title: Association of increased plasma cardiotrophin-1 with inappropriate left ventricular mass in essential hypertension.
abstract: Inappropriate left ventricular mass is present when the value of left ventricular mass exceeds individual needs to compensate hemodynamic load imposed by increased blood pressure. The goal of this study was to investigate whether plasma concentration of cardiotrophin-1, a cytokine that induces exaggerated hypertrophy in cardiomyocytes with hypertensive phenotype, is related to inappropriate left ventricular mass in patients with essential hypertension. The study was performed in 118 patients with never-treated hypertension and without prevalent cardiac disease. The left ventricular mass prediction from stroke work (systolic blood pressurexDoppler stroke volume), sex, and height (in meters(2.7)) was derived. An observed left ventricular mass/predicted left ventricular mass value >128% defined inappropriate left ventricular mass. Plasma cardiotrophin-1 was measured by an enzyme-linked immunosorbent assay. The studies were repeated in a group of 45 patients after 1 year of antihypertensive treatment. At baseline 67 and 51 patients presented with appropriate and inappropriate left ventricular mass, respectively. Plasma cardiotrophin-1 was higher (P<0.001) in patients with inappropriate mass than in patients with appropriate mass and normotensive controls. A direct correlation was found between cardiotrophin-1 and observed left ventricular mass/predicted left ventricular mass ratio (r=0.330, P<0.001) in all hypertensive patients. After treatment, plasma cardiotrophin-1 decreased and increased in patients in which inappropriate left ventricular mass regressed and persisted, respectively, despite a similar reduction of blood pressure in the 2 subgroups of patients. Albeit descriptive in nature, these results suggest the hypothesis that an excess of cardiotrophin-1 may contribute to inappropriate left ventricular growth in hypertensive patients.
authors.affiliation: Division of Cardiovascular Sciences, University Clinic, University of Navarra, Pamplona, Spain.
authors.forename: Begoña
authors.initials: B
authors.lastname: López
authors.forename: José M
authors.initials: JM
authors.lastname: Castellano
authors.forename: Arantxa
authors.initials: A
authors.lastname: González
authors.forename: Joaquín
authors.initials: J
authors.lastname: Barba
authors.forename: Javier
authors.initials: J
authors.lastname: Díez
mesh_terms: D000328:Adult; D000368:Aged; D057912:Angiotensin II Type 2 Receptor Blockers; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001262:Atenolol / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure / Q000187:drug effects; D016207:Cytokines / Q000097:blood*; D003971:Diastole; D005260:Female; D006352:Heart Ventricles / Q000187:drug effects / Q000503:physiopathology; D006801:Humans; D006852:Hydrochlorothiazide / Q000627:therapeutic use; D006973:Hypertension / Q000097:blood* / Q000188:drug therapy / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000097:blood* / Q000000981:diagnostic imaging / Q000188:drug therapy; D019808:Losartan / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood; D010446:Peptide Fragments / Q000097:blood; D013599:Systole; D014463:Ultrasonography
chemical_list: D057912:Angiotensin II Type 2 Receptor Blockers; D000959:Antihypertensive Agents; D015415:Biomarkers; D016207:Cytokines; D010446:Peptide Fragments; C109794:pro-brain natriuretic peptide (1-76); D006852:Hydrochlorothiazide; D020097:Natriuretic Peptide, Brain; D001262:Atenolol; C092073:cardiotrophin 1; D019808:Losartan