title: Relations of matrix remodeling biomarkers to blood pressure progression and incidence of hypertension in the community.
abstract: BACKGROUND
  Biomarkers of extracellular matrix remodeling are associated with prevalent hypertension in cross-sectional studies, but their relations to longitudinal changes in blood pressure (BP) and hypertension incidence are unknown.
  
  
  RESULTS
  We evaluated 595 nonhypertensive Framingham Offspring Study participants (mean age 55 years; 360 women) without prior heart failure or myocardial infarction who underwent routine measurements of plasma tissue inhibitor of metalloproteinase-1 (TIMP-1), metalloproteinase-9 (MMP-9), and procollagen III N-terminal peptide. We related plasma TIMP-1, procollagen III N-terminal peptide, and MMP-9 to the incidence of hypertension and progression of BP by >or=1 category (defined on the basis of the sixth report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure). On follow-up (4 years), 81 participants (51 women) developed hypertension, and 198 (114 women) progressed to a higher BP category. In multivariable models, a 1-SD increment of log-TIMP-1 was associated with a 50% higher incidence of hypertension (95% CI 1.08 to 2.08) and a 21% (95% CI 1.00 to 1.47) higher risk of BP progression. Individuals in the top TIMP-1 tertile had a 2.15-fold increased risk of hypertension (95% CI 0.99 to 4.68) and 1.68-fold (95% CI 1.05 to 2.70) increased risk of BP progression relative to the lowest tertile. Individuals with detectable MMP-9 had a 1.97-fold higher risk of BP progression (95% CI 1.06 to 3.64) than those with undetectable levels. Plasma procollagen III N-terminal peptide was not associated with hypertension incidence or BP progression.
  
  
  CONCLUSIONS
  In the present community-based sample, higher TIMP-1 and MMP-9 concentrations were associated with BP progression on follow-up. Additional studies are warranted to confirm our findings.
authors.affiliation: National Heart, Lung, and Blood Institute's Framingham Heart Study, Framingham, Mass, USA.
authors.forename: Ravi
authors.initials: R
authors.lastname: Dhingra
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Pencina
authors.forename: Peter
authors.initials: P
authors.lastname: Schrader
authors.forename: Thomas J
authors.initials: TJ
authors.lastname: Wang
authors.forename: Daniel
authors.initials: D
authors.lastname: Levy
authors.forename: Karol
authors.initials: K
authors.lastname: Pencina
authors.forename: Deborah A
authors.initials: DA
authors.lastname: Siwik
authors.forename: Wilson S
authors.initials: WS
authors.lastname: Colucci
authors.forename: Emelia J
authors.initials: EJ
authors.lastname: Benjamin
authors.forename: Ramachandran S
authors.initials: RS
authors.lastname: Vasan
mesh_terms: D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure / Q000502:physiology*; D015331:Cohort Studies; D018450:Disease Progression; D005109:Extracellular Matrix / Q000378:metabolism*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000453:epidemiology* / Q000209:etiology; D015994:Incidence; D008297:Male; D008404:Massachusetts / Q000453:epidemiology; D008875:Middle Aged; D012307:Risk Factors
chemical_list: D015415:Biomarkers