There was a dose-dependent decrease in blood pressure for aliskiren 75 mg , 150 mg and 300 mg .
Aliskiren had no effect on blood pressure variability .
Due to very limited information available regarding change in heart rate and pulse pressure , it was not possible to meta-analyze these outcomes .Mortality and non-fatal serious adverse events were not increased .
AUTHORS ' CONCLUSIONS Compared to placebo , aliskiren lowered BP and this effect is dose-dependent .
This magnitude of BP lowering effect is similar to that for angiotensin-converting enzyme ( ACE ) inhibitors and angiotensin receptor blockers ( ARBs ) .
There is no difference in mortality , nonfatal serious adverse events or withdrawal due to adverse effects with short term aliskiren monotherapy .
BACKGROUND Hypertension is a chronic condition associated with an increased risk of mortality and morbidity .
Renin is the enzyme responsible for converting angiotensinogen to angiotensin I , which is then converted to angiotensin II .
Renin inhibitors are a new class of drugs that decrease blood pressure ( BP ) by preventing the formation of both angiotensin I and angiotensin II .
OBJECTIVES To quantify the dose-related BP lowering efficacy of renin inhibitors compared to placebo in the treatment of primary hypertension .
To determine the change in BP variability , pulse pressure , and heart rate and to evaluate adverse events ( mortality , non-fatal serious adverse events , total adverse events , withdrawal due to adverse effects and specific adverse events such as dry cough , diarrhoea and angioedema ) .
Effect of the direct renin inhibitor aliskiren on left ventricular remodelling following myocardial infarction with systolic dysfunction.
AIMS Direct renin inhibitors provide an alternative approach to inhibiting the renin-angiotensin-aldosterone system ( RAAS ) at the most proximal , specific , and rate-limiting step . We tested the hypothesis that direct renin inhibition would attenuate left ventricular remodelling in patients following acute myocardial infa rct ion receiving stable , individually optimized therapy , including another inhibitor of the RAAS . METHODS AND RESULTS We r and omly assigned 820 patients between ∼2 and 8 weeks following acute myocardial infa rct ion , with the left ventricular ejection fraction ( LVEF ) ≤45 % , and regional wall motion abnormalities ( ≥20 % akinetic area ) , to  receive aliskiren ( n = 423 ) , titrated to 300 mg , or matched placebo ( n = 397 ) , added to the st and ard therapy . All patients were required to be on a stable dose of an ACE-inhibitor or ARB , and beta-blocker unless contraindicated or not tolerated . Echocardiograms were obtained at baseline , and following 26 - 36 weeks of treatment . The primary endpoint was change in left ventricular end-systolic volume from baseline to 36 weeks , and was evaluable in 329 patients in the placebo group and 343 patients in the aliskiren group . We observed no difference in the primary endpoint of end-systolic volume change between patients r and omized to aliskiren ( -4.4 ± 16.8 mL ) or placebo ( -3.5 ± 16.3 mL ) , or in secondary measures of end-diastolic volume , or LVEF . We also observed no differences in a composite endpoint of cardiovascular death , hospitalization for heart failure , or reduction in LVEF > 6 points . There were more investigator reported adverse events in the aliskiren group , including hypotension , increases in creatinine and hyperkalaemia . CONCLUSION Adding the direct renin inhibitor aliskiren to the st and ard therapy , including an inhibitor of the RAAS , in high-risk post-MI patients did not result in further attenuation of left ventricular remodelling , and was associated with more adverse effects . These findings do not suggest that dual RAAS blockade with aliskiren would provide additional benefit in these high-risk post-MI patients
There was a dose-dependent decrease in blood pressure for aliskiren 75 mg , 150 mg and 300 mg .
Aliskiren had no effect on blood pressure variability .
Due to very limited information available regarding change in heart rate and pulse pressure , it was not possible to meta-analyze these outcomes .Mortality and non-fatal serious adverse events were not increased .
AUTHORS ' CONCLUSIONS Compared to placebo , aliskiren lowered BP and this effect is dose-dependent .
This magnitude of BP lowering effect is similar to that for angiotensin-converting enzyme ( ACE ) inhibitors and angiotensin receptor blockers ( ARBs ) .
There is no difference in mortality , nonfatal serious adverse events or withdrawal due to adverse effects with short term aliskiren monotherapy .
BACKGROUND Hypertension is a chronic condition associated with an increased risk of mortality and morbidity .
Renin is the enzyme responsible for converting angiotensinogen to angiotensin I , which is then converted to angiotensin II .
Renin inhibitors are a new class of drugs that decrease blood pressure ( BP ) by preventing the formation of both angiotensin I and angiotensin II .
OBJECTIVES To quantify the dose-related BP lowering efficacy of renin inhibitors compared to placebo in the treatment of primary hypertension .
To determine the change in BP variability , pulse pressure , and heart rate and to evaluate adverse events ( mortality , non-fatal serious adverse events , total adverse events , withdrawal due to adverse effects and specific adverse events such as dry cough , diarrhoea and angioedema ) .