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 .
Potential mechanisms by which nonsteroidal anti-inflammatory drugs elevate blood pressure: the role of endothelin-1.
To determine whether endothelin-1 ( ET-1 ) contributes to hypertension associated with non-steroidal anti-inflammatory drug ( NSAID ) usage in healthy , elderly , normotensive individuals a r and omised , double-blind , placebo-controlled , crossover trial of indomethacin was undertaken in 41 healthy , elderly individuals with stable normotension or controlled hypertension ( blood pressure ( BP ) < or = 160/90 mm Hg ) . The main outcome measures were systolic and diastolic BP , heart rate , cardiac output , weight , creatinine clearance , plasma renin activity , aldosterone , endothelin-1 and arginine vasopressin concentrations and 24 h urinary endothelin-1 and 6 keto prostagl and in F1 alpha outputs . Analysis of covariance was used to evaluate the effect of indomethacin on BP and related parameters . Indomethacin treatment for 1 month increased systolic ( + /- s.e.m . : 4.1 + /- 2.2 mm Hg ; 95 % confidence interval 0 to 8.3 mm Hg ) and diastolic BP ( 2.7 + /- 1.1 mm Hg ; 0.4 to 4.9 mm Hg ) without altering cardiac output ( P = 0.59 ) , implying an increase in total peripheral resistance .  Indomethacin treatment produced a small increase in weight ( 1.4 + /- 0.4 kg ; 0.6 to 2.2 kg ) , a small reduction in renal function ( creatinine clearance : 6.8 + /- 1.8 mis/min ; 3.3 to 10.3 mis/min ) but a significant ( 83 % ) increase in daily urinary endothelin-1 production ( 13.1 + /- 3.4 ng/ml ; 6.4 to 19.8 ng/ml ) without altering plasma ET-1 concentration , suggesting increased renal synthesis . In conclusion , renal paracrine effects of ET-1 may contribute to NSAID-induced blood pressure elevation in humans
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 .