Cardiovascular Risk Factors in Chilean Patients with Rheumatoid Arthritis

MARCELA CISTERNAS, MIGUEL A. GUTIÉRREZ, JULIETA KLAASSEN, ANA MARÍA ACOSTA, and SERGIO JACOBELLI

ABSTRACT.

Objective. Epidemiologic studies have shown an increased mortality rate in patients with rheumatoid arthritis (RA). The most common cause of death in these patients is cardiovascular disease. We estimated the frequency of and examined risk factors for coronary artery disease in Chilean patients with RA.

Methods. Fifty-four patients with RA were studied: 87% were women, with a mean age (± standard deviation) of 51 ± 13 yrs, 92% were rheumatoid factor positive, and 51% had radiological erosions; 32 age and sex matched healthy controls were studied. Traditional cardiovascular risk factors and RA-specific variables were determined. Lipid profile, lipoprotein(a) [Lp(a)], homocysteine, ultrasensitive C-reactive protein (CRP), anticardiolipin (aCL), anti-ß₂-glycoprotein I (anti-ß₂-GPI) and antioxidized low density lipoprotein (ox-LDL) antibodies were measured.

Results. Median concentration of homocysteine was significantly higher in patients with RA than in controls: 10 (range 5.4-37.4) versus 8.3 (3.6-17.8) µmol/l (p = 0.001). Patients with RA who gave a history of cardiovascular disease had the highest concentrations of homocysteine: 15.1 (13.1-19.7) versus 9.9 (5.4-37.4) µmol/l (p = 0.001). We found no differences between patients and controls in lipid profiles or Lp(a), or for other traditional risk factors. Anti-ox-LDL, IgG aCL, and IgG anti-ß₂-GPI antibody levels were similar in both groups. IgM subtypes were higher in patients with RA than in controls, but in low titers.

Conclusion. Our data suggest that a high homocysteine concentration could be an important risk marker for cardiovascular disease in patients with RA. (J Rheumatol 2002;29:1619-22)

Key Indexing Terms:

ATHEROSCLEROSIS
RHEUMATOID ARTHRITIS
LIPID PROFILES
HOMOCYSTEINE

---

From the Departamento de Inmunología, Clínica y Reumatología, and Departamento de Nutrición, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile.

Supported by Escuela de Medicina Pontificia Universidad Católica de Chile and Fondo Nacional de Investigación Científica y Tecnológica (FONDECYT) #1980954 and #8.000-003.

M. Cisternas, MD; M.A. Gutiérrez, MD; S. Jacobelli, MD, Departamento de Inmunología Clínica y Reumatología; J. Klaassen, MD; A.M. Acosta, BSc, Departamento de Nutrición y Diabetes.

Address reprint requests to Dr. M. Cisternas, Departamento de Inmunología Clínica y Reumatología, Hospital Clínico, Pontificia Universidad Católica de Chile, Marcoleta 367, Santiago, Chile. E-mail: mcister@med.puc.cl

Submitted July 30, 2001; revision accepted February 27, 2002.

---