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 ketoprofen on blood pressure, endocrine and renal responses to chronic dosing with captopril in patients with essential hypertension.
The effects of non-steroidal anti-inflammatory drugs ( NSAIDs ) on the blood pressure and renal function of essential hypertensive patients depend on the specific type of NSAID and antihypertensive drug administered . Twelve patients with essential hypertension , aged 35 to 59 years , stabilized ( blood pressure less than 140/90 mmHg ) with captopril  , received ketoprofen ( 100 mg bid for 7 days ) or matching placebo in a r and omized double-blind cross-over fashion . A 3-week wash-out period was included between treatment periods . Blood pressure on the first and last days of the placebo treatment period ( 137 + /- 7 (SD)/80 + /- 8 and 139 + /- 11/81 + /- 9 mmHg ) was similar to respective values during ketoprofen therapy ( 136 + /- 10/79 + /- 7 and 143 + /- 10/81 + /- 9 mmHg ) . The mean differences in systolic and diastolic blood pressures , at the end of the treatment periods , between ketoprofen and placebo were 4 ( 95 % confidence intervals -5 , + 13 ) and 0 (-8 , + 8) mmHg , respectively . Ketoprofen had no effect on 24-h urinary sodium excretion ( 160 + /- 33 and 147 + /- 39 mmol/24 h for ketoprofen and placebo , respectively ) . Ketoprofen was without effect on glomerular filtration rate , renal plasma flow and filtration fraction . In conclusion , our data suggest that ketoprofen is a safe choice when short-term treatment with a NSAID is indicated in an essential hypertensive patient treated with a converting enzyme inhibitor such as 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 .