Browsing by Author "Yilmaz, Mehmet Birhan"

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Carotis Intima-Media Thickness, Coronary Calcium Score at Different Stages of Coronary Artery Disease
(Dokuz Eylul Univ Inst Health Sciences, 2024) Okan, Taha; Doruk, Mehmet; Ozturk, Ali; Topaloglu, Caner; Yilmaz, Mehmet Birhan
Purpose: Coronary Artery Calcium Score (CACS) and Carotid Artery Intima-Media Thickness (CIMT) are surrogate markers for atherosclerosis. CACS is a recognized indicator of coronary artery disease (CAD), but CIMT's role in CAD diagnosis is debated. This study aimed to assess how well CIMT and CACS predict CAD presence and severity as detected by coronary computed tomography angiography (CCTA). Materials and Methods: In the study, 88 participants (57 CAD and 31 controls) underwent coronary angiography and CACS calculation using computerized tomography and CIMT measured according to the guidelines. Patients with CAD were classified by CACT results and further subdivided by CACS into three groups: Group I (<100), Group II (100-300), and Group III (>= 300). The relationship between CIMT and CAD groups with zero Agatston scores, as well as the control group, was also examined. Results: The CACS had 82% sensitivity and 100% specificity for predicting CAD, excluding CAD with 75.6% specificity. A CIMT max cut-off of >= 0.78 mm showed 76% sensitivity and 54% specificity for CAD. A CIMT max cut-off of >= 1.03 mm had 93% specificity but only 35% sensitivity, while <= 0.59 mm excluded CAD with 96% specificity but just 10% sensitivity. Patients with CIMT levels between 0.59 mm and 1.03 mm may need further testing to assess CAD risk accurately. Conclusion: The CACS is more sensitive than CIMT in predicting CAD, and CIMT is not helpful when the CACS is zero. Determining an optimal CIMT cutoff for CAD prediction is challenging, and patients with CIMT between 0.59 mm and 1.03 mm may require additional testing.
Diagnostic Potential of Ctrp5 and Chemerin for Coronary Artery Disease: a Study by Coronary Computed Tomography Angiography
(Mdpi, 2025) Okan, Taha; Altin, Cihan; Topaloglu, Caner; Doruk, Mehmet; Yilmaz, Mehmet Birhan
Background/Objectives: As an endocrine organ, adipose tissue produces adipokines that influence coronary artery disease (CAD). The objective of this study was to assess the potential value of CTRP5 and chemerin in differentiating coronary computed tomography angiography (CCTA)-confirmed coronary artery disease (CAD) versus non-CAD. Secondarily, within the CCTA-confirmed CAD group, the aim was to investigate the relationship between the severity and extent of CAD, as determined by coronary artery calcium score (CACS), and the levels of CTRP5 and chemerin. Methods: Consecutive individuals with chest pain underwent CCTA to evaluate coronary artery anatomy and were divided into two groups. The CCTA-confirmed CAD group included patients with any atherosclerotic plaque (soft, mixed, or calcified) regardless of calcification, while the non-CAD group consisted of individuals without plaques on CCTA, with zero CACS, and without ischemia on stress ECG. Secondarily, in the CCTA-confirmed CAD group, the severity and extent of CAD were evaluated using CACS. Blood samples were collected and stored at -80 degrees C for analysis of CTRP5 and chemerin levels via ELISA. Results: Serum CTRP5 and chemerin levels were significantly higher in the CAD group compared to the non-CAD group (221.83 +/- 103.81 vs. 149.35 +/- 50.99 ng/mL, p = 0.003 and 105.02 +/- 35.62 vs. 86.07 +/- 19.47 ng/mL, p = 0.005, respectively). Receiver operating characteristic (ROC) analysis showed that a CTRP5 cutoff of 172.30 ng/mL had 70% sensitivity and 73% specificity for identifying CAD, while a chemerin cutoff of 90.46 ng/mL had 61% sensitivity and 62% specificity. A strong positive correlation was observed between CTRP5 and chemerin, but neither adipokine showed a correlation with the Agatston score, a measure of CAD severity and extent, nor with coronary artery stenosis as determined by CCTA. Conclusions: CTRP5 and chemerin were significantly elevated in the CCTA-confirmed CAD group compared to the non-CAD group, with CTRP5 showing greater sensitivity and specificity. However, neither adipokine was linked to CAD severity and extent, differing from findings based on invasive coronary angiography (ICA). CTRP5 may serve as a promising "all-or-none biomarker" for CAD presence.
Pentraxin 3: a Marker for the Presence and Severity of Coronary Artery Disease
(Kare Publ, 2025) Okan, Taha; Topaloglu, Caner; Altin, Cihan; Doruk, Mehmet; Yilmaz, Mehmet Birhan
Objective: Atherosclerosis, a major contributor to coronary artery disease (CAD), is characterized by chronic arterial inflammation. Pentraxin 3 (PTX-3), a biomarker of inflammation, serves as an indicator of both atherosclerosis and the progression of CAD. The aim of this study was to investigate the association between PTX-3 levels and the presence and severity of CAD, as determined by coronary computed tomography angiography (CCTA). Method: In this study, 94 participants (54 with CAD and 40 controls) underwent CCTA and coronary artery calcium scoring (CACS) using computed tomography. PTX-3 levels were measured using the enzyme-linked immunosorbent assay (ELISA) method. CAD patients were categorized based on CCTA findings and furthersubdivided into three groups according to their CACS: Group I (CACS < 100), Group II (CACS 100-299), and Group III (CACS >= 300). Results: Serum PTX-3 levels were significantly higher in the CAD group. A PTX3 cut-off value of 5.80 ng/mL predicted CAD with 68% sensitivity and 66% specificity. A strong positive correlation was observed between CACS and PTX-3 levels (r = 0.521, P < 0.001). In high-risk patients with a CACS >= 300, PTX-3 levels were significantly higher than those in low- and intermediate-risk groups a CACS < 300. However, no significant difference in PTX-3 levels was observed between the normal coronary group and the low- and intermediate-risk groups. Furthermore, no correlation was found between the degree of coronary artery stenosis and PTX-3 levels. Conclusion: Pentraxin 3 might serve as a valuable biomarkerforthe diagnosis and severity of CAD.