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 .
Different patterns of renal prostaglandins I2 and E2 in patients with essential hypertension with low to normal or high renin activity
Objective Differences in renal synthesis between prostagl and ins I2 and E2 , and the relationships of the amounts synthesized to renin release were investigated in patients with essential hypertension . Methods Of 12 in patients , six had low to normal plasma renin activity and six had high renin activity . Before and 30 min after intravenous injection of aspirin D , L-lysine ( 18 mg/kg ) , abdominal aortic and renal venous plasma was sample d and assayed for renin activity , 6-keto-prostagl and in F1α ( as an index of prostagl and in I2 ) , and prostagl and in E2 . Results In patients with low to normal renin activity  , mean ± SD plasma levels of 6-keto-prostagl and in F1α were lower in the right and left renal veins ( 3.6 ± 1.4 and 4.1 ± 1.5 pg/ml , respectively ) than in the aorta ( 5.5 ± 2.0 pg/ml ) , but in the other patients , the levels in these veins ( 7.0 ± 2.4 and 6.5 ± 1.5 pg/ml ) were higher than in the aorta ( 5.4 ± 0.9 pg/ml ) . Plasma prostagl and in E2 levels in both veins were higher than in the aorta in both groups and , at each site , the levels were similar in the two groups . Aspirin suppressed renin release in the patients with high renin activity . Conclusions In patients with essential hypertension with low to normal renin activity , either less prostagl and in I2 than prostagl and in E2 is produced in the kidney or else more is metabolized there , and in such patients with high renin activity , the renal synthesis of prostagl and in I2 , more than that of prostagl and in E2 , seems to be related to the increased renin release
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 .