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 .
Changes in peripheral hemodynamics and vasodilating prostaglandins after high-dose short-term ibuprofen in chronically treated hypertensive patients.
The use of cyclooxygenase inhibitors has been seen to reduce the efficacy of many antihypertensive drugs . However , cyclooxygenase inhibitors are normally non-selective because they affect both vascular tissue , where the endothelial prostanoids exert principally a vasodilatory action , and the kidneys , where they also play an important role in regulating hydroelectrolytic metabolism by redistribution of intraparenchymal flow . To evaluate the relative importance of vascular district in the hypertensive patient , we administered ibuprofen - a drug acting with only a minimal antagonist activity . A group of 20 male hypertensives were r and omly allocated , according to a single-blind protocol , to treatment with amlodipine ( A , 10 mg/day ) or lisinopril ( L , 20 mg/day ) . Blood pressure was significantly reduced after 30 days , with a mean difference of -21.75 mmHg for systolic blood pressure ( SBP ) ( 95 % confidence interval ( Cl ) : -27.46 to -16.04 ; P < 0.0001 ) and -14.15 mmHg for diastolic blood pressure ( DBP ) ( 95 % Cl : -17.13 to -11.17 ; P < 0.0001 ) . Brachial artery compliance showed a mean increase of 1.657 x 10(-7 ) dyn-1 cm(4 ) ( 95 % Cl : 1.188 to 2.126 ; P<0.001 ) , and forearm resistances showed a mean decrease of -41.973 mmHg ml(-1)s ( 95 % Cl : -75.479 to -8.467 ; P = 0.017 ) . Changes in compliance were significantly related to those in SBP ( r= -0.546 ; P= 0.013 ) . The administration of ibuprofen ( 400 mg , three times a day for 3 days ) was accompanied by a slight but significant increase in SBP , but not in brachial artery compliance or forearm resistances . Only SBP was affected , showing a mean increase of 4.25 mmHg ( 95 % Cl : 1.26 to 7.24 ; P = 0.008 ) . There was also reduced urinary excretion of PGI(2 ) and TXA(2 ) metabolites . The mean change in 6-keto-PGF(1 alpha ) and 2,3-dinor-6-keto-PGF(1 alpha ) was 45.71 ng per g urinary creatinine ( uCr ) ( 95 % Cl : -0.16 to-91.25 ; P= 0.049 ) and -73.17 ng ( g uCr)(-1 ) ( 95 % Cl : -38.81 to -107.53 ; P<0.001 ) , respectively . The mean decrease in TXA(2 ) catabolites was highly significant : -39.2 ng ( g uCr)(-1 ) ( 95 % Cl : -18.17 to-60.22 ; P < 0.001 ) and -102.87 ng ( g uCr)(-1 ) ( 95 % Cl : -61.86 to -143.88 ; P < 0.001 ) for TXB(2 ) and 2,3-dinor-TXB(2 ) , respectively . Our study highlighted an inverse correlation between changes in blood pressure and those in urinary 2,3-dinor-6-keto-PGF(1alpha ) excretion , irrespective of antihypertensive regimen . This suggests that , in the hypertensive patient treated with NSAIDs , inhibition of vascular prostanoid synthesis may play an important role in countering the efficacy of an important vascular tone regulatory mechanism
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 .