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 .
Assessment of blood pressure during naproxen therapy in hypertensive patients treated with nicardipine.
Nonsteroidal antiinflammatory drugs ( NSAIDs ) are known to attenuate the antihypertensive effects of a variety of antihypertensive agents including diuretics , beta-blockers , and vasodilators . Because of their unique mechanisms of actions , calcium channel blockers may not be subject to this interaction . This multicenter , double-blind , r and omized , placebo-controlled study was design ed to assess the effect of NSAID therapy on blood pressure control in stable hypertensive patients treated with a calcium channel blocker . One hundred patients with stable blood pressure control on 30 mg nicardipine three times a day were treated with 375 mg naproxen twice a day or placebo for 4 weeks . The mean diastolic blood pressures and estimated mean arterial pressures in both groups changed < 1 mm Hg during the 4 weeks of study drug treatment . None of the changes was significantly different from baseline and the two treatment groups were not significantly different from each other . Body weight in the placebo-treated patients did not change significantly whereas body weight in the naproxen-treated patients increased significantly , from 90.3 + /- 3.2 kg to 91.0 + /- 3.2 kg ( mean = 0.7 , P = .0003 ) . At 4 weeks there was a mean loss of 0.1 kg in the placebo group and a mean gain of 0.4 kg in the naproxen group compared to baseline weights , neither of which was statistically significant ( P = .60 and P = .071 , respectively ) . These results indicate that despite a significant increase in body weight , the antihypertensive action of the calcium channel blocker nicardipine is not significantly affected by cotreatment with naproxen
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 .