This study was designed to investigate whether plasma concentration of cardiotrophin-1 (CT-1), a cytokine that induces cardiomyocyte hypertrophy and stimulates cardiac fibroblasts, is related to hypertensive heart disease, as defined by the presence of echocardiographically assessed left ventricular hypertrophy (LVH).
The study was performed in 31 normotensive subjects and 111 patients with never-treated essential hypertension (54 without LVH and 57 with LVH). Causes of LVH other than hypertension were excluded after a complete medical workup. A novel enzyme-linked immunosorbent assay was developed to measure plasma CT-1.
Plasma CT-1 was increased (P < 0.001) in hypertensives compared with normotensives. The value of CT-1 was higher (P < 0.001) in hypertensives with LVH than in hypertensives without LVH. Some 31% of patients without LVH exhibited values of CT-1 above the upper normal limit in normotensives. A direct correlation was found between CT-1 and left ventricular mass index (r = 0.319, P < 0.001) in all subjects. Receiver operating characteristic curves showed that a cutoff of 39 fmol/ml for CT-1 provided 75% specificity and 70% sensitivity for predicting LVH with a relative risk of 6.21 (95% confidence interval, 2.95 to 13.09).
These results show an association between LVH and the plasma concentration of CT-1 in essential hypertension. Although preliminary, these findings suggest that the determination of CT-1 may be an easy and reliable method for the initial screening and diagnosis of hypertensive heart disease.
aArea of Cardiovascular Pathophysiology, Centre for Applied Medical Research, School of Medicine
bDivision of Gene Therapy and Hepatology, Centre for Applied Medical Research, School of Medicine, University of Navarra, Navarra
cDepartment of Cardiology and Cardiovascular Surgery, University Clinic, School of Medicine, University of Navarra, Navarra
dPrimary Care Navarra Health Service
eDepartment of Epidemiology and Public Health, University of Navarra, Navarra
fDepartment of Clinical Biochemistry, University Clinic, School of Medicine, University of Navarra, Navarra
gDepartment of Internal Medicine, University Clinic, School of Medicine, University of Navarra, Navarra, Spain
Received 29 July, 2004
Revised 12 October, 2004
Accepted 14 October, 2004
Sponsorship: This work was supported by a grant from the UTE Project FIMA and by a grant (FIS 02/1484) from the Fondo de Investigaciones Sanitarias, Ministry of Health, Spain.
Correspondence and requests for reprints to Javier Díez, Área de Fisiopatología Cardiovascular, CIMA – Facultad de Medicina, C/ Pío XII 55, 31080 Pamplona, Spain. Tel: +34 948 194700, fax: +34 948 194716; e-mail: email@example.com
*These authors contributed equally to this work.