title: Is left ventricular hypertrophy a low-level inflammatory state? A population-based cohort study.
abstract: OBJECTIVE
  Cross-sectional studies have shown that chronic sub-clinical inflammation is associated with left ventricular hypertrophy (LVH), but results are conflicting. We investigated the association between baseline LVH and high-sensitivity C-reactive protein (CRP) values, both cross-sectionally and after a six-year-follow-up, in a population-based cohort (n = 1564) and a subgroup from this cohort (n = 515), without obesity, diabetes, metabolic syndrome or any drugs.
  
  
  RESULTS
  ECG tracings at baseline were interpreted according to the Cornell voltage-duration product criteria: 166/1564 subjects (10.6%) showed LVH. Patients with baseline LVH showed increased BMI, waist circumference, blood pressure, and a worse metabolic pattern. Their CRP values both at baseline and at follow-up were almost two-fold higher than in patients without LVH. Similar results were found in the healthier sub-sample. In a multiple regression model, CRP at follow-up was directly associated with baseline LVH (expressed as Cornell voltage-duration product) in the whole cohort (β = 0.0003; 95%CI 0.0002-0.0006; p < 0.001) and in the sub-sample (β = 0.0003; 0.0002-0.0004; p < 0.001), after adjusting for age, sex, BMI, waist circumference, smoking, exercise levels, blood pressure and baseline CRP values.
  
  
  CONCLUSIONS
  Baseline LVH, which is associated with systemic inflammation, predicts increased CRP values at follow-up, independently of cardiovascular and metabolic risk factors, both in a population-based cohort and a healthier sub-sample. The inflammatory consequences of LVH might be an intriguing subject for further researches.
authors.affiliation: Department of Internal Medicine, University of Turin, Corso Dogliotti 14, 10126 Turin, Italy. sbo@molinette.piemonte.it
authors.forename: S
authors.initials: S
authors.lastname: Bo
authors.forename: C
authors.initials: C
authors.lastname: Mandrile
authors.forename: N
authors.initials: N
authors.lastname: Milanesio
authors.forename: A
authors.initials: A
authors.lastname: Pagani
authors.forename: L
authors.initials: L
authors.lastname: Gentile
authors.forename: R
authors.initials: R
authors.lastname: Gambino
authors.forename: P
authors.initials: P
authors.lastname: Villois
authors.forename: L
authors.initials: L
authors.lastname: Ghinamo
authors.forename: S
authors.initials: S
authors.lastname: Canil
authors.forename: M
authors.initials: M
authors.lastname: Durazzo
authors.forename: M
authors.initials: M
authors.lastname: Cassader
authors.forename: P
authors.initials: P
authors.lastname: Cavallo-Perin
mesh_terms: D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism*; D016009:Chi-Square Distribution; D003430:Cross-Sectional Studies; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000097:blood* / Q000175:diagnosis / Q000453:epidemiology / Q000276:immunology; D007249:Inflammation / Q000097:blood* / Q000175:diagnosis / Q000453:epidemiology / Q000276:immunology; D018836:Inflammation Mediators / Q000097:blood*; D007558:Italy / Q000453:epidemiology; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D016017:Odds Ratio; D018570:Risk Assessment; D012307:Risk Factors; D013997:Time Factors; D015854:Up-Regulation
chemical_list: D015415:Biomarkers; D018836:Inflammation Mediators; D002097:C-Reactive Protein