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 .
[Reduction of the antihypertensive effects of enalapril by indomethacin. Its independence from renal sodium retention].
OBJECTIVE To evaluate in hypertensive patients whether or not the sodium-retaining effects of indomethacin can explain the indomethacin-induced attenuation of enalapril antihypertensive effects . DESIGN R and omized , single-blinded , placebo controlled study with a placebo phase ( 2 weeks ) followed by enalapril 20 mg/d ( 4 weeks , once daily ) and enalapril 20 mg + indomethacin 75 mg/d ( 1 week ) . Enalapril dose increased up to 40 mg/d if inadequate response to 20 mg . PATIENTS Twenty-four patients with mild-moderated hypertension , showing an adequate response to enalapril ( 20 - 40 mg/d ) . METHODS Blood pressure evaluated by " casual " methods and by 24-hour ambulatory blood pressure monitoring , measurement of 24-hour urinary sodium excretion and fractional excretion of sodium : at the end of placebo , enalapril and enalapril + indomethacin treatments . Determination of the correlations between the changes induced by indomethacin ( when added to enalapril ) on the blood pressure and on sodium excretion effects of enalapril . RESULTS Enalapril significantly reduced casual blood pressure ( systolic/diastolic ) by 33/18 mmHg and 24-hour blood pressure by 20/9 mmHg . When added to enalapril , indomethacin attenuated ( by 50 % ) the antihypertensive effects of enalapril and significantly decreased the 24-hour ( from 120 + /- 11 mmol to 106 + /- 10 mmol ) and fractional excretion of sodium ( from 1.11 + /- 0.09 % to 0.75 + /- 0.06 % ) . However , the indomethacin-induced attenuation of enalapril hypotensive effects did not correlate with indomethacin-induced changes of sodium excretion . CONCLUSIONS When indomethacin is administrated to hypertensive patients that are well controlled with enalapril , it produces a marked attenuation of enalapril hypotensive effects and produces sodium retention . However , the amount of the attenuation of the hypotensive effects of enalapril by indomethacin are completely independent of the amount of the indomethacin-induced sodium retention . These results suggest that the mechanisms involved in interaction between both drugs at the blood pressure domain are probably localized at an extra-renal level
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 .