title: Usefulness of C-reactive protein and left ventricular diastolic performance for prognosis in patients with left ventricular systolic heart failure.
abstract: High-sensitivity C-reactive protein (hs-CRP) is a hepatocyte-derived inflammatory cytokine shown to be increased in the setting of acute heart failure (HF), particularly with increased intracardiac filling pressures. In the chronic HF setting, the relation between hs-CRP and echocardiographic indexes of left ventricular (LV) diastolic performance has not been examined. We measured plasma hs-CRP levels using a particle-enhanced immunonephelometry assay (Dade Behring, Inc., Deerfield, Illinois) in 136 subjects with chronic HF (LV ejection fraction [EF]<or=35%, New York Heart Association functional classes II to IV). We performed echocardiography, including color M-mode and tissue Doppler methods. We prospectively examined subjects' death, cardiac transplantation, and HF hospitalization status over 33+/-17 months. In our study cohort (mean LVEF 26+/-6%, median plasma hs-CRP 3.19 mg/L), plasma hs-CRP levels progressively increased with worsening LV diastolic dysfunction. In particular, plasma hs-CRP levels correlated with mitral E/A wave ratio (Spearman r=0.25, p=0.004), mitral deceleration time (r=-0.28, p=0.002), pulmonary vein systolic wave/diastolic wave ratio (r=-0.32, p<0.001), mitral E wave/color M-mode velocity of propagation ratio (r=0.28, p=0.001), and mitral E wave/tissue Doppler septal E' wave ratio (r=0.28, p=0.001). Plasma hs-CRP levels independently predicted adverse clinical events even after adjustment for LVEF and mitral E wave/tissue Doppler septal E' wave ratio (hazard ratio 2.28, 95% confidence interval 1.18 to 4.39). In conclusion, in patients with chronic systolic HF, expression of circulating CRP was associated with increasing echocardiographic indexes of diastolic dysfunction. High plasma hs-CRP levels portend poor long-term outcomes, particularly in those with severe concomitant systolic and diastolic dysfunctions.
authors.affiliation: Department of Cardiovascular Medicine, Cleveland Clinic Foundation, Cleveland, Ohio, USA. tangw@ccf.org
authors.forename: W H Wilson
authors.initials: WH
authors.lastname: Tang
authors.forename: Kevin
authors.initials: K
authors.lastname: Shrestha
authors.forename: Frederick
authors.initials: F
authors.lastname: Van Lente
authors.forename: Richard W
authors.initials: RW
authors.lastname: Troughton
authors.forename: Maureen G
authors.initials: MG
authors.lastname: Martin
authors.forename: Allen G
authors.initials: AG
authors.lastname: Borowski
authors.forename: Sue
authors.initials: S
authors.lastname: Jasper
authors.forename: Allan L
authors.initials: AL
authors.lastname: Klein
mesh_terms: D000328:Adult; D000368:Aged; D002097:C-Reactive Protein / Q000032:analysis*; D003971:Diastole / Q000502:physiology*; D015150:Echocardiography, Doppler; D005260:Female; D054143:Heart Failure, Systolic / Q000000981:diagnostic imaging / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D018754:Ventricular Dysfunction / Q000000981:diagnostic imaging / Q000503:physiopathology*; D016277:Ventricular Function, Left / Q000502:physiology*
chemical_list: D002097:C-Reactive Protein