０．２９，ｎ＝６１，Ｐ均＜０．０１），急性心肌梗死并发心力衰竭死亡时ＳＴＮＦＲ升高达正常值７．７倍（７．２３±１．６０，ｎ＝５），心肌缺血患者中心功能ＩＩ、ＩＶ级（２．５３±０．４６，ｎ＝７）较Ｉ、Ｉ级者（１．７３±０．５０，ｎ＝１６）升高明显（Ｐ＜０．０１）。结论：冠心病患者中ＳＴＮＦＲ水平与病情严重程度密切相关，并能预测急性心肌梗死患者预后。     

墓碑形ST段抬高对急性心肌梗死患者近期预后的影响

目的：研究墓碑形ＳＴ段抬高是急性心肌梗死（ＡＭＩ）早期或超急性期严重心肌损伤的表现形式，探讨其近期预后险恶的特点。方法：自１９８１年１月至１９９５年５月间收治ＡＭＩ１０８０例，根据心电图ＳＴ段抬高形式分墓碑形组３３例，通常形组１０４７例进行多项指标对照分析。结果：墓碑形组ＳＴ段抬高的振幅为１５．８±１．４ｍｍ，通常组为７．６±１．１ｍｍ（Ｐ＜０．０１），血清肌酸激酶（ＣＫ）峰值两组分别为８７９±１４９ＩＵ／Ｌ及３６７±１１８ＩＵ／Ｌ（Ｐ＜０．０１），墓碑形组心肌梗死部位以前壁多见（Ｐ＜０．０５），心肌梗死后并发症以泵衰竭、心肌梗死后心绞痛、恶性心律失常及１周内病死率均明显增高（Ｐ＜０．０１）。结论：墓碑形ＳＴ段抬高是ＡＭＩ近期预后险恶的独立指标，应引起急诊和住院医师高度重视。     

血清肌钙蛋白Ⅰ浓度对急性心肌梗塞溶栓疗效的判定价值探讨

目的观察急性心肌梗塞（ＡＭＩ）患者接受静脉溶栓治疗时,血清肌钙蛋白Ⅰ（ｃＴｎⅠ）浓度变化,探讨其对溶栓疗效的判定价值。方法选择ＡＭＩ患者５３例,２６例接受溶栓治疗。采用ＯＰＵＳ自动生化分析仪,以ＥＬＩＳＡ法测定ｃＴｎⅠ浓度。结果显示：（１）从发病到达ｃＴｎⅠ峰值时间,２２例溶栓再通组（１５．７±３．９小时）比４例溶栓未通组（２２．０±２．３１小时）及２７例未溶栓组（２６．２±１１．１小时）均明显提前（Ｐ＜０．０５）。（２）血清ｃＴｎⅠ峰值水平在溶栓再通组（３２８．０±２４５．２μｇ／Ｌ）比溶栓未通组（１７０．５±５０．２μｇ／Ｌ）及未溶栓组（１３０．７３±１００．０３μｇ／Ｌ）明显增高（Ｐ＜０．０１）。（３）以ｃＴｎⅠ峰值到达时间≤１８小时判定ＡＭＩ后溶栓再通,其敏感性、准确性（分别为７２．７％和７３．１％）,均高于ＣＫ－ＭＢ≤１４小时（分别为６３．６％和６５．４％）,特异性二者相同（均为７５％）。结论血清ｃＴｎⅠ水平,在ＡＭＩ溶栓再通患者中峰值时间前移,其≤１８小时对ＡＭＩ溶栓再通具有一定的判定价值。     

缩短第一产程提高日间分娩率的前瞻性研究

作者对３８７例头位分娩初产妇进行缩短第一产程，施行日间分娩研究，其日间分娩率达９５．６１％，高于对照组的５８％（Ｐ〈０．０１）；第一产程３．１５±１．０６小时，较对照组的７．１４±４．２５小时明显缩短（Ｐ〈０．０１）；手术产率为１６．０２％，低于对照组的２９．５０％（Ｐ〈０．０１）；围产儿低Ａｐｇａｒ评分率１．８１％，低于对照组的７．５％（Ｐ〈０．０１）；研究组无围产儿死亡，对照组围产儿死亡率为１     

环孢菌素A和吡喹酮联合应用预防小鼠血吸虫性肝纤维化的研究

目的：观察环孢菌素Ａ和吡喹酮联合应用对小鼠血吸虫性肝纤维化的影响。方法：感染第５ｗｋ末给药，吡喹酮８００ｍｇ／ｋｇ１次喂服及环孢菌素Ａ３０ｍｇ／ｋｇ皮下注射，每日１次，连续５日。结果：联合用药组血清游离羟脯氨酸水平在９、１２、１５ｗｋ分别为７．９１±０．２１、９．０３±１．６６、９．６９±１．２３μｍｏｌ／Ｌ，显著低于单独应用吡喹酮组的１０．１３±１．４５、１１．２３±１．３４和１１．８９±１．６２μｍｏｌ／Ｌ（Ｐ＜０．０１或Ｐ＜０．０５）；第９ｗｋ时肝脏虫卵肉芽肿面积（１．０８×１０５μｍ２）和其中胶原纤维的百分含量（１８．９１％±７．８２％），分别显著小于单独应用吡喹酮组（１．７２×１０５μｍ２和２９．４１％±１３．０９％）（Ｐ均＜０．０５）。结论：联合用药组的肝脏纤维化程度较单独用吡喹酮者为轻。     

心脏肌钙蛋白T在急性心肌梗死中心的应用价值

目的 探讨血清肌钙蛋白Ｔ（ｃＴｎＴ）在急性心肌梗死（ＡＭＩ）后的释放特点及其对ＡＭＩ溶栓后的疗效判定。方法 采用酶联免疫法对２８例ＡＭＩ患者进行动态血清ｃＴｎＴ观察,同时测定ＣＫ及ＣＫ－ＭＢ。结果 溶栓２小时阳性率６７．９％、发病８小时至５天为１００％,发病７、９、１１、１３、１５、１７、１９天分别为９２．９％、８２．１％、６７．９％、６０．７％、３９．３％、２１．４％、７．１％。明显比ＣＫ和ＣＫ     

长期心肌缺血对急性心肌梗塞预后的影响

目的:探讨长期心肌缺血对急性心肌梗塞(AMI)临床表现与近期预后的影响.方法: 回顾性分析了596例心绞痛(AP)病程≥2周的AMI的临床资料,并与无AP史或AP<2周的患者比较.结果: AP组合并休克、心衰者少于对照组(分别为10.9% 比15.8%和19.8% 比25.0%,均P<0.05),住院病死率也较低(11.4% 比15.7%,P<0.05),AP组梗塞前正规治疗者多于对照组(58.4%比29.1%,P<0.001),患高血压者也较多(53.1% 比41.2%,P<0.001),但大面积梗塞较少,肌酸激酶峰值较低.结论: 长期心肌缺血可能也有缺血预适应作用,有益于AMI的近期预后.     

Seasonal Pattern of Acute Myocardial Infarction in the National Registry of Myocardial Infarction

Objectives. The purpose of this study was to determine whether the rate of hospital admission for acute myocardial infarction (AMI) varies seasonally in a large, prospective U.S. registry.

Background. Identification of specific patterns in the timing of the onset of AMI is of importance because it implies that there are triggers external to the atherosclerotic plaque. Using death certificate data, most investigators have noted a seasonal pattern to the death rate from AMI. However, it is unclear whether this observation is due to variation in the prevalence of AMI or to other factors that may alter the likelihood of a fatal outcome.

Methods. We examined the seasonal mean number of cases of AMI (adjusted for the length of days in each season) that were submitted to the National Registry of Myocardial Infarction (NRMI) by 138 high volume core hospitals over a 3-year period (December 21, 1990 through December 20, 1993) during which the number of hospitals participating in the Registry was stable. Data were analyzed using general linear modeling and analysis of variance.

Results. High volume core hospitals reported 83,541 cases of AMI to the Registry during the study period. Approximately 10% more such cases were entered into the Registry in winter or spring than in summer (p < 0.05). The same trends were seen in both northern and southern states, men and women, patients <70 versus ≥70 years of age and those with Q wave versus non-Q wave AMI.

Conclusions. We conclude that there is a seasonal pattern to the reporting rate of cases of AMI in the NRMI. This observation further supports the hypothesis that acute cardiovascular events may be triggered by events that are external to the atherosclerotic plaque.

(J Am Coll Cardiol 1996;28:1684–8)>     

长期心肌缺血对急性心肌梗塞预后的影响

目的 :探讨长期心肌缺血对急性心肌梗塞 (AMI)临床表现与近期预后的影响。方法 :　回顾性分析了 5 96例心绞痛 (AP)病程≥ 2周的 AMI的临床资料 ,并与无 AP史或 AP<2周的患者比较。结果 :　 AP组合并休克、心衰者少于对照组 (分别为 10 .9%比 15 .8%和 19.8%比 2 5 .0 % ,均 P<0 .0 5 ) ,住院病死率也较低 (11.4%比 15 .7% ,P<0 .0 5 ) ,AP组梗塞前正规治疗者多于对照组 (5 8.4%比 2 9.1% ,P<0 .0 0 1) ,患高血压者也较多(5 3.1%比 41.2 % ,P<0 .0 0 1) ,但大面积梗塞较少 ,肌酸激酶峰值较低。结论 :　长期心肌缺血可能也有缺血预适应作用 ,有益于 AMI的近期预后     

Seasonal Distribution of Acute Myocardial Infarction in the Second National Registry of Myocardial Infarction

Objectives. This observational study sought to determine whether cases of acute myocardial infarction (AMI) reported to the second National Registry of Myocardial Infarction (NRMI-2) varied by season.Background. The existence of circadian variation in the onset of AMI is well established. Examination of this periodicity has led to new insights into pathophysiologic triggers of atherosclerotic plaque rupture. Although a seasonal pattern for mortality from AMI has been previously noted, it remains unclear whether the occurrence of AMI also displays a seasonal rhythmicity. Documentation of such a pattern may foster investigation of new pathophysiologic determinants of plaque rupture and intracoronary thrombosis.Methods. We analyzed the number of cases of AMI reported to NRMI-2 by season during the period July 1, 1994 to July 31, 1996. Data were normalized so that seasonal occurrence of AMI was reported according to a standard 90-day length.Results. A total of 259,891 cases of AMI were analyzed during the study period. Approximately 53% more cases were reported in winter than during the summer. The same seasonal pattern (decreasing occurrence of reported cases from winter to fall to spring to summer) was seen in men and women, in different age groups and in 9 of 10 geographic areas. In-hospital case fatality rates for AMI also followed a seasonal pattern, with a peak of 9% in winter.Conclusions. The present results suggest that there is a seasonal pattern in the occurrence of AMIs reported to NRMI-2 that is characterized by a marked peak of cases in the winter months and a nadir in the summer months. This pattern was seen in all subgroups analyzed as well as in different geographic areas. These findings suggest that the chronobiology of seasonal variation in AMI may be affected by variables independent of climate.     

Methodologic and Clinical Validation of the TIMI Myocardial Perfusion Grade in Acute Myocardial Infarction

Improved microvascular perfusion using the TIMI myocardial perfusion grade (TMPG) has been related to reduced in hospital, 30-day and 2-year mortality following thrombolytic administration. We sought to validate this measure using the more quantitative technique of digital subtraction angiography (DSA) and to correlate TMPG with ST segment resolution. DSA was used to analyze films from the LIMIT AMI acute myocardial infarction trial of front loaded r-tPA and rhuMAb CD18. Dye kinetics were also characterized using DSA in 88 arteries from patients without acute coronary syndromes in the absence of an obstructive lesion. Compared to normal patients, microvascular perfusion was reduced in acute myocardial infarction patients on DSA as demonstrated by a reduction in peak Gray (brightness) (p < 0.0001), the rate of rise in Gray/sec (p < 0.0001), the blush circumference (p < 0.0001), and the rate of growth in circumference (cm/sec) (p < 0.0001). However, while DSA perfusion was impaired overall in the setting of acute myocardial infarction, TMPG grade 3 in the setting of acute myocardial infarction did not differ from that in normal patients when studied quantitatively as shown by similar rates of growth in brightness and circumference (p = NS). ST resolution and the TMPG were significantly associated (p = 0.04). Compared to normal patients, acute myocardial infarction reduces the peak brightness of the myocardium, the rate of rise in brightness, the circumference of blush and the rate of growth in circumference as assessed using digital subtraction angiography. However, acute myocardial infarction patients with TMPG 3 had rates of growth in brightness and circumference that were nearly identical to normal patients. Thus, DSA validates that TMPG 3 is associated with normal kinetics of myocardial perfusion, and this likely accounts for the low (0.7%) 30 day mortality observed among those patients with TFG 3 and TMPG 3.     

The Role of the Myocardial Microvasculature in Mental Stress–Induced Myocardial Ischemia

There is increasing evidence that mental stress can manifest as physical diseases. One such condition is mental stress–induced myocardial ischemia (MSIMI); a silent, transient, myocardial ischemic response to stressful conditions. We propose that the cardiac microvasculature may be an important site for the interplay between mental stress and MSIMI. This study is a review of the literature discussing the prevalence and emerging mechanisms underlying MSIMI. We identified several aspects underlying MSIMI, including psychological, genetic, and physiological causes. Several sources suggested that dysfunctional cardiac microvasculature might be a contributing factor in the development of stress‐induced myocardial ischemia. The literature also suggested that although MSIMI has distinct features and pathophysiology, its occurrence might indicate an increased future risk of cardiovascular events. We found that dysfunctional cardiac microvasculature may be the key point of interaction between mental stress and transient myocardial ischemia and that the development of MSIMI might be a “silent” indicator for future cardiac events.     

Inflammatory Alterations in the Myocardial Microcirculation

Inflammatory mechanisms are involved in the pathophysiology of cardiovascular disease and the present review focus us on the association between inflammation and microvascular endothelial dysfunction in the heart, i.e. reduced endothelium-dependent vasodilation of coronary resistance vessels. This abnormality is caused by reduced bioactivity of nitric oxide (NO), and it is found in a variety of conditions, including ischemic heart disease, cardiac allograft vasculopathy, diabetes, hypercholesterolemia, and smoking. At the level of the myocardial microcirculation, reperfusion injury manifests itself as endothelial dysfunction, no-reflow, and increased permeability, which are all probably the result of reperfusion-induced augmentation of the inflammatory response. In other animal models of cardiovascular disease, inflammatory alterations have been described that can contribute to microvascular endothelial dysfunction and reactive oxygen species, neutrophils, tumour necrosis factor-α, and inducible NO synthase are among the mediators that have been incriminated. Circulating levels of inflammatory mediators may serve as molecular markers of cardiovascular disease, and antiinflammatory interventions hold some promise for future cardiovascular therapy.     

Myocardial infarction in the diabetic patient

It has long been thought that the symptomatology and prognosis of coronary events in patients with diabetes may differ from those in nondiabetic persons. A review of recent data demonstrates a higher mortality during the acute phase of myocardial infarction for diabetic patients than for their nondiabetic counterparts, possibly related to a higher incidence of congestive heart failure and cardiogenic shock. The clinical course of diabetic patients with infarction and the role of insulin in myocardial adaptation to ischemia are both reviewed. Diabetic patients surviving the acute phase of myocardial infarction have a lower survival in follow-up than nondiabetic survivors, although some improvement in survival has been noted following beta-adrenergic-blocker therapy.