The SA Journal Diabetes & Vascular Disease Vol 11 No 2(June 2014) - page 13

VOLUME 11 NUMBER 2 • JUNE 2014
59
SA JOURNAL OF DIABETES & VASCULAR DISEASE
RESEARCH ARTICLE
categorised according to abdominal circumference or measures of
body fat content and distribution which are most closely linked to
an adverse risk state. Additionally, data on other measures of body
fat distribution such as dual-energy X-ray absorptiometry (DEXA)
scan was notavailable for these subjects. However, viscerally obese
subjects with a normal BMI are rare when compared to those
with an elevated BMI.
21,54
Although we observed a correlation
between obesity or MetS and the epicardial responses to ACH after
univariate analysis, these differences were no longer significant after
adjustment for other risk factors. Because coronary atherosclerosis
causes epicardial constriction with ACH, and the majority of our
cohort had CAD, we may have underestimated the influence of
these factors on epicardial endothelial function in this cohort.
Since this was a cross sectional study, its findings do not infer
causality between obesity or MetS and endothelial dysfunction.
However, the emergence of obesity as an independent risk factor
in recent surveys linking it to cardiovascular events supports our
observations.
55
Furthermore, although the ability of angiography to
confirm a diagnosis of normal coronaries is limited, as eccentric
atheroma is often undetectable with this technique, those with
abnormal angiographic appearances are likely to have a greater
disease burden than those with angiographically ‘smooth’ vessels.
Finally, our cohort consists of highly selected patients and although
not entirely representative of the population as a whole, is well
representative of subjects with and at risk of CAD undergoing
cardiac catheterization in routine clinical practice.
Conclusion
We have shown that clustering of MetS components is an important
and independent determinant of coronary endothelial dysfunction
in subjects with and without CAD. Since, endothelial dysfunction
predates development of overt disease, aggressive risk factor
prevention and earlier therapeutic interventions to ameliorate
endothelial dysfunction in these individuals are likely to be of great
value and require further study.
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