title: Relations of plasma matrix metalloproteinase-9 to clinical cardiovascular risk factors and echocardiographic left ventricular measures: the Framingham Heart Study.
abstract: BACKGROUND
  Plasma levels of matrix metalloproteinase-9 (MMP-9), a key determinant of extracellular matrix degradation, are increased in heart failure and in acute coronary syndromes. We investigated cross-sectional relations of plasma MMP-9 to vascular risk factors and echocardiographic left ventricular (LV) measurements.
  
  
  RESULTS
  We studied 699 Framingham Study participants (mean age, 57 years; 58% women), free of heart failure and previous myocardial infarction, who underwent routine echocardiography. We examined sex-specific distributions of LV internal dimensions (LVEDD) and wall thickness (LVWT) and sampled persons with both LVEDD and LVWT below the sex-specific median (referent, n=299), with increased LVEDD (LVEDD > or =90th percentile, n=204) and increased LVWT (LVWT > or =90th percentile, n=221) in a 3:2:2 ratio. Plasma MMP-9 was detectable in 138 persons (20%). In multivariable models, increasing heart rate (OR per SD, 1.41; 95% CI, 1.17 to 1.71) and antihypertensive treatment (OR, 1.63; 95% CI, 1.06 to 2.50) were key clinical correlates of detectable plasma MMP-9. In multivariable-adjusted models, detectable plasma MMP-9 was associated with increased LVEDD (OR, 2.84; 95% CI, 1.13 to 7.11), increased LVWT (OR, 2.54; 95% CI, 1.00 to 6.46), and higher LV mass (P=0.06) in men but not in women (OR for increased LVEDD, 1.37; 95% CI, 0.54 to 3.46; for increased LVWT, 0.99; 95% CI, 0.39 to 2.52; P=0.59 for LV mass).
  
  
  CONCLUSIONS
  In our community-based sample, detectable plasma MMP-9 levels were associated with increased LV diastolic dimensions and increased wall thickness in men. These observations indicate that plasma MMP-9 level may be a marker for cardiac extracellular matrix degradation, a process involved in LV remodeling.
authors.affiliation: The Framingham Heart Study, Framingham, Mass 01702-5803, USA.
authors.forename: Johan
authors.initials: J
authors.lastname: Sundström
authors.forename: Jane C
authors.initials: JC
authors.lastname: Evans
authors.forename: Emelia J
authors.initials: EJ
authors.lastname: Benjamin
authors.forename: Daniel
authors.initials: D
authors.lastname: Levy
authors.forename: Martin G
authors.initials: MG
authors.lastname: Larson
authors.forename: Douglas B
authors.initials: DB
authors.lastname: Sawyer
authors.forename: Deborah A
authors.initials: DA
authors.lastname: Siwik
authors.forename: Wilson S
authors.initials: WS
authors.lastname: Colucci
authors.forename: Patrice
authors.initials: P
authors.lastname: Sutherland
authors.forename: Peter W F
authors.initials: PW
authors.lastname: Wilson
authors.forename: Ramachandran S
authors.initials: RS
authors.lastname: Vasan
mesh_terms: D000368:Aged; D015415:Biomarkers; D002318:Cardiovascular Diseases / Q000000981:diagnostic imaging / Q000201:enzymology* / Q000453:epidemiology; D015331:Cohort Studies; D018618:Echocardiography, Doppler, Color; D005109:Extracellular Matrix / Q000378:metabolism; D005260:Female; D006352:Heart Ventricles / Q000000981:diagnostic imaging*; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000201:enzymology; D008297:Male; D020780:Matrix Metalloproteinase 9 / Q000097:blood*; D008875:Middle Aged; D012307:Risk Factors; D020257:Ventricular Remodeling / Q000502:physiology
chemical_list: D015415:Biomarkers; D020780:Matrix Metalloproteinase 9