Acetylsalicylic acid ( ASA ) did not reduce stroke or ' all cardiovascular events ' compared to placebo in primary prevention patients with elevated blood pressure and no prior cardiovascular disease .
Antiplatelet therapy with ASA for primary prevention in patients with elevated blood pressure provides a benefit , reduction in myocardial infa rct ion , which is negated by a harm of similar magnitude , increase in major haemorrhage .
The benefit of antiplatelet therapy for secondary prevention in patients with elevated blood pressure is many times greater than the harm .
Benefit has not been demonstrated for warfarin therapy alone or in combination with aspirin in patients with elevated blood pressure .
BACKGROUND Elevated systemic blood pressure results in high intravascular pressure but the main complications , coronary heart disease ( CHD ) , ischaemic strokes and peripheral vascular disease ( PVD ) , are related to thrombosis rather than haemorrhage .
Some complications related to elevated blood pressure , heart failure or atrial fibrillation , are themselves associated with stroke and thromboembolism .
Therefore it is important to investigate if antithrombotic therapy may be useful in preventing thrombosis-related complications in patients with elevated blood pressure .
OBJECTIVES To conduct a systematic review of the role of antiplatelet therapy and anticoagulation in patients with high blood pressure , including those with elevations in both systolic and diastolic blood pressure , isolated elevations of either systolic or diastolic blood pressure , 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 .
Ticlopidine , clopidogrel and newer antiplatelet agents such as prasugrel and ticagrelor have not been sufficiently evaluated in patients with high blood pressure .
Effects of non-steroidal anti-inflammatory drugs on prostacyclin and thromboxane biosynthesis in patients with mild essential hypertension.
1 . The effects of non-steroidal anti-inflammatory drugs ( NSAID ) on prostacyclin and thromboxane bio synthesis and on blood pressure were determined in 46 patients with mild essential hypertension . Patients who had abstained from antihypertensive therapy for 2 weeks before study were treated with either aspirin , ibuprofen , sulindac or placebo for 7 days . 2 . Excretion rates of 2,3-dinor-6-oxo-prostagl and in ( PG ) F1 alpha , 6-oxo-PGF1 alpha , 2,3-dinorthromboxane ( TX ) B2 and TXB2 were measured as indices of prostacyclin and TXA2 bio synthesis . Sample s were assayed using immunoaffinity chromatography and gas chromatography/electron capture chemical ionisation mass spectrometry . 3 . Aspirin and ibuprofen reduced urinary excretion of all prostacyclin- and thromboxane-derived products . Sulindac inhibited excretion of 2,3-dinor-6-oxo-PGF1 alpha , 6-oxo-PGF1 alpha and 2,3-dinor-TXB2 , but had no significant effect on TXB2 . 4 . Systolic blood pressure increased in the ibuprofen-treated group when compared with the placebo group . There were no other significant changes in systolic or diastolic pressure in any of the treatment groups . Among the patients as a whole , there was a significant negative correlation between change in blood pressure and change in excretion of the prostacyclin-derived but not of the thromboxane-derived products . 5 . We conclude that , in patients with mild essential hypertension , neither sulindac nor aspirin ( in the doses used ) selectively spares prostacyclin bio synthesis by the kidney . The significant relationship between increase in blood pressure and reduction in prostacyclin bio synthesis favours the possibility that in individuals who become hypertensive , prostacyclin bio synthesis determines , in part , the severity of the hypertensive state
Acetylsalicylic acid ( ASA ) did not reduce stroke or ' all cardiovascular events ' compared to placebo in primary prevention patients with elevated blood pressure and no prior cardiovascular disease .
Antiplatelet therapy with ASA for primary prevention in patients with elevated blood pressure provides a benefit , reduction in myocardial infa rct ion , which is negated by a harm of similar magnitude , increase in major haemorrhage .
The benefit of antiplatelet therapy for secondary prevention in patients with elevated blood pressure is many times greater than the harm .
Benefit has not been demonstrated for warfarin therapy alone or in combination with aspirin in patients with elevated blood pressure .
BACKGROUND Elevated systemic blood pressure results in high intravascular pressure but the main complications , coronary heart disease ( CHD ) , ischaemic strokes and peripheral vascular disease ( PVD ) , are related to thrombosis rather than haemorrhage .
Some complications related to elevated blood pressure , heart failure or atrial fibrillation , are themselves associated with stroke and thromboembolism .
Therefore it is important to investigate if antithrombotic therapy may be useful in preventing thrombosis-related complications in patients with elevated blood pressure .
OBJECTIVES To conduct a systematic review of the role of antiplatelet therapy and anticoagulation in patients with high blood pressure , including those with elevations in both systolic and diastolic blood pressure , isolated elevations of either systolic or diastolic blood pressure , 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 .
Ticlopidine , clopidogrel and newer antiplatelet agents such as prasugrel and ticagrelor have not been sufficiently evaluated in patients with high blood pressure .