Acetylsalicylic acid ( ASA ) did not reduce stroke or ‘ all cardiovascular events ’ compared to placebo in primary prevention patients with elevated BP and no prior cardiovascular disease .
To conclude for primary prevention in patients with elevated BP , antiplatelet therapy with ASA can not be recommended since the magnitude of benefit , a reduction in myocardial infa rct ion , is negated by a harm of similar magnitude , an increase in major haemorrhage .
Although elevated systemic blood pressure ( BP ) results in high intravascular pressure , the main complications of hypertension are related to thrombosis rather than haemorrhage .
It therefore seemed plausible that use of antithrombotic therapy may be useful in preventing thrombosis-related complications of elevated BP .
The objectives were to conduct a systematic review of the role of antiplatelet therapy and anticoagulation in patients with BP , to address the following hypotheses : ( i ) antiplatelet agents reduce total deaths and /or major thrombotic events when compared to placebo or other active treatment ; and ( ii ) oral anticoagulants reduce total deaths and /or major thromboembolic events when compared to placebo or other active treatment .
Randomized Trial of Thrombolysis Versus Heparin in Unstable Angina
Background The clinical usefulness of intravenous thrombolytic therapy in unstable angina is currently unknown , despite the pathogenetic similarity of this entity to acute myocardial infa rct ion , for which thrombolysis has enjoyed great success . To compare the clinical benefit of intravenous urokinase with that of conventional antithrombotic therapy in preventing the progression of unstable angina to new myocardial infa rct ion , intractable angina , or death within the first 96 hours after hospitalization , 149 patients with unstable angina were r and omized to one of two intravenous thrombolytic strategies . Methods and Results Forty-nine patients received 3 million units urokinase i.v . over 90 minutes plus intravenous heparin ( group A ) ; 47 patients received unblinded 3 million units urokinase i.v . plus 325 mg aspirin p.o . daily ( group B ) ; and 53 patients received placebo thrombolytic infusion plus full-dose heparin ( group C ) . The primary end point of this trial was 96-hour clinical status . There were no significant differences in the baseline characteristics ( age , sex , previous myocardial infa rct ion , hypertension prevalence , diabetes , tobacco use , or previous revascularization ) among the three groups . Despite an excess of minor untoward reactions for the urokinase groups ( chills , 26.5 % and 23.4 % for groups A and B versus 0 % for group C ; p<0.01 ) , there was no significant difference with respect to major bleeds ( two , none , and two for groups A , B , and C , respectively;p = NS ) . At 96 hours after presentation , no significant difference emerged in the incidence of new cardiac events : new myocardial infa rct ions developed in 10.2 % of group A , 6.4 % of group B , and 3.8 % of group C ( p = NS ) ; intractable angina occurred in 6.1 % of group A , 10.6 % of group B , and 9.4 % of group C ( p = NS ) . There were no deaths . All three groups encountered a similar incidence of overall cardiac events : 16.31 % , 17.0 % , and 13.2 % for groups A , B , and C , respectively ( p = NS ) . Although trial enrollment was to extend to 600 patients , interim analysis led to early cessation of enrollment due to a negative trend in respect to outcome after thrombolysis . Conclusions High-dose intravenous urokinase followed by either heparin or aspirin can be safely administered to a broad , unselected group of patients with unstable angina . However , this study suggests that no clinical advantage is conferred by urokinase , with either adjunctive antithrombotic therapy over st and ard heparin therapy alone , when given relatively late ( mean , 8.7 hours ) after admission for unstable angina . A possible detrimental effect can not be excluded
Acetylsalicylic acid ( ASA ) did not reduce stroke or ‘ all cardiovascular events ’ compared to placebo in primary prevention patients with elevated BP and no prior cardiovascular disease .
To conclude for primary prevention in patients with elevated BP , antiplatelet therapy with ASA can not be recommended since the magnitude of benefit , a reduction in myocardial infa rct ion , is negated by a harm of similar magnitude , an increase in major haemorrhage .
Although elevated systemic blood pressure ( BP ) results in high intravascular pressure , the main complications of hypertension are related to thrombosis rather than haemorrhage .
It therefore seemed plausible that use of antithrombotic therapy may be useful in preventing thrombosis-related complications of elevated BP .
The objectives were to conduct a systematic review of the role of antiplatelet therapy and anticoagulation in patients with BP , to address the following hypotheses : ( i ) antiplatelet agents reduce total deaths and /or major thrombotic events when compared to placebo or other active treatment ; and ( ii ) oral anticoagulants reduce total deaths and /or major thromboembolic events when compared to placebo or other active treatment .