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Kozáni, Greece

Kadoglou N.P.E.,Mamatsio General Hospital | Gkontopoulos A.,Mamatsio General Hospital | Kapelouzou A.,Surgery Academy | Fotiadis G.,Hippokratio General Hospital | And 3 more authors.
Clinica Chimica Acta | Year: 2011

Background: The association of novel adipokines, vaspin and visfatin, with atherosclerosis is still obscure. The present study aimed to investigate the relationship of those adipokines with the existence as well as the extent of coronary artery disease (CAD), suggesting a link between adiposity and atherosclerosis. Methods: We enrolled a total of 108 patients with angiographically proven stable, asymptomatic CAD and 65 healthy controls (HC) without cardiovascular diseases. The severity of CAD was assessed using coronary angiography by the Gensini score. Clinical parameters, glycemic and lipid profile, high-sensitivity CRP (hsCRP), vaspin and visfatin levels were assayed. Results: Serum levels of vaspin were significantly lower in subjects with CAD [0.91 (0.44-1.29) ng/ml] than healthy controls [1.42 (0.96-2.42) ng/ml] (p=0.009). Inversely, visfatin (p=0.016) and hsCRP (p<0.001) levels were considerably up-regulated in CAD vs HC group. Multivariate analysis demonstrated decreased vaspin and increased visfatin levels to correlate with CAD presence, independent of other cardiovascular risk factors (p<0.05). Standard multiple regression revealed HDL, LDL-C and vaspin to be independent determinants of Gensini score (R2=0.189, p=0.019). Notably, statin-free patients had even lower vaspin levels compared to statin users (p=0.018). Conclusions: Decreased vaspin and increased visfatin serum levels were observed in asymptomatic patients with CAD. Low vaspin concentrations seemed to correlate with CAD severity. © 2010 Elsevier B.V.


Kadoglou N.P.E.,Attikon University Hospital | Tahmatzidis D.K.,Mamatsio General Hospital | Giannakoulas C.,Mamatsio General Hospital | Kapelouzou A.,Surgery Academy | And 4 more authors.
Journal of Cardiovascular Medicine | Year: 2015

Objectives The role of the novel adipokines, omentin-1 and chemerin, in coronary artery disease is still obscure. The present study analyzed the serum levels of omentin-1 and chemerin in patients with acute myocardial infarction (AMI) as well as prospectively 6 months post-AMI. Methods Seventy-eight patients (63 men and 15 women) with first AMI were enrolled. Thirty-two age-matched and sex-matched individuals without overt cardiovascular disease served as healthy controls. Serum levels of omentin-1, chemerin, interleukin-18 (IL-18), high-sensitivity C-reactive protein (hsCRP), glycemic and lipid profiles, blood pressure, BMI and ejection fraction were assayed. In AMI patients, blood samples were obtained at hospital admission and after 6 months, whereas coronary angiography was performed within 7 days after admission. Results At baseline, AMI group appeared with significantly lower ejection fraction, omentin-1 and high-density lipoprotein serum levels, whereas it had higher concentrations of white blood cells count (WBC), hsCRP, IL-18 and chemerin compared with healthy controls (P<0.05). After 6 months of follow-up, the concentrations of WBC, hsCRP and IL-18 significantly downregulated, whereas omentin-1 levels considerably increased (from 18.73±3.66ng/ml to 28.62±5.61ng/ml, P<0.001) within AMI group. In contrast, serum chemerin did not significantly change (263.37±73.32ng/ml vs. 195.90±84.32ng/ml, P=0.190). In standard multiple regression analyses, baseline levels and changes of hsCRP and IL-18 levels during follow-up remained independent determinants of omentin-1, respectively at baseline and after follow-up. Conclusion Patients with AMI showed at admission lower omentin-1 and higher chemerin serum levels compared with healthy controls. The suppression of inflammation in the 6-month post-AMI period might have mediated the significant upregulation of omentin-1, implicating a novel target of treatment. © Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.


Kadoglou N.P.E.,Mamatsio General Hospital | Kadoglou N.P.E.,Surgery Academy | Lampropoulos S.,Mamatsio General Hospital | Kapelouzou A.,Surgery Academy | And 4 more authors.
Translational Research | Year: 2010

Apelin and ghrelin have emerged as novel adipokines, but their role in coronary artery disease (CAD) remains obscure. In the present study, we analyzed their serum levels in patients with acute coronary syndromes (ACS) or established asymptomatic CAD. A total of 355 participants were enrolled. Among them were 80 patients with unstable angina (UA) and 115 patients with acute myocardial infarction (AMI) hospitalized in the coronary care unit. We also included 88 asymptomatic patients with established CAD (asymptomatic CAD) and 72 age-and sex-matched healthy controls (HCs). All groups with CAD underwent coronary angiography, and the Gensini score was determined. Clinical parameters, glycemic and lipid profile, high-sensitivity CRP (hsCRP), insulin resistance (HOMA-IR), as well as apelin and ghrelin were assayed. Patients with ACS (UA or AMI) were sampled at hospital admission. All 3 groups with CAD (UA, AMI, or asymptomatic CAD) showed significantly higher levels of hsCRP, HOMA-IR, and white blood cells than controls (P < 0.01). Conversely, apelin and ghrelin concentrations were considerably (P < 0.05) lower in CAD patients with respect to the control group. Most importantly, UA (6.72 ± 3.51 ng/mL) and AMI (6.02 ± 4.07 ng/mL) groups had even lower apelin levels on admission compared with the asymptomatic CAD group (13.53 ± 5.2 ng/mL) (P < 0.05). Logistic regression analysis showed an independent association of low apelin and ghrelin levels with CAD presence. Besides this result, apelin showed an inverse relationship with ACS incidence and a Gensini score independent of other cardiovascular risk factors (P < 0.05). In conclusion, CAD seemed to correlate with low serum apelin and ghrelin levels. Moreover, apelin concentrations inversely were associated with the severity and the acute phase of CAD, which suggests its involvement in the progression and destabilization of coronary atherosclerotic plaques. © 2010 Mosby, Inc. All rights reserved.

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