Subclinical coronary atherosclerosis is more pronounced in men and women with lower socio-economic status: associations in a population-based study Coronary atherosclerosis and social status

Background Social inequalities of manifest coronary heart diseases are well documented in modern societies. Less evidence is available on subclinical atherosclerotic disease despite the opportunity to investigate processes underlying this association. Therefore, we examined the relationship between coronary artery calcification as a sign of subclinical coronary atherosclerosis, socio-economic status and established cardiovascular risk factors in a healthy population. Design Cross-sectional. Methods In a population-based sample of 4487 men and women coronary artery calcification was assessed by electron beam computed tomography quantified by the Agatston score. Socio-economic status was assessed by two indicators, education and income. First, we investigated associations between the social measures and calcification. Second, we assessed the influence of cardiovascular risk factors on this association. Results After adjustment for age, men with 10 and less years of formal education had a 70% increase in calcification score compared with men with high education. The respective increase for women was 80%. For income the association was weaker (among men 20% higher for the lowest compared with the highest quartile; and among women 50% higher, respectively). Consecutive adjustment for cardiovascular risk factors significantly attenuated the observed association of socio-economic status with calcification. Conclusions Social inequalities in coronary heart diseases seem to influence signs of subclinical coronary atherosclerosis as measured by coronary artery calcification. Importantly, cumulation of major cardiovascular risk factors in lower socio-economic groups accounted for a substantial part of this association.

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Elevated serum uric acid predicts the development of moderate coronary artery calcification independent of conventional cardiovascular risk factors

Atherosclerosis ◽

10.1016/j.atherosclerosis.2018.02.014 ◽

2018 ◽

Vol 272 ◽

pp. 233-239 ◽

Cited By ~ 11

Author(s):

Ji Eun Jun ◽

You-Bin Lee ◽

Seung-Eun Lee ◽

Ji Yeon Ahn ◽

Gyuri Kim ◽

...

Keyword(s):

Risk Factors ◽

Uric Acid ◽

Cardiovascular Risk ◽

Coronary Artery ◽

Cardiovascular Risk Factors ◽

Serum Uric Acid ◽

Coronary Artery Calcification ◽

Elevated Serum

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Abstract 6133: Microvascular Dysfunction and Chronic Inflammation in Patients without Cardiovascular Risk Factors

Circulation ◽

10.1161/circ.118.suppl_18.s_1068-b ◽

2008 ◽

Vol 118 (suppl_18) ◽

Author(s):

Alejandro Recio-Mayoral ◽

Justin C Mason ◽

Juan C Kaski ◽

Michael B Rubens ◽

Olivier A Harari ◽

...

Keyword(s):

Risk Factors ◽

Coronary Artery Disease ◽

Cardiovascular Risk ◽

Coronary Artery ◽

Cardiovascular Risk Factors ◽

Chronic Inflammation ◽

Coronary Atherosclerosis ◽

Microvascular Dysfunction ◽

Early Marker ◽

Artery Disease

Premature coronary atherosclerosis, which is actually seen as an active inflammatory process, is an established complication of systemic autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). We hypothesized that exposure to chronic inflammation, even in the absence of classical cardiovascular risk factors (CVRF), could result in coronary microvascular dysfunction (CMD), an early marker of coronary atherosclerosis. By means of positron emission tomography in combination with oxygen-15 labeled water, myocardial blood flow (MBF) was measured at rest and during iv adenosine infusion (140 μg/kg/min) in 13 SLE and 12 RA patients (mean [±SD] age 44±10 years) without CVRF. All patients underwent coronary angiography using multi-slice (64 slices) computed tomography and only those with none or trivial coronary artery disease (<30% luminal stenosis) were included. A group of 25 age- and gender-matched controls were also studied. There were no differences between patients and controls regarding body-mass index, blood pressure and lipid parameters. RA and SLE patients showed similar mean disease duration (16±11 and 11±7 years, respectively; p=0.12). Resting MBF was similar in patients and controls (1.25±0.27 vs 1.15±0.24 ml/min/g, p=0.15). However, during adenosine stress patients had lower MBF compared with controls (2.94±0.83 vs 4.11±0.84 ml/min/g, p<0.001). As result, coronary flow reserve (CFR; adenosine/resting MBF) was significantly reduced in patients (2.44±0.78) compared with controls (3.81±1.07; p<0.001). Seven patients showed ischemic electrocardiographic changes during adenosine and had a more severe reduction in CFR (1.76±0.81) and more years of disease (21±7 years) compared with those patients without ischemic changes (CFR 2.49±0.54; p=0.006; duration of disease 14±5 years; p=0.03). CFR was inversely correlated with years of disease (r=−0.65, p<0.001), but not with corticosteroid cumulative dose (r=0.20, p=0.39). Chronic inflammation in the absence of traditional CVRF is characterized by severe CMD. This may represent an early marker of disease which precedes and contributes to premature coronary artery disease in patients with RA and SLE.

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