RESUMO
OBJECTIVES: we sought to evaluate the relationship between angina and coronary artery calcium (CAC) in women, and among women without CAC, the associations between angina and clinical, vascular, and inflammatory factors. BACKGROUND: angina in women without coronary atherosclerosis is associated with significant morbidity, yet its determinants are poorly understood. METHODS: women ages 30 to 65 years from the Dallas Heart Study, a multiethnic probability sample of Dallas County residents, who completed a Rose angina questionnaire and had complete data for CAC by computed tomography were selected for this analysis. Soluble intercellular adhesion molecule-1, soluble vascular cell adhesion molecule-1, high sensitivity C-reactive protein, monocyte chemoattractant protein-1 and aortic compliance by magnetic resonance imaging were measured. RESULTS: among the 1,480 women in this cohort (mean age 45 years, 49% African-American), angina was present in 6.9% but was not associated with CAC (19% CAC prevalence with angina vs. 15% without, p = 0.2). Among women without CAC, angina was related to variables reflecting obesity and insulin resistance and was independently associated with African-American ethnicity, premature family history of myocardial infarction, and waist circumference (all p < 0.05). Such women with angina also had higher levels of soluble intercellular adhesion molecule-1 (668 vs. 592 ng/ml, p = 0.02) and soluble vascular cell adhesion molecule-1 (1,106 vs. 968 ng/ml, p = 0.01) and reduced aortic compliance (mean 22 vs. 26 ml/mm Hg, p = 0.007) than such women without angina. Conversely, there was no difference in C-reactive protein or monocyte chemoattractant protein-1 levels for women with and without angina (p = not significant, each). CONCLUSIONS: angina among women in the general population is common and is not associated with subclinical atherosclerosis. Additionally, angina in the absence of subclinical atherosclerosis is not related to many traditional atherosclerotic risk factors but is associated with clinical, inflammatory, and vascular factors that reflect endothelial dysfunction and vascular stiffness, suggesting a distinct vascular etiology and alternative potential therapeutic targets.
