Rate of fibrinogen breakdown related to coronary patency and bleeding complications in patients with thrombolysis in acute myocardial infarction--results from the PRIMI trial.

Four hundred and one patients with acute myocardial infarction of less than 4 h duration were randomized to receive intravenous thrombolytic treatment with either 80 mg of full length unglycosylated single-chain-urokinase plasminogen activator (INN saruplase) or 1.5 million IU of streptokinase delivered over a 60 min period. Angiographic patency rates were higher at 60 min in saruplase treated patients (71.8% vs 48%; P less than 0.001), but did not differ significantly at 90 min (71.2% vs 63.9%; P = 0.15). Fibrinogen levels dropped markedly in both groups, the decrease being delayed and less pronounced with saruplase. Total fibrin and fibrinogen degradation products and D-dimer values rose earlier and to higher peak values in streptokinase treated patients. In both groups marked plasminogen and alpha 2-antiplasmin consumption was observed. Lower fibrinogen levels, and in particular the faster rate of fibrinogen breakdown, were associated with higher patency rates at 90 min (P less than 0.05). Patients with bleeding complications had lower 'lowest points' and a more rapid decrease in fibrinogen (P less than 0.05). These findings were not related to the drug used. Increased heparin levels at 6 to 12 h were correlated to bleeding complications in streptokinase treated patients. It is concluded that the rate of fibrinogen breakdown during and following thrombolytic treatment for acute myocardial infarction is related to early vessel patency and bleeding complications.     

Efficacy and safety of low-dose streptokinase plus desmopressin in acute myocardial infarction: A pilot study

In this pilot study the combined use of desmopressin, which releases tissue plasminogen activator from vascular endothelium, and a low dose of streptokinase as a new thrombolytic regimen for acute myocardial infarction is proposed. Eighteen patients with acute myocardial infarction were treated intravenously with 150,000 U (4 patients) or 250,000 U (14 patients) of streptokinase infused over 10 minutes, followed by 24 g of desmopressin infused over 5–10 minutes. Aspirin and beta-blockers were administered at admission, and heparin and oral anticoagulants were started at the end of the thrombolytic regimen. Hemostatic parameters were studied before and 30, 60, 120, and 240 minutes after starting thrombolytic therapy. Fifteen patients (83.3%) had evidence of clinical reperfusion. Angiography was performed with a mean delay of 8.8 hours (range 1.5–22 hours) from the start of thrombolytic therapy. Fourteen patients (77.8%) had patency of the infarct-related artery: 10 patients (55.6%) achieved TIMI grade 3, and 4 patients (22%) achieved TIMI grade 2. Two patients (one TIMI grade 1 and one TIMI grade 2) underwent coronary angioplasty. No patient died during the in-hospital period. At 18 months follow-up, all patients are alive. No major or minor bleeding was detected. The significant decline in plasma fibrinogen and in the euglobulin lysis time, and the increase in fibrinogen/fibrin degradation products, indicate a plasma lytic state. Crosslinked fibrin degradation products increased from 310±120 ng/ml to 670 ±310 ng/ml (p=0.009), suggesting that fibrin digestion occurred in vivo. This pilot study provides data supporting the feasibility and efficacy of a new and more economic thrombolytic treatment of acute myocardial infarction without hemorrhagic complications.     

The incidence and mechanism of hypotension following thrombolytic therapy for acute myocardixal infarction with streptokinase-containing agents -- lack of relationship to pretreatment streptokinase resistance

The incidence, amplitude, mechanism and relationship to priorexposure to streptococcal antigen of bloodpressure changes tostreptokinase-containing thrombolytic agents were investigatedin 125 patients treated with either 15 x 10⁶ IU streptokinaseover 60 min or 30 U anistreplase over 5 min, within 6 h of onsetof acute myocardial infarction. Twenty-one of 52 patients withanterior and 34 of 73 with inferior myocardial infarction hada hypotensive response. There were no signficant differencesin the incidence, duration or amplitude of hypotension betweenthe two treatment groups. The maximum mean fall in systolicblood pressure was 16.9 mmHg (95% confidence limits, CL 12.2to 24.5 mmHg), and the maximum mean fall in diastolic bloodpressure was 13.7 mmHg (CL 10.3 to 17.1 mmHg), starting 4 minafter start of therapy and resolving within 34 min. Blood pressurechanges were well tolerated. Hypotension was not related topretreatment streptokinase resistance titre, or anti-SK IgGconcentration, to changes in plasma fibrinogen, B-ß15–42 peptide, D-dimer—as indices of thrombin activationand fibrin (-ogen) breakdown — to plasma viscosity. The blood pressure changes following treatment with streptokinase-containingthrombolytic agents in acute myocardial infarction are frequentbut well tolerated. The mechanism of hypotension remains unclear,but is not related to prior exposure to streptococcal antigen.     

溶栓治疗对急性心肌梗死者纤维蛋白溶解指标的影响

目的 研究急性心肌梗死(AMI)患者溶栓治疗过程中,血浆纤维蛋白溶解系统各指标的变化.方法 首次AMI者26例,男性17例、女性9例,给予尿激酶150万单位(U)溶栓治疗,测定溶栓前、及溶栓后0.5、6、12、24、72小时的血浆总体纤维蛋白溶解活力(GFC)、纤维蛋白原(Fg)、纤维蛋白溶解酶原(PLG)、组织型纤维蛋白溶解酶原激活因子(t-PA)及其抑制因子(PAI)水平.结果(1)血浆Fg、PLG浓度在尿激酶静脉注射后6小时显著降低至治疗前的50%,在24～72小时又逐渐回升至治疗前水平,72小时Fg浓度超过治疗前(P<0.05);血浆GFC、PAI则在治疗后0.5小时立即升高至峰值水平,在6～72小时迅速下降甚至低于治疗前水平(P<0.05);而t-PA水平在治疗后有所升高但变化无显著差异(P>0.05).(2)溶栓治疗后临床再灌注与无再灌注组血浆GFC的峰值水平及时间存在显著差异(P<0.05).结论 血浆GFC水平比其他指标更能揭示纤维蛋白溶解药物对体内纤维蛋白溶解系统的作用机制,溶栓治疗后血浆总体纤维蛋白溶解活力被激活的程度及时间是决定临床再灌注的重要因素.     

Thrombolytic therapy is indicated for patients over 75 years of age with st-elevation acute myocardial infarction: protagonist viewpoint

Although the benefits of thrombolytic therapy are well established in patients younger than age 75 years with acute ST-elevation myocardial infarction, the value of thrombolytic treatment in patients 75 years of age or older remains controversial. This is due in part to conflicting data from clinical trials and observational studies and in part because of concerns about increased risk for major bleeding complications in the very elderly, particularly intracranial hemorrhage. However, in a recent meta-analysis based on data from 3322 patients aged 75 years or older presenting with ST-elevation myocardial infarction within 6 hours of symptom onset, thrombolytic therapy was associated with an absolute mortality reduction of 3.4% (26.0% vs. 29.4%), an effect similar to that seen in younger patients. In addition, although the risk of stroke increased with age, the absolute excess risk of stroke in patients older than age 75 years receiving thrombolytic treatment was <1%, and there was no age-associated excess in the risk of other major bleeding complications. These findings indicate that thrombolytic therapy is beneficial in carefully selected elderly patients with acute myocardial infarction and that the risk of major adverse events is acceptably low.     

基层医院急性心肌梗死早期溶栓治疗104例观察

目的观察基层医院对急性心肌梗死（AMI）患者在无条件做急诊冠状动脉介入治疗时，早期溶栓治疗的临床疗效。方法对发病3h内符合溶栓条件的104例AMI患者实施瑞替普酶（Reteplase）溶栓治疗。溶栓前查血常规、血小板计数、出凝血时间、血型、心肌酶谱及心电图，给予吸氧、镇静、止痛、心电监护。溶栓前口服阿司匹林300mg，静脉推注肝素5000IU，然后2min内静脉推注瑞替普酶10MU，间隔30min再静脉推注10MU。第1次静脉推注肝素1h后开始静脉点滴肝素700-1000IU／h，持续24-48h。结果104例AMI患者中有94例溶栓后符合冠状动脉再通指标，可判断为再通，再通率为90．4％。住院死亡7例（6．7％），脑出血1例（0．96％），消化道出血3例（2．9％），牙龈出血17例（16．3％）。结论基层医院对AMI患者在无条件做急诊冠状动脉介入治疗时早期溶栓治疗疗效显著。     

急性心肌梗死患者溶栓治疗的观察与护理

目的探讨对急性心肌梗死患者溶栓治疗的观察与护理体会。方法对我院2008年1—12月收治的68例AMI患者进行护理干预,重点在溶栓治疗前做好准备工作,强调心理和饮食注意事项;治疗过程中密切观察病情,严格各项技能操作;治疗后积极预防出血、再灌注心律失常、低血压等并发症,并给予康复指导。结果本组患者治疗顺利,静脉再通率为72．8％,均无严重并发症发生,痊愈出院。结论积极有效的护理可以提高急性心肌梗死患者溶栓治疗的临床效果。     

Correlation of baseline plasminogen activator inhibitor activity with patency of the infarct artery after thrombolytic therapy in acute myocardial infarction

Increased levels of plasminogen activator inhibitor (PAI) have recently been described in patients with acute myocardial infarction (AMI). To correlate PAI levels to patency of infarct arteries after thrombolytic therapy with recombinant tissue-type plasminogen activator (rt-PA), 125 consecutive patients with AMI were examined. Blood levels of fibrinogen, plasminogen, tissue plasminogen activator (t-PA) and PAI were measured before treatment initiation, 10 minutes after completion of rt-PA infusion and 24 and 48 hours after treatment. Coronary angiography, performed in all patients 72 hours after beginning rt-PA infusion, revealed patent infarct arteries in 97 patients and occluded infarct arteries in 28 patients. Pretreatment levels of PAI were significantly higher in patients with occluded infarct arteries (18.0 +/- 11.5 vs 10.5 +/- 9.3 IU/ml, p less than 0.01). Conceivably, higher levels of PAI may interfere with the natural thrombolytic process and make pharmacologic thrombolytic intervention less effective.     

Diabetic Retinopathy Should Not Be a Contraindication to Thrombolytic Therapy for Acute Myocardial Infarction: Review of Ocular Hemorrhage Incidence and Location in the GUSTO-I Trial

Objectives. This study sought to evaluate the incidence of ocular hemorrhage in patients with and without diabetes after thrombolytic therapy for acute myocardial infarction.

Background. Ocular hemorrhage after thrombolysis has been reported rarely. However, there is concern that the risk is increased in patients with diabetes. In fact, diabetic hemorrhagic retinopathy has been identified as a contraindication to thrombolytic therapy without clear evidence that these patients have an increased risk for ocular hemorrhage.

Methods. We identified all suspected ocular hemorrhages from bleeding complications reported in patients enrolled in the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (GUSTO)-I trial. Additional information was collected on a one-page data form. We compared the incidence and location of ocular hemorrhages in patients with and without diabetes.

Results. There were 40,899 patients (99.7%) with information about diabetic history and ocular bleeding. Twelve patients (0.03%) had an ocular hemorrhage. Intraocular hemorrhage was confirmed in only one patient. There were 6,011 patients (15%) with diabetes, of whom only 1 had an ocular hemorrhage (eyelid hematoma after a documented fall). The upper 95% confidence intervals for the incidence of intraocular hemorrhage in patients with and without diabetes were 0.05% and 0.006%, respectively.

Conclusions. Ocular hemorrhage and, more important, intraocular hemorrhage after thrombolytic therapy for acute myocardial infarction is extremely uncommon. The calculated upper 95% confidence interval for the incidence of intraocular hemorrhage in patients with diabetes was only 0.05%. We conclude that diabetic retinopathy should not be considered a contraindication to thrombolysis in patients with an acute myocardial infarction.     

Platelet glycoprotein IIb/IIIa inhibitor therapy in non-ST segment elevation acute coronary syndromes

Platelet glycoprotein (GP) IIb/IIIa inhibitors prevent fibrinogen binding and platelet aggregation. They decrease ischemic complications associated with non-ST segment elevation acute coronary syndromes and percutaneous coronary intervention. Meta-analyses of 6 randomized trials of parenteral GP IIb/IIIa inhibitors in patients with acute coronary syndromes suggest a significant reduction in death and myocardial infarction in high risk patients. These include patients undergoing early percutaneous coronary intervention or those with high TIMI risk score, elevated troponin values, or diabetes mellitus. Despite guideline recommendations supporting therapy for these indications, only a minority of appropriate candidates are being treated. The risk of major bleeding is small; thrombocytopenia can result from abciximab therapy. Optimal dosing strategies continue to evolve.     

Randomized,Double-Blind Study Comparing Saruplase With Streptokinase Therapy in Acute Myocardial Infarction: The COMPASS Equivalence Trial

Objectives. This study sought to demonstrate the equivalence of saruplase and streptokinase in terms of 30-day mortality.Background. The use of thrombolytic agents in the treatment of acute myocardial infarction is well established and has been shown to substantially reduce post-myocardial infarction mortality.Methods. Three thousand eighty-nine patients with symptoms compatible with those of acute myocardial infarction for <6 h entered the study at a total of 104 centers and were randomized to receive streptokinase (1.5-MU infusion over 60 min) or saruplase (20-mg bolus and 60-mg infusion over 60 min). In the saruplase group, a bolus of heparin (5,000 IU) was administered before saruplase, and a corresponding blinded double-dummy placebo bolus was administered before streptokinase. All patients received intravenous heparin infusions for ≥24 h starting 30 min after the end of the thrombolytic infusions; the infusions were titrated to maintain an activated partial thromboplastin time at 1.5 to 2.5 times that of normal.Results. Death of any cause up to 30 days after randomization occurred in 88 (5.7%) of 1,542 patients randomized to receive saruplase and 104 (6.7%) of 1,547 patients randomized to receive streptokinase (odds ratio 0.84, p < 0.01 for equivalence). Hemorrhagic strokes occurred more often in patients receiving saruplase (0.9% vs. 0.3%), whereas thromboembolic strokes were more prevalent in the streptokinase-treated patients (0.5% vs. 1.0%). The rate of bleeding was similar in the two treatment groups (10.4% vs. 10.9%). Hypotension and cardiogenic shock occurred less frequently in the saruplase group. Reinfarction rates were similar.Conclusions. Saruplase is a clinically safe and effective thrombolytic medication. This profile ranks saruplase favorably among the currently available thrombolytic agents.     

New-onset angina preceding acute myocardial infarction is associated with improved contractile recovery after thrombolysis

Background Ischaemic preconditioning reduces myocardial infarct size inanimal models. Clinical data suggest that episodes of anginaimmediately before acute myocardial infarction may be associatedwith smaller infarct size in man. However, it is unclear whetherischaemic episodes preceding acute myocardial infarction alsoaffect contractile recovery in patients. Objective In this study we investigated the recovery of regional myocardialfunction after thrombolysis in two groups of patients at theirfirst Q-wave acute myocardial infarction; in one group (n=42)myocardial infarction occurred unheralded, whereas patientsof the second group (n=48) had experienced new-onset anginain the 48h that preceded infarction. Echocardiographic analysisof myocardial regional function in the infarct area was doneat 2, 24 and 72h after thrombolysis, and at 1 week, and 1 and3 months follow-up. Results Peak level of MB-creatine kinase was significantly lower inpatients with new-onset angina (96±47 as compared with221±108IU.l^–1, P<0·01), as was the areaunder the MB-creatine kinase curve (1321±876 as comparedto 3879±1555U.l^–1/36h, P<0·01). Hypokineticsegments were fewer in patients with pre-infarction angina.Similarly, wall motion score improved significantly earlierin patients who had new-onset angina before acute myocardialinfarction. Thus, contractile recovery was more rapid in patientswith previous angina than in those in whom infarction occurredunheralded. Complications during the in-hospital outcome andother variables considered during the 4-week follow-up weresimilar between groups. Conclusions Patients who experienced new-onset angina before acute myocardialinfarction showed better recovery of regional function afterthrombolysis. Our study supports the hypothesis that brief periodsof ischaemia immediately before myocardial infarction may preconditionthe human heart, thus improving contractile recovery.     

Thrombolysis in Myocardial Infarction (TIMI) Trial, Phase I: A comparison between intravenous tissue plasminogen activator and intravenous streptokinase. Clinical findings through hospital discharge

Intravenous administration of 80 mg of recombinant tissue plasminogen activator (rt-PA, 40, 20, and 20 mg in successive hours) and streptokinase (SK, 1.5 million units over 1 hr) was compared in a double-blind, randomized trial in 290 patients with evolving acute myocardial infarction. These patients entered the trial within 7 hr of the onset of symptoms and underwent baseline coronary arteriography before thrombolytic therapy was instituted. Ninety minutes after the start of thrombolytic therapy, occluded infarct-related arteries had opened in 62% of 113 patients in the rt-PA and 31% of 119 patients in the SK group (p less than .001). Twice as many occluded infarct-related arteries opened after rt-PA compared with SK at the time of each of seven angiograms obtained during the first 90 min after commencing thrombolytic therapy. Regardless of the time from onset of symptoms to treatment, more arteries were opened after rt-PA than SK. The reduction in circulating fibrinogen and plasminogen and the increase in circulating fibrin split products at 3 and 24 hr were significantly less in patients treated with rt-PA than in those treated with SK (p less than .001). The occurrence of bleeding events, administration of blood transfusions, and reocclusion of the infarct-related artery was comparable in the two groups. Thus, in patients with acute myocardial infarction, rt-PA elicited reperfusion in twice as many occluded infarct-related arteries as compared with SK at each of seven serial observations during the first 90 min after onset of treatment.     

Influence of heparin on fibrinogen and D-dimer plasma levels in acute myocardial infarction treated with streptokinase

The purpose of this study was to investigate whether, to whatextent, and through which mechanisms intravenous heparin, administeredbefore and after streptokinase, affects the plasma levels ofD-dimer and fibrinogen in myocardial infarction. Data concerningmortality and incidence of coronary recanalization in patientsreceiving heparin and thrombolytic therapy after acute myocardialinfarction are controversial; furthermore, the mechanisms throughwhich heparin acts in combination with thrombolytic therapyare unclear. Thirty-eight patients with acute myocardial infarctiontreated with streptokinase were considered. Nineteen of themreceived, immediately before the beginning of thrombolytic treatment,a bolus of heparin (100 U. kg¹ intravenously) and, 2 h later,intravenous heparin in doses raising the partial thromboplastintime to 2-2.5 times the normal value (Group 1); the remaining19 did not receive anticoagulant treatment (Group 2). Multipledeterminations of plasma D-dimer and fibrinogen levels wereobtained in all patients before, and in the seven days followingthrombolytic treatment. Six hours after streptokinase, fibrinogendecreased from 304 ± 34 to 61 ± 34 mg. dt¹ inGroup 1 and from 312 ± 29 to 38 ±21 mg. dt¹ inGroup 2 (P<002 versus Group 1). The same difference betweengroups persisted at the 12th and at the 18th hour. D-dimer values,from 0-5 ± 01 \ig. dl¹ in Group 1 and 04 ±01 fig.dt¹ in Group 2, increased at the 1st hour to 37.2 ± 36.5fig. dt¹ and 52.2 ± 39.8 µg. dl¹, respectively.A peak value was reached in both groups at the 6th hour, whichwas followed by a slow decrease. A significant difference betweenthe two groups (P<0.05) was observed at the 1st, 2nd, 4thand 6th hour. An inverse correlation between maximal changesof fibrinogen and of D-dimer was found in both groups (r= 0.89,P<0.001 in Group 1; r=-0.81, P<0.001 in Group 2). The relationship between D-dimer and fibrinogen variations afterstreptokinase and changes induced by heparin, support the hypothesisthat the decrease of fibrinogen, following thrombolysis, isnot only the consequence of its direct degradation, but alsothe result of its transformation by streptokinase into fibrin,fibrin cross-linked (with facilitation of thrombogenic condition)and then into the stable catabolite, D-dimer. These data confirma thrombogenic effect of streptokinase therapy; this tendencycan be limited by prompt use of high doses of heparin.     

Intracranial hemorrhage in association with thrombolytic therapy: incidence and clinical predictive factors.

In a period of 18 months, 2,469 patients with acute myocardial infarction treated with a thrombolytic agent were prospectively registered in 61 hospitals. Most patients (73%) were treated with streptokinase. Intracranial hemorrhage was observed in 24 patients, corresponding to an incidence rate of 1% (95% confidence interval 0.6% to 1.3%). The median time interval between the start of thrombolytic therapy and the first clinical signs of intracranial bleeding was 16 h (range 3 to 36). In total, 16 (66%) of the 24 patients died as a result of cerebral hematoma. To determine clinical predictive factors, a case-control study was conducted. For every patient with intracranial hemorrhage, two control patients who received thrombolytic therapy because of acute infarction in the same hospital and in the same period were selected. Detailed clinical characteristics of 22 of the 24 patients as well as of 7 other patients with documented intracerebral bleeding from the European Cooperative Study Group and of 2 patients who sustained intracranial hemorrhage outside the registry period were compared with 62 control patients. The results of multivariate logistic regression analysis indicate that patients taking an oral anticoagulant before admission, patients with a body weight less than 70 kg and those greater than 65 years old are at higher risk for intracranial hemorrhage during thrombolytic therapy.     

Role of heparin after intravenous thrombolytic therapy for acute myocardial infarction

The optimal approach to management of patients after thrombolytic therapy for acute myocardial infarction (AMI) is unclear. The role of anticoagulation with heparin was evaluated in 75 consecutive patients who received intravenous streptokinase for AMI. Heparin therapy was titrated to keep the partial thromboplastin time (PTT) between 90 and 120 seconds. Seventeen episodes of definite myocardial ischemia (associated with reversible electrocardiographic changes) were observed in 13 patients. When episodes of probable myocardial ischemia are included (typical chest pain relieved by nitroglycerin or associated with more than a 15-mm Hg change in blood pressure but without electrocardiographic changes), 52 episodes occurred in 28 patients. Four episodes of definite and 4 of probable myocardial ischemia occurred within 24 hours of discontinuation of heparin. Analysis of the level of anticoagulation as assessed by PTT at the time of the ischemic events shows that ischemia occurred more often at lower PTTs. Nine hemorrhagic complications occurred, all within 24 hours of streptokinase infusion. In 4 patients bleeding was believed to be major and heparin administration was discontinued; 2 patients with gastrointestinal bleeding required blood transfusions. Our data suggest that after thrombolytic therapy for AMI, the level of anticoagulation is inversely related to the frequency of recurrent ischemic events; that discontinuation of heparin is frequently associated with ischemia; and that administration of heparin is associated with a low incidence of hemorrhagic complications.     

Elevated serum D dimer: a degradation product of cross-linked fibrin (XDP) after intravenous streptokinase during acute myocardial infarction

D dimer, a degradation product of cross-linked fibrin, is generated by lysis of fibrin but not by lysis of fibrinogen and can be reliably detected by specific monoclonal antibody techniques. The generation of D dimer after intravenous streptokinase in acute myocardial infarction was studied with the use of a semiquantitative latex agglutination immunoassay. This assay utilizes the monoclonal antibody DD-3B6/22, raised by conventional hybridoma technology, against a highly purified preparation of human D dimer and is adjusted to give a positive agglutination at a D dimer serum concentration of greater than 200 ng/ml (upper limit of normal). Twenty-one patients with acute transmural myocardial infarction of less than 3 hours' duration were studied. Fifteen patients received 0.75 to 1.5 million U intravenous streptokinase and 6 patients were treated conventionally without thrombolytic therapy. An elevated serum level of D dimer was detected before treatment in only 1 of 15 patients receiving intravenous streptokinase and within 2 hours of treatment in the remaining 14 patients who received streptokinase. In contrast, an elevated serum D dimer level was not detected during the first 24 hours in any of the six conventionally treated patients, including two patients who manifested the clinical syndrome of spontaneous reperfusion. The data suggest that in patients with acute myocardial infarction, an elevated serum level of D dimer, a cross-linked fibrin degradation product occurs early after administration of a large dose of streptokinase, but is infrequent during the first 24 hours in conventionally treated patients with acute infarction. Measurement of D dimer may be potentially useful for monitoring thrombolysis in patients with acute myocardial infarction.     

Prognostic value of plasma C-reactive protein and fibrinogen determinations in patients with acute myocardial infarction treated with thrombolysis

OBJECTIVES: To investigate the prognostic value of plasma C-reactive protein (CRP) and fibrinogen determinations in patients with acute myocardial infarction treated with thrombolysis. DESIGN: Longitudinal study of morbidity and mortality. SETTING: Coronary care unit at Danderyd Hospital, Stockholm, Sweden. SUBJECTS: A total of 222 patients aged 75 years or below, treated with thrombolysis because of typical symptoms of myocardial infarction and electrocardiogram showing ST-segment elevation or bundle branch block were included in the study. The patients were followed for 24-60 months (mean 40 +/- 16 months). MAIN OUTCOME MEASURES: Cardiovascular death or new myocardial infarction. RESULTS: Concentrations of CRP were significantly higher at 48 h than at 3 months, whilst the levels of fibrinogen were similar. CRP and fibrinogen concentrations measured during the acute phase of myocardial infarction were associated with cardiovascular death or a new myocardial infarction during follow-up in univariate analysis. CRP levels measured 3 months after the acute event were not associated with subsequent events whereas fibrinogen concentrations showed a borderline prognostic significance (P = 0.05). When CRP and fibrinogen were entered into multivariate analysis together with the previously established prognostic factors in the patient group (age, diabetes mellitus and left ventricular function), these markers of inflammation did not add further prognostic information. CONCLUSION: C-reactive protein and fibrinogen do not carry the same independent prognostic information after acute myocardial infarction treated with thrombolysis as in studies previously reported for patients with unstable angina or non-Q-wave myocardial infarction.     

Thromboembolic complications of percutaneous transluminal coronary angioplasty for myocardial infarction

To determine the incidence of thromboembolic complications of percutaneous transluminal coronary angioplasty (PTCA) in the setting of recent and acute myocardial infarction, the clinical sequelae and coronary angiographic findings were examined in a series of 13 patients who underwent PTCA either as acute intervention during the infarction or as treatment for recurrent myocardial ischemia that occurred soon after the initial completed infarction. In all cases, the angiographic appearance in the infarct-related artery was that of thrombus in the setting of total or subtotal occlusion. Balloon dilatation without antecedent thrombolytic therapy, was performed in 14 arteries and was successful in establishing reperfusion with reduction of the degree of intraluminal narrowing to less than 50% in all cases. Residual thrombus at the site of inflation was noted in two cases (15%), and embolization was noted in four cases (29%), for an incidence of complication of 44%. In five of six instances in which either residual thrombus or embolization were noted, the initial infarction had occurred greater than 24 h before. In only one of seven cases in which PTCA was used as acute intervention during infarction of less than 4 h duration was the presence of residual thrombus noted after PTCA. Therefore, these findings suggest that thromboembolic complications after PTCA in the setting of recent or acute myocardial infarction are uncommon when the syndrome is less than 4 h duration; however, complications are relatively frequent when infarction has occurred greater than 24 h before. PTCA as a primary intervention in this latter setting should be approached cautiously.     

急性心肌梗死患者溶栓前后患者血浆中NO、vWF的动态观察

目的　探讨急性心肌梗死 (AMI)溶栓前后患者血浆中NO、vWF的动态变化及其临床意义。方法　对 4 1例AMI溶栓前及溶栓后 2h、2 4h分别采血 ,测取血浆中NO及vWF的含量 ,并进行统计学处理比较。结果　 2 4例溶栓再通后2h ,患者血浆中NO显著降低 ,P <0 0 1,vWF无明显变化 >0 0 5 ;2 4h ,患者血浆中NO显著增高 ,P >0 0 1,vWF显著降低 ,P <0 0 1;而未再通组溶栓后 2h、2 4hNO及vWF的含量均无显著差异P >0 0 5。结论　AMI溶栓再通患者血浆中NO明显增高 ,vWF明显下降 ;溶栓后无再通患者血浆中NO和vWF无明显变化