title: Association of central pulse pressure with contrast-induced nephropathy and clinical outcomes in patients undergoing coronary intervention.
abstract: OBJECTIVE
  The increase in pulse pressure (PP) may be transmitted to the glomerulus and thus impair renal blood flow autoregulation. This subtle change could predispose patients to the detrimental effect of contrast media. We sought to determine whether elevated central PP is associated with increased contrast-induced nephropathy (CIN) and future cardiovascular events in patients undergoing percutaneous coronary intervention (PCI).
  
  
  METHODS
  In total, 448 consecutive patients receiving PCI were enrolled. In each patient, central and peripheral blood pressures were measured before PCI. The occurrence of CIN was identified and defined as a rise in serum creatinine of 0.5 mg/dl or a 25% increase from the baseline value within 48 h after the procedure. All patients were then followed up for at least 3 years or until the occurrence of a major adverse cardiovascular event (MACE) including death, nonfatal myocardial infarction, and ischemic stroke after coronary intervention.
  
  
  RESULTS
  Overall, CIN occurred in 52 (11.6%) patients. Patients developing CIN had higher baseline central PP (P = 0.004). Patients were then stratified into three groups (low/intermediate/high) according to baseline central PP. Compared to that with the lowest tertile of central PP, patients with the highest tertile of central PP had a significantly increased incidence of CIN after PCI (odds ratio, 2.94; 95% confidence interval, CI 1.02-8.51). By Cox regression analysis, elevated central PP was an independent predictor of future MACE in all patients undergoing PCI (hazard ratio, 2.07; 95% CI 1.04-4.12).
  
  
  CONCLUSIONS
  Elevated baseline central PP was associated with an increased risk of CIN and future cardiovascular events in patients with PCI. Further clinical study may be indicated to determine whether pharmacological modulation on baseline central PP could prevent CIN and future MACE after PCI.
authors.affiliation: aDivision of Cardiology, Department of Internal Medicine bDepartment of Medical Research and Education, Taipei Veterans General Hospital cInstitute of Clinical Medicine dCardiovascular Research Center eInstitute and Department of Pharmacology, National Yang-Ming University, Taipei, Taiwan.
authors.forename: Shao-Sung
authors.initials: SS
authors.lastname: Huang
authors.forename: Po-Hsun
authors.initials: PH
authors.lastname: Huang
authors.forename: Hsin-Bang
authors.initials: HB
authors.lastname: Leu
authors.forename: Tao-Cheng
authors.initials: TC
authors.lastname: Wu
authors.forename: Shing-Jong
authors.initials: SJ
authors.lastname: Lin
authors.forename: Jaw-Wen
authors.initials: JW
authors.lastname: Chen
mesh_terms: D000368:Aged; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D003287:Contrast Media / Q000009:adverse effects*; D003404:Creatinine / Q000097:blood; D005260:Female; D006801:Humans; D015994:Incidence; D007674:Kidney Diseases / Q000097:blood / Q000139:chemically induced* / Q000453:epidemiology / Q000503:physiopathology; D007677:Kidney Function Tests; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000209:etiology; D016017:Odds Ratio; D062645:Percutaneous Coronary Intervention / Q000009:adverse effects; D012044:Regression Analysis; D020521:Stroke / Q000209:etiology; D013997:Time Factors
chemical_list: D003287:Contrast Media; D003404:Creatinine