[Early intravenous thrombolysis with recombinant tissue plasminogen activator for acute cerebral infarction]. [Randomized controlled clinical trial of a home care unit intervention to reduce readmission and death rates in patients discharged from hospital following admission for heart failure]. Intravenous heparin for the prevention of stroke progression in acute partial stable stroke. Reduction in sudden deaths by a multifactorial intervention programme after acute myocardial infarction. A controlled clinical trial of streptokinase and heparin in the treatment of major pulmonary embolism. A comparison of thrombolytic therapy with operative revascularization in the initial treatment of acute peripheral arterial ischemia. A comparison of six weeks with six months of oral anticoagulant therapy after a first episode of venous thromboembolism. Duration of Anticoagulation Trial Study Group. A randomized controlled study of peripheral parenteral nutrition in moderate and severe alcoholic hepatitis. Early changes in coagulation following a paracetamol overdose and a controlled trial of fresh frozen plasma therapy.
To evaluate the efficacy and safety of recombinant tissue plasminogen activator (rt-PA) and to explore the most suitable dosage of rt-PA in the early treatment of the Chinese patients with acute cerebral infarction (ACI).
                The patients who suited for the standard were divided into three groups. Group A received rt-PA at 0.9 mg/kg, group B received rt-PA at 0.7 mg/kg, and group C did not receive any thrombolytic therapy. In thrombolytic groups, rt-PA at 8 mg was injected intravenously in a bolus at first and then the rest was given over 60 minutes. The maximal dosage was 90 mg. The Chinese stroke scale (CSS) and Barthel Index (BI) were used to evaluate the recovery of neurological functions after rt-PA treatment for 24 hours and 90 days. The hemorrhagic rate and 30 days mortality rate were also analysed.
                In group A the CSS significant effective rate was 41.18 percent at 24 hours and 76.47 percent at 90 days after thrombolysis. At 90 days BI significant effective rate was 58.82 percent. At 30 days hemorrhagic rate was 8.82 percent and mortality rate was 5.88 percent. In group B, the CSS significant effective rate was 39.39 percent at 24 hours and 69.70 percent at 90 days. At 90 days, BI significant effective rate was 54.55 percent, and at 30 days, hemorrhagic rate was 9.09 percent and mortality rate was 9.09 percent. In group C, the CSS significant effective rate was 21.21 percent, at 24 hours and 30.30 percent at 90 days (P>0.05). At 90 days, BI was 21.21 percent the mortality rate was 9.09 percent. At 30 days the mortality rate was no significant difference within three groups At 90 days, significant effective rate was 73.13 percent vs. 30.30 percent in thrombolytic and control groups (P=0.001 7). The significant disability rate was 13.43 percent vs. 24.24 percent.
                For Chinese individuals, with ACI, rt-PA thrombolysis was effective and safe. The dosage of 0.9 mg/kg for foreign people also fitted for Chinese individuals. To determine the effectiveness of a primarily educational intervention in heart failure (HF) patients implemented in a home care unit.
                This randomized controlled clinical trial involved 279 HF patients who were discharged from a tertiary-care hospital between February 2001 and June 2002. Patients with dementia, terminal non-cardiac disease, or chronic obstructive pulmonary disease were excluded. Data collected included the cause of cardiac decompensation. A primarily educational intervention was implemented in the patient's home for up to 15 days after hospital discharge. Treatment was adjusted during the first week if necessary. The primary outcome measure was the 1-year cumulative incidence of readmission or death. Secondary measures were the incidence of readmission, mortality, and emergency department admission. Telephone interviews were carried out 3, 6 and 12 months after discharge, and clinical records were updated when necessary. Emergency department admission in the first 6 months was monitored.
                At 1-year follow-up, 62 of the 137 patients (45.3%) in the intervention group had been readmitted or died, compared with 75 of the 142 (52.8%) in the control group, (relative risk=0.86, P=.232). Among patients who suffered decompensation because failure to adhere to treatment, 16 of the 45 (35.6%) in the intervention group were readmitted or died, compared with 34 of the 56 (60.7%) control group patients (relative risk=0.59, P=.016).
                This intervention is feasible but, when applied indiscriminately to every discharged heart failure patient, the best that can be expected is only a modest reduction in readmission and death rates, which, in this study in particular, did not achieve statistical significance. In a double-blind, placebo-controlled trial, 225 patients with acute partial stable thrombotic stroke were randomly assigned to receive continuous intravenous heparin therapy or placebo for 7 days for the prevention of stroke progression or death. No statistically significant difference between the two groups was found in degree of neurologic change; incidence of stroke progression after 7 days; or functional activity level of survivors at 7 days, 3 months and at 1 year after treatment. Compared with controls, a statistically significant greater number of patients in the group receiving heparin died in the year after the stroke. These deaths occurred 3 to 12 months after the initial stroke and probably were not related to treatment. Results of this study do not support the use of intravenous heparin to treat patients who have had acute partial stroke. 375 consecutive patients below 65 years who had an acute myocardial infarction (AMI) took part in a randomised rehabilitation and secondary prevention trial (part of a W.H.O.-coordinated project) designed to study the effects of a multifactorial intervention programme on morbidity, mortality, return to work, &c. After three years' follow-up the cumulative coronary mortality was significantly smaller in the intervention group than in the controls (18.6% versus 29.4%, p = 0.02). This difference was mainly due to a reduction of sudden deaths in the intervention group (5.8% versus 14.4%, p less than 0.01). The reduction was greatest during the first six months after AMI. 18.1% in the intervention group and 11.2% in the controls (p less than 0.10) presented with non-fatal reinfarctions. The number of patients with new Q-QS findings at the end of the three years was, however, almost the same in both groups. The results suggest that organised aftercare during the first six months after AMI with special emphasis on optimum medical control and health education contributes significantly to a reduction in the number of sudden deaths. Treatment with streptokinase or heparin was allocated randomly to 20 patients with major pulmonary embolism verified by angiography. In addition, 4 patients treated with streptokinase and 1 patient treated with heparin were included in the trial prior to the start of treatment. Streptokinase of heparin was given for 72 hours and pulmonary angiography was repeated. The angiographic evidence of thrombolysis was significantly greater (p less than 0.01) in the 14 patients treated with streptokinase than in the 11 treated with heparin. In the heparin group, 1 patient died from massive embolism 15 hours after the start of treatment. In another patient who died 4 weeks later from cerebral glibolastoma, persistent massive embolism contributed to the fatal outcome. In the streptokinase group, 1 patient with a metastatic pulmonary carcinoma died 3 weeks after the start of treatment from gangrene of both legs following thrombotic occlusion of the inferior vena cava. Bleeding was more common after treatment with streptokinase than with heparin, but was not a serious problem in any patient. It is concluded that patients with life-threatening pulmonary embolism should be offered the benefits of streptokinase. Despite the widespread use of intraarterial thrombolytic therapy for peripheral arterial occlusive disease, a randomized study comparing its efficacy with that of operative intervention has never been performed. This study evaluates the potential of intraarterial urokinase infusion to provide clinical benefits in patients with acute peripheral arterial occlusion.
                Patients with limb-threatening ischemia of less than 7 days' duration were randomly assigned to intraarterial catheter-directed urokinase therapy or operative intervention. Anatomic lesions unmasked by thrombolysis were treated with balloon dilation or operation. The primary end points of the study were limb salvage and survival.
                A total of 57 patients were randomized to the thrombolytic therapy group, and 57 patients were randomized to the operative therapy group. Thrombolytic therapy resulted in dissolution of the occluding thrombus in 40 (70%) patients. Although the cumulative limb salvage rate was similar in the two treatment groups (82% at 12 months), the cumulative survival rate was significantly improved in patients randomized to the thrombolysis group (84% vs 58% at 12 months, p = 0.01). The mortality differences seemed to be primarily attributable to an increased frequency of in-hospital cardiopulmonary complications in the operative treatment group (49% vs 16%, p = 0.001). The benefits of thrombolysis were achieved without significant differences in the duration of hospitalization (median 11 days) and with only modest increases in hospital cost in the thrombolytic treatment arm (median $15,672 vs $12,253, p = 0.02).
                Intraarterial thrombolytic therapy was associated with a reduction in the incidence of in-hospital cardiopulmonary complications and a corresponding increase in patient survival rates. These benefits were achieved without an appreciable increase in the duration of hospitalization and with only modest increases in hospital cost, suggesting that thrombolytic therapy may offer a safe and effective alternative to operation in the initial treatment of patients diagnosed with acute limb-threatening peripheral arterial occlusion. The optimal duration of oral anticoagulant therapy after a first episode of venous thromboembolism is still a matter of debate.
                We performed a multicenter trial comparing six weeks of oral anticoagulant treatment with six months of such therapy in patients who had a first episode of venous thromboembolism. Anticoagulant therapy consisted of warfarin or dicumarol. Of the 902 patients enrolled, 5 were later excluded because they had congenital protein C deficiency; 443 were randomly assigned to receive six weeks of oral anticoagulant therapy with a targeted international normalized ratio (INR) of 2.0 to 2.85, and 454 were randomly assigned to receive six months of such therapy. The initial diagnoses were confirmed by means of venography in cases of deep-vein thromboses (n = 790) and with perfusion-ventilation scanning or angiography in cases of pulmonary embolism (n = 107); recurrences were confirmed in the same way.
                After two years of follow-up, there had been 123 recurrences of venous thromboembolism that met the diagnostic criteria, 80 in the six-week group (18.1 percent; 95 percent confidence interval, 14.5 to 21.6) and 43 in the six-month group (9.5 percent; 95 percent confidence interval, 6.8 to 12.2). The odds ratio for recurrence in the six-week group was 2.1 (95 percent confidence interval, 1.4 to 3.1). There was no difference in mortality or the rate of major hemorrhage between the six-week and six-month groups.
                Six months of prophylactic oral anticoagulation after a first episode of venous thromboembolism led to a lower recurrence rate than did treatment lasting for six weeks. The difference between the two groups occurred between 6 weeks and 6 months after the start of treatment, and the rates of recurrence remained nearly parallel for 1 1/2 years thereafter. We performed a controlled trial of peripheral hyperalimentation in moderate and severe alcoholic hepatitis to determine whether improvement in survival and liver function could be obtained. Twelve patients with moderate and 22 with severe alcoholic hepatitis were randomized to 28 days of peripheral parenteral nutrition (PPN) or standard therapy (ST). In the moderate group, six were treated with each therapy. In the severe group, 10 were treated with PPN and 12 with ST. Routine liver tests, hepatocyte function (galactose elimination capacity), estimated hepatic blood flow (galactose clearance) and assessment of ascites and encephalopathy were performed at randomization and at 28 days. Groups were equally matched at randomization. In the moderate group PPN produced no improvement in morbidity (liver tests) and mortality (no deaths). In the severe group there were seven deaths (4 PPN, 3 ST). PPN produced greater improvement than ST in serum bilirubin and transferrin concentrations and a trend toward greater improvement in prothrombin time, serum albumin and galactose elimination capacity. PPN had no deleterious effect on encephalopathy or ascites as only ST patients developed ascites or encephalopathy after randomization. We conclude that PPN compared to ST (1) provides no benefit in moderate alcoholic hepatitis, but (2) did more rapidly improve morbidity (liver tests) and probably liver function in severe alcoholic hepatitis; (3) PPN did not improve early mortality, and (4) it had no deleterious effect on encephalopathy or ascites. Early changes in coagulation were found in patients following a paracetamol overdose. Low levels of clotting factors II, V and VII were present within 24 hours of the overdose. As the levels of factor II correlated with plasma fibrinogen values at this time, it is possible that they were consumed in the process of intravascular coagulation, although this was not supported by the presence of raised titres of fibrin degradation products. The prothrombin time ratio was greater than 2-2 within 30 hours of ingestion of the overdose in all patients who eventually died, whereas it was less than this in those developing only moderate liver damage. The administration of fresh frozen plasma to patients did appear to reduce the maximum abnormality of the prothrombin time ratio, which was significantly less three days after the overdose in the group receiving fresh frozen plasma. However, the coagulation disturbance was of short duration, and the prothrombin time ratio had also returned to normal within one week of the overdose in the control patients, and the administration of fresh frozen plasma did not appear to reduce the morbidity or mortality in the treated patients.
Sonothrombolysis appears to reduce death or dependency at three months (although CIs are quite wide), and increases recanalisation without clear hazard. A larger clinical trial is warranted.