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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:436.)
© 2007 American Heart Association, Inc.

Letter to the Editor

Letter to the Editor

Monocyte cAMP Content Is Decreased in Patients With Stable Angina

Marie Anne Punchard; Aranzazu Ortega Pozzi; Teresa Perez de Prada; Monica Torres Coronado; Pablo Gonzalez; Panayotis Fantidis

From the Laboratorio de Cardiología Experimental (Lab 5), Medicina y Cirugía Experimentales and Hospital Clínico San Carlos, Prof Martín Lagos, 28040 Madrid, Spain.

Correspondence to Panayotis Fantidis, MD, C/ Los Arcos 3, Esc Cent. 2° 4, 28033 Madrid, Spain. Email pfantidis@yahoo.es

An extract of the first 250 words of the full text is provided, because this article has no abstract.

A crucial event in atherosclerosis is the formation of foam cells. Vascular cell adhesion molecule-1 (VCAM-1), intercellular cell adhesion molecule-1 (ICAM-1), macrophage chemoattractant protein-1 (MCP-1), and macrophage colony stimulating factor (M-CSF) are important molecules that contribute to foam cell formation.¹ Removal of excess free cholesterol from macrophages, neutralization of monocyte migration inhibitory factor (MIF), and reduction of proinflammatory cytokine concentrations are important goals for the prevention of foam cell formation and the development of atherosclerosis.^2,3

Increases in intracellular cAMP concentration inhibit the expression of ICAM-1 and VCAM-1,⁴ decrease the production of MCP-1⁵ and M-CSF,⁶ increase the expression of antiinflammatory cytokines, and decrease the expression of MIF and proinflammatory interleukins.⁷ In addition, cAMP analogs induce the ABCA1 secretory pathway, by which apolipoproteins (apoA-I) actively remove free cholesterol from cells; treatment of macrophages with cAMP analogs causes parallel increases in apo-I–mediated cholesterol efflux.⁸

On the basis of the role of cAMP in the expression of proatherogenic and antiatherogenic molecules, we postulated that the intracellular cAMP concentrations of peripheral monocytes may be low in patients with coronary artery disease.

We studied 80 patients with chronic stable angina (SA) who were consecutively admitted to our hospital, and 67 healthy age-matched healthy volunteers with no known coronary artery disease or risk factors. Coronary angiography was carried out with all patients

Total plasma cholesterol (mg/dL), LDL-cholesterol (mg/dL), and HDL-cholesterol (mg/dL) were measured by colorimetric methods (Sigma Diagnostics Inc). Serum interleukin (IL)-6 (pg/mL) was measured by enzyme immunoassay (EIA; Diagnostic Products Corporation).

Peripheral blood mononuclear cells were . . . [Full Text of this Article]