Abstract

Background:

Coronary artery disease (CAD) and osteoporosis (OP) are common diseases in postmenopausal women. In both cross-sectional and longitudinal epidemiologic studies, low bone mass has been related to increased frequency of CAD. However, available data on the relationship between bone mineral density (BMD) and severity of coronary lesions is limited.

Objective:

To investigate association between the BMD and severity of coronary lesions assessed by Gensini score in postmenopausal women.

Methods:

This study included 122 postmenopausal women who were diagnosed with CAD. These patients were divided into two groups according to the severity of coronary lesions assessed by the Gensini score – patients with mild coronary lesions (Gensini score < 25) and patients with severe coronary lesions (Gensini score ≥ 25). Femoral neck mineral density was measured with dual energy X-ray absorptiometry (DXA).

Results:

The study included postmenopausal women aged 64.31 ± 4.71 years, 85 of whom (69.7%) exhibited severe coronary lesions. Participants with severe coronary lesions had a significantly higher T score than did those with mild coronary lesions at the femoral neck (p < 0.05). The mean T-score was −0.84 ± 1.01 in mild coronary lesions group, −1.42 ± 1.39 in severe coronary lesions group (p < 0.05). Multivariable logistic regression analysis showed that osteopenia-osteoporosis at the Femoral neck (odds ratio 2.73; 95% confidence interval 1.06 to 6.13) was associated with an increased risk of developing severe coronary lesions. The multiple regression model showed that T-scores (b = −0.407, SE = 0.151, p=0.007) were the independent predictors of Gensini score.

Conclusion:

The relationship between severity of coronary lesions and BMD was significant in postmenopausal women. BMD, a low-cost technique involving minimal radiation exposure, widely used for osteoporosis screening, is a promising marker of severity of coronary lesions.

In recent years, the association between osteoporosis and atherosclerotic disease has been described, regardless of patients’ age, and highlighted epidemiologic and pathophysiologic similarities between arterial wall calcification and osteogenesis.^, Cross-sectional, prospective studies have pointed out significant negative association between cardiovascular mortality and low bone mass, osteoporotic fractures, vascular calcification, extension of coronary artery disease and abdominal aortic injury.^– Concomitant occurrence of both diseases seems to result from common pathophysiologic and molecular mechanisms between these conditions. However, it is still controversial whether a low bone mass is caused by arterial calcification or vice-versa, or whether these conditions only have the same pathophysiological mechanism.

Risk factors for osteoporosis and atherosclerotic disease include estrogen, parathyroid hormone, homocysteine and vitamin K deficiency, lipid oxidation products, inflammatory process, vitamin D excess, molecular pathways involved in both bone and vascular mineralization, and similar mechanisms of calcification involving vascular and bone structures. Arterial calcification is found in more than 90% of atherosclerotic lesions. The process starts with formation of vesicles in the endothelial matrix, followed by proliferation and mineralization of the arterial intima-media wall, similarly to the bone tissue. Many bone remodeling regulators have been described in calcified atherosclerotic lesions, including osteocalcin, hydroxyapatite crystals, osteopontin, bone morphogenetic protein 2 osteoprotegerin, sclerostin, dickkopf factor (DKK), leptin, oxidized lipids and calcium sensor-related factor.

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