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 .
Effect of low-dose aspirin on thromboxane production and the antihypertensive effect of captopril.
Some of the antihypertensive effects of angiotensin-converting enzyme ( ACE ) inhibitors occur through nonangiotensin II-mediated mechanisms . One of these is through decreased kinin degradation , leading to enhanced production of vasodilator arachidonic acid metabolites . It was reasoned that if ACE inhibition also leads to an increase in the production of the potent vasoconstrictor thromboxane A2 , then maneuvers that selectively inhibit thromboxane production without reducing prostagl and ins ( PG ) E2 + PGI2 might enhance the antihypertensive effect of ACE inhibition . This double-blinded , r and omized , crossover study was therefore undertaken to determine : ( 1 ) if captopril increases platelet and /or renal thromboxane production ; and ( 2 ) if low-dose aspirin enhances the antihypertensive effect of captopril .  Patients with mild essential hypertension and no other significant medical problems were studied . In a double-blinded , r and om order , patients took captopril alone ( 25 mg every 12 h ) for 2 wk and captopril plus aspirin ( 75 mg/day ) for another 2 wk . Active treatment periods were preceded by 2 wk of single-blind placebo .  Fifteen patients with a mean age of 53 yr and an average mean arterial pressure ( MAP ) of 114 + /- 8 ( + /- SD ) mm Hg were studied .  Serum thromboxane B2 was higher ( P < 0.05 ) during treatment with captopril/placebo ( 600 + /- 46 ( + /- SE ) pg/mL ) than during the two washout periods combined ( 420 + /- 57 and 553 + /- 78 ) and was lowest ( P < 0.0005 ) during treatment with captopril/aspirin ( 302 + /- 36 ) . Captopril treatment significantly increased the urinary excretion of PGE2 ( P = 0.038 ) . Captopril/placebo significantly lowered MAP ( P < 0.05 ) to 105.0 + /- 3.7 mm Hg compared with the washout period . However , the addition of aspirin to captopril caused no additional lowering of MAP ( 105.2 + /- 2.8 mm Hg ) . It was concluded that treatment with captopril does increase platelet thromboxane production . However , lowering platelet thromboxane with low doses of aspirin may not enhance the antihypertensive effect of captopril
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 .