p. 6−12
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p. 13−19
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p. 20−26
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50% and 40.69±8.96 byCVG vs 43.90±10.71% by echocardiography in EFs≤50%). By linear regression analysis, thepresence of pathologic Q wave, atrial fibrillation and left bundle branch block, moderate andsevere mitral regurgitation, increased LV size, and increased interventricular septal diameterresulted in a higher EF value via CVG, whereas in those with EFs of 50% or less, the EF byechocardiography was higher. No effect of time gap between the measurements was found.Conclusions: According to our study, the EF measurements obtained by echocardiography and CVGvaried on an individual basis. The level of the EF was the most important factor correlating withthe difference between the measurements by the methods.]]>
p. 27−35
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p. 36−43
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p. 44−49
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p. 50−56
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30 ng/mL), insufficient (20–30 ng/mL), mildly-to-moderately deficient (10–20ng/mL), and severely deficient (<10 ng/mL).Results: There was no significant relationship between vitamin D deficiency and the number ofinvolved coronary vessels (P=0.423), and nor was there any difference in the serum level ofvitamin D in the individuals with CAD (24.84±18.53 ng/dL) and those without CAD(22.37±16.88 ng/mL) (P=0.409). Our multivariate logistic regression model showed thatvitamin D deficiency could not predict the presence of CAD (OR=0.963, 95% CI: 0.666 to1.392; P=0.842). Analysis of the area under the ROC curve indicated a low value for themeasurement of the vitamin D level in discriminating CAD from the normal coronary status(AUC=0.533, 95% CI: 0.437 to 0.629; P=0.496).Conclusions: Our study could not demonstrate a predictive role for vitamin D deficiency concerningthe severity of CAD in type 2 diabetes. Among the different CAD risk factors, smoking andopium use were significantly correlated with vitamin D deficiency.]]>
p. 57−64
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