title: High sodium intake adversely affects oxidative-inflammatory response, cardiac remodelling and mortality after myocardial infarction.
abstract: OBJECTIVE
  Enhanced sodium intake increases volume overload, oxidative stress and production of proinflammatory cytokines. In animal models, increased sodium intake favours ventricular dysfunction after myocardial infarction (MI). The aim of this study was to investigate, in human subjects presenting with ST-segment elevation MI (STEMI), the impact of sodium intake prior the coronary event.
  
  
  METHODS
  Consecutive patients (n=372) admitted within the first 24 h of STEMI were classified by a food intake questionnaire as having a chronic daily intake of sodium higher (HS) or lower (LS) than 1.2 g in the last 90 days before MI. Plasma levels of 8-isoprostane, interleucin-2 (IL-2), tumour necrosis factor type α (TNF-α), C-reactive protein (CRP) and brain natriuretic peptide (BNP) were measured at admission and at the fifth day. Magnetic resonance imaging was performed immediately after discharge. Total mortality and recurrence of acute coronary events were investigated over 4 years of follow-up.
  
  
  RESULTS
  The decrease of 8-isoprostane was more prominent and the increase of IL-2, TNF-α and CRP less intense during the first 5 days in LS than in HS patients (p<0.05). Sodium intake correlated with change in plasma BNP between admission and fifth day (r=0.46; p<0.0001). End-diastolic volumes of left atrium and left ventricle were greater in HS than in LS patients (p<0.05). In the first 30 days after MI and up to 4 years afterwards, total mortality was higher in HS than in LS patients (p<0.05).
  
  
  CONCLUSIONS
  Excessive sodium intake increases oxidative stress, inflammatory response, myocardial stretching and dilatation, and short and long-term mortality after STEMI.
authors.affiliation: University of Brasilia Medical School (UnB), Brasilia, DF, Brazil.
authors.forename: Ana Paula R
authors.initials: AP
authors.lastname: Costa
authors.forename: Rafaela C S
authors.initials: RC
authors.lastname: de Paula
authors.forename: Guilherme F
authors.initials: GF
authors.lastname: Carvalho
authors.forename: Juliana P
authors.initials: JP
authors.lastname: Araújo
authors.forename: Joalbo M
authors.initials: JM
authors.lastname: Andrade
authors.forename: Osorio L R
authors.initials: OL
authors.lastname: de Almeida
authors.forename: Eliana C
authors.initials: EC
authors.lastname: de Faria
authors.forename: Wladimir M
authors.initials: WM
authors.lastname: Freitas
authors.forename: Otavio R
authors.initials: OR
authors.lastname: Coelho
authors.forename: Jose A F
authors.initials: JA
authors.lastname: Ramires
authors.forename: Jose C
authors.initials: JC
authors.lastname: Quinaglia e Silva
authors.forename: Andrei C
authors.initials: AC
authors.lastname: Sposito
mesh_terms: D000328:Adult; D002097:C-Reactive Protein / Q000378:metabolism; D052279:Creatine Kinase, MB Form / Q000097:blood; D015237:Dinoprost / Q000031:analogs & derivatives / Q000097:blood; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007376:Interleukin-2 / Q000097:blood; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000401:mortality* / Q000503:physiopathology; D020097:Natriuretic Peptide, Brain / Q000097:blood; D018384:Oxidative Stress / Q000502:physiology; D012964:Sodium / Q000008:administration & dosage* / Q000009:adverse effects*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D020257:Ventricular Remodeling / Q000502:physiology
chemical_list: D007376:Interleukin-2; D014409:Tumor Necrosis Factor-alpha; D020097:Natriuretic Peptide, Brain; C075750:8-epi-prostaglandin F2alpha; D002097:C-Reactive Protein; D012964:Sodium; D015237:Dinoprost; D052279:Creatine Kinase, MB Form