title: Inflammatory markers and serum lipids in idiopathic dilated cardiomyopathy.
abstract: Coronary microcirculation is impaired in idiopathic dilated cardiomyopathy (IDC), possibly because of endothelial dysfunction. High-density lipoproteins (HDLs) have the potential to regulate endothelial function and modulate inflammation and the innate immune response. This study investigated whether reduced HDLs, concomitantly with the activation of inflammation, are associated with IDC. Fifty-five patients with IDC, without evidence of other organ or systemic, chronic, or recurrent diseases, were compared with 55 healthy controls for HDLs and complete lipid profiles, C-reactive protein, C3 and C4 complement fractions, soluble intercellular adhesion molecule-1 and soluble endothelial leukocyte adhesion molecule-1, haptoglobin, and ceruloplasmin. Patients with IDC differed from controls, with lower HDL levels, lower apolipoprotein A-I and A-II levels, and higher triglyceride levels, but not on total and low-density lipoprotein cholesterol, apolipoprotein B, or lipoprotein(a). In addition, all measured inflammation markers were significantly greater in patients with IDC than in controls and were negatively correlated with HDLs. A strong and independent association with IDC was found for age, soluble intercellular adhesion molecule-1, and HDLs that, when categorized as <40 or >40 mg/dl, showed the strongest association (prevalence odds ratio 0.10, p <0.0005) with the disease. In conclusion, the data here reported on reduced HDLs and increased endothelial inflammatory activation and the linear negative correlation between HDLs and inflammation markers, particularly soluble intercellular adhesion molecule-1, could suggest a role for HDLs in the endothelial-microvascular dysfunction seen in IDC.
authors.affiliation: CNR Institute of Clinical Physiology, Pisa, Italy. tizisamp@ifc.cnr.it
authors.forename: Tiziana
authors.initials: T
authors.lastname: Sampietro
authors.forename: Danilo
authors.initials: D
authors.lastname: Neglia
authors.forename: Alberto
authors.initials: A
authors.lastname: Bionda
authors.forename: Beatrice
authors.initials: B
authors.lastname: Dal Pino
authors.forename: Federico
authors.initials: F
authors.lastname: Bigazzi
authors.forename: Mariarita
authors.initials: M
authors.lastname: Puntoni
authors.forename: Umberto
authors.initials: U
authors.lastname: Startari
authors.forename: Aurora
authors.initials: A
authors.lastname: Morales
authors.forename: Fabrizio
authors.initials: F
authors.lastname: Minichilli
authors.forename: Fabrizio
authors.initials: F
authors.lastname: Bianchi
authors.forename: Antonio
authors.initials: A
authors.lastname: L'Abbate
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism*; D002311:Cardiomyopathy, Dilated / Q000097:blood* / Q000150:complications / Q000276:immunology; D002570:Ceruloplasmin / Q000378:metabolism; D008076:Cholesterol, HDL / Q000097:blood*; D003176:Complement C3 / Q000378:metabolism; D003181:Complement C4 / Q000378:metabolism; D018450:Disease Progression; D050171:Dyslipidemias / Q000097:blood / Q000150:complications / Q000276:immunology; D019040:E-Selectin / Q000097:blood; D005260:Female; D006242:Haptoglobins / Q000378:metabolism; D006801:Humans; D007113:Immunity, Innate / Q000502:physiology; D007249:Inflammation / Q000097:blood; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood*
chemical_list: D015415:Biomarkers; D008076:Cholesterol, HDL; D003176:Complement C3; D003181:Complement C4; D019040:E-Selectin; D006242:Haptoglobins; D014280:Triglycerides; D018799:Intercellular Adhesion Molecule-1; D002097:C-Reactive Protein; D002570:Ceruloplasmin