title: Perindopril-based blood pressure-lowering therapy reduces amino-terminal-pro-B-type natriuretic peptide in individuals with cerebrovascular disease.
abstract: OBJECTIVE
  The plasma amino-terminal-pro-B-type natriuretic peptide (NT-proBNP) level predicted congestive heart failure, myocardial infarction, and ischaemic stroke in participants of the Perindopril Protection Against Recurrent Stroke Study (PROGRESS), a placebo-controlled study of the effects of blood pressure lowering on cardiovascular events among individuals with cerebrovascular disease. Active treatment comprised a flexible regimen based on perindopril, with the addition of indapamide at the discretion of treating physicians. Active treatment reduced cardiovascular events, and we therefore investigated whether active treatment modified NT-proBNP and other cardiovascular risk factors.
  
  
  METHODS
  We measured NT-proBNP and other cardiovascular risk factors at randomization and after 13 months of therapy in a subset of 357 PROGRESS participants.
  
  
  RESULTS
  Baseline systolic and pulse pressures were higher in individuals with elevated baseline NT-proBNP levels. In comparison with placebo, active treatment reduced the blood pressure and NT-proBNP levels, and increased renin levels. Reduction of NT-proBNP levels by active treatment was most evident in individuals with baseline NT-proBNP levels in the highest quarter (> 26 pmol/l), with a median reduction of 16 pmol/l (interquartile range 0-51 pmol/l, P = 0.004), corresponding to a median decrease of 39% (interquartile range 0-69%). Active treatment reduced blood pressure similarly for individuals in each of the four quarters of baseline NT-proBNP. Active therapy had no effect on plasma lipid, C-reactive protein, homocysteine, or soluble vascular cell adhesion molecule 1 levels.
  
  
  CONCLUSIONS
  We conclude that plasma NT-proBNP level, in addition to predicting cardiovascular risk, may provide a measure of risk reduction by blood pressure-lowering therapy.
authors.affiliation: St Vincent's Institute of Medical Research, Fitzroy, Victoria, Australia. dcampbell@svi.edu.au
authors.forename: Duncan J
authors.initials: DJ
authors.lastname: Campbell
authors.forename: Mark
authors.initials: M
authors.lastname: Woodward
authors.forename: John P
authors.initials: JP
authors.lastname: Chalmers
authors.forename: Samuel A
authors.initials: SA
authors.lastname: Colman
authors.forename: Alicia J
authors.initials: AJ
authors.lastname: Jenkins
authors.forename: Bruce E
authors.initials: BE
authors.lastname: Kemp
authors.forename: Bruce C
authors.initials: BC
authors.lastname: Neal
authors.forename: Anushka
authors.initials: A
authors.lastname: Patel
authors.forename: Stephen W
authors.initials: SW
authors.lastname: MacMahon
mesh_terms: D000368:Aged; D000959:Antihypertensive Agents / Q000494:pharmacology*; D015415:Biomarkers; D001794:Blood Pressure / Q000187:drug effects*; D002318:Cardiovascular Diseases / Q000517:prevention & control*; D002561:Cerebrovascular Disorders / Q000150:complications* / Q000517:prevention & control; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood* / Q000187:drug effects; D010446:Peptide Fragments / Q000097:blood* / Q000187:drug effects; D020913:Perindopril / Q000494:pharmacology*; D012307:Risk Factors
chemical_list: D000959:Antihypertensive Agents; D015415:Biomarkers; D010446:Peptide Fragments; C109794:pro-brain natriuretic peptide (1-76); D020097:Natriuretic Peptide, Brain; D020913:Perindopril