Original article Herz DOI 10.1007/s00059-015-4313-4 Received: 22 January 2015 Revised: 20 March 2015 Accepted: 28 March 2015
Huseyin Altug Cakmak1 · Serkan Aslan2 · Ahmet Arif Yalcin2 · Ibrahim Faruk Akturk2 · Burce Yalcin3 · Fatih Uzun2 · Derya Ozturk2 · Mehmet Erturk2 · Mehmet Gul2
© Urban & Vogel 2015
3 Department of Microbiology, Kanuni Sultan Suleyman Education and Training Hospital, Istanbul, Turkey
1 Department of Cardiology, Rize Kackar Government Hospital, Rize, Turkey 2 Department of Cardiology, Mehmet Akif Ersoy Thoracic and Cardiovascular Surgery Education and
Training Hospital, Istanbul, Turkey
Relationship between serum visfatin levels and coronary slow-flow phenomenon The coronary slow-flow (CSF) phenomenon is a delayed antegrade progression of contrast agent to the distal branch of a coronary artery in the absence of obstructive coronary artery disease (CAD), coronary ectasia, coronary vasospasm, valvular or myocardial disease, or acute coronary syndrome [1]. It is a relatively common angiographic finding, with a reported incidence of 1–34 % in patients undergoing coronary angiography for suspected CAD [2, 3]. The presence of CSF has been related with various clinical events, such as hypertension, acute myocardial infarction, stable and unstable angina pectoris, life-threatening arrhythmias, and sudden cardiac death [4, 5]. The precise etiologies and pathophysiological mechanisms are not yet understood, nor have the clinical significance and long-term course of CSF been established, but several mechanisms have been proposed. Visfatin (nicotinamide phosphoribosyl transferase, or pre-beta colony-enhancing factor), a novel adipokine expressed predominantly in visceral adipose tissue, was originally isolated from peripheral blood lymphocytes [6]. It has insulin-mimetic effects and may cause insulin sensitivity [6]. In vivo, it promotes angiogenesis but impairs vascular endothelial function [7, 8]. Recently, visfatin was identified in foam cell macrophages within human unstable atherosclerotic plaques and was demonstrated to induce tumor necrosis factor alpha (TNF)-α and interleukin (IL)-6 in human monocytes, indicating a possible role in acute coronary events [9, 10]. A recent study demonstrated a neg-
ative relationship between visfatin and flow-mediated vasodilatation in type 2 diabetes mellitus [8], which may also indicate an involvement of visfatin in endothelial dysfunction and microvascular disease. Plasma visfatin levels have been reported to be increased in patients with obesity [11], type 2 diabetes [11], inflammatory bowel disease [12], rheumatic arthritis [13], and atherosclerosis of the coronary and carotid arteries [14]. Only one study in the literature has reported an association between visfatin levels and presence of CSF in patients with stable angina pectoris [15]. The aim of the present study was therefore to investigate the relationship between serum visfatin levels and the presence and extent of CSF in patients with stable angina pectoris undergoing elective coronary angiography.
Patients and methods Patient selection and study protocol This was a cross-sectional observational study. Coronary angiography was performed on 2,812 consecutive patients between March 2013 and June 2014. Of these, 90 (3.2 %) patients who had angiographically confirmed normal coronary arteries and slow coronary flow were included in the study. During this period, of the 208 (7.4 %) patients who had normal coronary arteries and normal coronary flow, 50 patients were randomly enrolled as the control group by three different experienced cardiologists without knowledge of the
patient’s demographic, clinical, and laboratory data. All patients had angiographically normal coronary arteries, with varying coronary flow rates and without any atherosclerotic lesions. Study participants were divided into two groups according to their coronary flow rates: 90 patients with isolated CSF and 50 control subjects with normal coronary flow. All study patients had chest pain or angina-equivalent symptoms, with positive results from either a treadmill test or a myocardial perfusion study. Demographic, clinical, and laboratory characteristics of the study groups were recorded from each patient’s history and physical examination, collected by physicians from the cardiology clinics at the time of cardiac catheterization, and stored in the database of the coronary angiography laboratory. The exclusion criteria for the present study were acute coronary syndromes, coronary ectasia (dilatation of the coronary artery diameter more than 1.5-fold compared with an adjacent healthy reference segment) or anomaly, coronary vasospasm, systolic (left ventricular ejection fraction 3 times the upper limit of normal), evidence of ongoing infection or inflammation, hematological disorders, chronic obstructive lung disease, medications that affect coagulation pathways, known malignancy, autoimmune diseases, major trauma or surgery in the previous 3 months, and thyroid dysfunctions such as hypothyroidism and hyperthyroidism. Study participants who were taking vasoactive drugs underwent a 3-day “wash-out” before the coronary angiography procedure. All study participants underwent a transthoracic echocardiographic examination using a Vivid S6 device with a 3.5MHz phased array transducer (GE Medical Systems, Horten, Norway) to evaluate left ventricular function. Recordings were performed with the patients in the left lateral decubitus position. Left ventricular ejection fraction was measured using Simpson’s method of disks, using two-dimensional images. The study protocol was approved by the local ethics committee, and all patients provided informed consent. The study was conducted in accordance with the ethical principles described by the Declaration of Helsinki.
Definitions The CSF phenomenon is a delayed antegrade progression of contrast agent to the distal branch of a coronary artery in the absence of obstructive CAD, coronary ectasia, coronary vasospasm, valvular or myocardial disease, and acute coronary syndrome. Angiographic evidence of CSF is defined by: (a) no evidence of obstructive epicardial CAD, (b) delayed distal vessel contrast opacification as evidenced by either TIMI-II flow or corrected TIMI frame count of > 27 frames, and (c) delayed distal vessel opacification in at least one epicardial vessel. Smoking was defined as the current regular use of cigarettes. Hypertension was diagnosed if systolic arterial pressure exceeded 140 mmHg and/or diastolic arterial pressure exceeded 90 mmHg, or if the patient was taking antihypertensive drugs [16]. Diabetes mellitus was defined as: a previous history of the disease; use of diet, insulin, or oral antidiabetic
2
Herz
drugs; or a fasting venous blood glucose level ≥ 126 mg/dl on two occasions in previously untreated patients [17]. The GFR for each patient was calculated using the measured plasma creatinine levels and the Cockcroft–Gault formula for the estimation of renal function [18]. Hyperlipidemia was defined as fasting total serum cholesterol > 200 mg/dl, low-density lipoprotein (LDL) cholesterol > 130 mg/dl, or serum triglycerides (TG) > 180 mg/dl, or use of lipid-lowering drugs because of a history of hypercholesterolemia [19]. The height and weight of each study participant were measured, and body mass index (BMI) was calculated as body weight in kilograms divided by the square of the height in meters (kg/m2).
cera Bioscience Inc., Santa Clara, Calif.), with a lower sensitivity limit of 0.2 ng/ml. Samples were measured in duplicate in a single experiment. The intra- and interassay coefficients of variance of this kit are 6–8 and 10–12 % respectively. The detection range of visfatin was 1–64 ng/ml. We used the turbidimetric method to measure high-sensitivity C-reactive protein (hsCRP; Hitachi 917 analyzer, Boehringer Mannheim, Germany). The detection limit was 0.1 mg/l, with intra- and interassay coefficients of variances of 1.38 and 5.8 %, respectively, for hsCRP.
Biochemical measurements
Coronary angiography was performed via a femoral approach using the standard Judkins technique, with a monoplane cineangiography system. Coronary angiograms were recorded in right and left oblique planes using cranial and caudal angulations, with a rate of 30 frames/s. During the coronary angiography procedures, iopromide (Ultravist 370, Schering AG, Berlin, Germany) was used as the contrast agent for all study participants. The patients were evaluated for the presence of CSF during coronary angiography. Coronary blood flow rates were measured quantitatively, using the thrombolysis in myocardial infarction (TIMI) frame count method (TFC), by two experienced interventional cardiologists who were totally blinded to the study [20]. The intraand interobserver coefficients of variation were 4.8 and 7.6 %, respectively. This method notes the number of cine frames required for the contrast agent to reach standard distal coronary landmarks in the left anterior descending (LAD), left circumflex (LCX), and right coronary (RCA) arteries. The initial frame count is defined as the frame in which concentrated dye occupies the full width of the proximal coronary artery lumen, touching both borders of the lumen, and having forward motion distal to the artery. The final frame is designated when the leading edge of the contrast column first reaches the distal end. Predefined distal landmarks are the distal bifurcation for the LAD, commonly referred to as the “mous-
Blood samples were drawn by venipuncture, using the vacutainer system from Becton Dickinson (Franklin Lakes, N.J.), into tubes containing anticoagulant EDTA. Samples were collected between 8:00 and 10:00 a.m. after a 12-h overnight fast from the antecubital vein, with the patient in a sitting position. The serum was obtained by centrifugation at 3,000 rpm at 4 °C for 15 min. Obtained sera were stored at − 80 °C until analysis. All routine biochemical and hematological parameters were measured on the day of blood draw. Biochemical parameters, including fasting blood glucose, creatinine, total cholesterol, high-density lipoprotein (HDL) cholesterol, LDL cholesterol, and TG, were measured using an Abbott Diagnostics C8000i (Abbott, Germany) auto-analyzer with commercial kits. The LDL cholesterol was assayed by applying Friedewald’s formula for samples with TG ≤ 400 mg/dl. Hematological parameters were obtained using the Coulter LH 780 Hematology Analyzer (Beckman Coulter Ireland, Inc., Mervue, Galway, Ireland). The neutrophil–lymphocyte ratio (NLR) was calculated from the differential count by dividing the absolute neutrophil count by the absolute lymphocyte count. Serum visfatin levels were measured with a commercially available kit using an enzyme-linked immunosorbent assay (ELISA) method (Human visfatin ELISA kit, catalogue no. SK00121-01, Avis-
Coronary angiography procedure and determination of coronary slow flow
Abstract · Zusammenfassung tache,” “pitchfork,” or “whale’s tail,” the distal bifurcation of the segment with the longest total distance for the LCX, and the first branch of the posterolateral artery for the RCA. The LAD artery is usually longer than the other major coronary arteries, so the TFC for this vessel is often higher. The corrected TIMI frame count (CTFC) for the LAD was obtained by dividing the TFC by 1.7. The mean TFC for each patient and control subject was calculated by totaling the TFC for the LAD, LCX, and RCA and then dividing by 3. The standard corrected mean values for normal visualization of the coronary arteries are 36.2 ± 2.6 frames for the LAD, 22.2 ± 4.1 frames for the LCX, and 20.4 ± 3 frames for the RCA [20]. The standard corrected mean value (cTFC) for the LAD coronary artery is 21.1 ± 1.5 frames. All study participants with a TFC that exceeded the previously published range for the particular vessel by more than 2 standard deviations (SDs) were considered to have CSF. In our study, values obtained above these thresholds in any of the three coronary arteries (not all three) were considered to be indicative of CSF.
Statistical analysis Continuous, normally distributed variables are presented as mean ± SD. Categorical variables are presented as frequencies and/or percentages. The Kolmogorov–Smirnov test was used to evaluate whether the continuous variables were normally distributed. Student’s t test was used for the comparison of normally distributed continuous numerical variables, the Mann–Whitney U test was used for non-normally distributed numerical variables, and the χ2test was used for comparing categorical variables between the two groups. Any correlation between data was tested by Spearman or Pearson correlation analysis. A receiver operating characteristic (ROC) analysis was performed to investigate the diagnostic value of serum visfatin and hsCRP levels in discriminating patients with CSF in at least one of the coronary arteries from patients without CSF. A logistic regression analysis was performed to detect the independent predictors of angiographically confirmed CSF. The covariates that signifi-
Herz DOI 10.1007/s00059-015-4313-4 © Urban & Vogel 2015 H.A. Cakmak · S. Aslan · A.A. Yalcin · I.F. Akturk · B. Yalcin · F. Uzun · D. Ozturk · M. Erturk · M. Gul
Relationship between serum visfatin levels and coronary slow-flow phenomenon Abstract Background. Increased levels of visfatin, a novel adipocytokine, are reported in atherosclerosis, obesity, and type 2 diabetes. The aim of the present study was to investigate the relationship between coronary slow flow (CSF) and visfatin in patients undergoing elective coronary angiography for suspected coronary artery disease. Patients and methods. A total of 140 recruited participants (90 patients with CSF and 50 controls) were divided into two groups according to their coronary flow rates. Coronary flow was quantified by thrombolysis in myocardial infarction (TIMI) frame count (TFC). Results. Serum visfatin levels were higher in the CSF group than in the control group (3.29 ± 1.11 vs. 2.70 ± 1.08 ng/ml, p = 0.003).
A significant correlation was found between TFC and visfatin (r = 0.535, p
Huseyin Altug Cakmak1 · Serkan Aslan2 · Ahmet Arif Yalcin2 · Ibrahim Faruk Akturk2 · Burce Yalcin3 · Fatih Uzun2 · Derya Ozturk2 · Mehmet Erturk2 · Mehmet Gul2
© Urban & Vogel 2015
3 Department of Microbiology, Kanuni Sultan Suleyman Education and Training Hospital, Istanbul, Turkey
1 Department of Cardiology, Rize Kackar Government Hospital, Rize, Turkey 2 Department of Cardiology, Mehmet Akif Ersoy Thoracic and Cardiovascular Surgery Education and
Training Hospital, Istanbul, Turkey
Relationship between serum visfatin levels and coronary slow-flow phenomenon The coronary slow-flow (CSF) phenomenon is a delayed antegrade progression of contrast agent to the distal branch of a coronary artery in the absence of obstructive coronary artery disease (CAD), coronary ectasia, coronary vasospasm, valvular or myocardial disease, or acute coronary syndrome [1]. It is a relatively common angiographic finding, with a reported incidence of 1–34 % in patients undergoing coronary angiography for suspected CAD [2, 3]. The presence of CSF has been related with various clinical events, such as hypertension, acute myocardial infarction, stable and unstable angina pectoris, life-threatening arrhythmias, and sudden cardiac death [4, 5]. The precise etiologies and pathophysiological mechanisms are not yet understood, nor have the clinical significance and long-term course of CSF been established, but several mechanisms have been proposed. Visfatin (nicotinamide phosphoribosyl transferase, or pre-beta colony-enhancing factor), a novel adipokine expressed predominantly in visceral adipose tissue, was originally isolated from peripheral blood lymphocytes [6]. It has insulin-mimetic effects and may cause insulin sensitivity [6]. In vivo, it promotes angiogenesis but impairs vascular endothelial function [7, 8]. Recently, visfatin was identified in foam cell macrophages within human unstable atherosclerotic plaques and was demonstrated to induce tumor necrosis factor alpha (TNF)-α and interleukin (IL)-6 in human monocytes, indicating a possible role in acute coronary events [9, 10]. A recent study demonstrated a neg-
ative relationship between visfatin and flow-mediated vasodilatation in type 2 diabetes mellitus [8], which may also indicate an involvement of visfatin in endothelial dysfunction and microvascular disease. Plasma visfatin levels have been reported to be increased in patients with obesity [11], type 2 diabetes [11], inflammatory bowel disease [12], rheumatic arthritis [13], and atherosclerosis of the coronary and carotid arteries [14]. Only one study in the literature has reported an association between visfatin levels and presence of CSF in patients with stable angina pectoris [15]. The aim of the present study was therefore to investigate the relationship between serum visfatin levels and the presence and extent of CSF in patients with stable angina pectoris undergoing elective coronary angiography.
Patients and methods Patient selection and study protocol This was a cross-sectional observational study. Coronary angiography was performed on 2,812 consecutive patients between March 2013 and June 2014. Of these, 90 (3.2 %) patients who had angiographically confirmed normal coronary arteries and slow coronary flow were included in the study. During this period, of the 208 (7.4 %) patients who had normal coronary arteries and normal coronary flow, 50 patients were randomly enrolled as the control group by three different experienced cardiologists without knowledge of the
patient’s demographic, clinical, and laboratory data. All patients had angiographically normal coronary arteries, with varying coronary flow rates and without any atherosclerotic lesions. Study participants were divided into two groups according to their coronary flow rates: 90 patients with isolated CSF and 50 control subjects with normal coronary flow. All study patients had chest pain or angina-equivalent symptoms, with positive results from either a treadmill test or a myocardial perfusion study. Demographic, clinical, and laboratory characteristics of the study groups were recorded from each patient’s history and physical examination, collected by physicians from the cardiology clinics at the time of cardiac catheterization, and stored in the database of the coronary angiography laboratory. The exclusion criteria for the present study were acute coronary syndromes, coronary ectasia (dilatation of the coronary artery diameter more than 1.5-fold compared with an adjacent healthy reference segment) or anomaly, coronary vasospasm, systolic (left ventricular ejection fraction 3 times the upper limit of normal), evidence of ongoing infection or inflammation, hematological disorders, chronic obstructive lung disease, medications that affect coagulation pathways, known malignancy, autoimmune diseases, major trauma or surgery in the previous 3 months, and thyroid dysfunctions such as hypothyroidism and hyperthyroidism. Study participants who were taking vasoactive drugs underwent a 3-day “wash-out” before the coronary angiography procedure. All study participants underwent a transthoracic echocardiographic examination using a Vivid S6 device with a 3.5MHz phased array transducer (GE Medical Systems, Horten, Norway) to evaluate left ventricular function. Recordings were performed with the patients in the left lateral decubitus position. Left ventricular ejection fraction was measured using Simpson’s method of disks, using two-dimensional images. The study protocol was approved by the local ethics committee, and all patients provided informed consent. The study was conducted in accordance with the ethical principles described by the Declaration of Helsinki.
Definitions The CSF phenomenon is a delayed antegrade progression of contrast agent to the distal branch of a coronary artery in the absence of obstructive CAD, coronary ectasia, coronary vasospasm, valvular or myocardial disease, and acute coronary syndrome. Angiographic evidence of CSF is defined by: (a) no evidence of obstructive epicardial CAD, (b) delayed distal vessel contrast opacification as evidenced by either TIMI-II flow or corrected TIMI frame count of > 27 frames, and (c) delayed distal vessel opacification in at least one epicardial vessel. Smoking was defined as the current regular use of cigarettes. Hypertension was diagnosed if systolic arterial pressure exceeded 140 mmHg and/or diastolic arterial pressure exceeded 90 mmHg, or if the patient was taking antihypertensive drugs [16]. Diabetes mellitus was defined as: a previous history of the disease; use of diet, insulin, or oral antidiabetic
2
Herz
drugs; or a fasting venous blood glucose level ≥ 126 mg/dl on two occasions in previously untreated patients [17]. The GFR for each patient was calculated using the measured plasma creatinine levels and the Cockcroft–Gault formula for the estimation of renal function [18]. Hyperlipidemia was defined as fasting total serum cholesterol > 200 mg/dl, low-density lipoprotein (LDL) cholesterol > 130 mg/dl, or serum triglycerides (TG) > 180 mg/dl, or use of lipid-lowering drugs because of a history of hypercholesterolemia [19]. The height and weight of each study participant were measured, and body mass index (BMI) was calculated as body weight in kilograms divided by the square of the height in meters (kg/m2).
cera Bioscience Inc., Santa Clara, Calif.), with a lower sensitivity limit of 0.2 ng/ml. Samples were measured in duplicate in a single experiment. The intra- and interassay coefficients of variance of this kit are 6–8 and 10–12 % respectively. The detection range of visfatin was 1–64 ng/ml. We used the turbidimetric method to measure high-sensitivity C-reactive protein (hsCRP; Hitachi 917 analyzer, Boehringer Mannheim, Germany). The detection limit was 0.1 mg/l, with intra- and interassay coefficients of variances of 1.38 and 5.8 %, respectively, for hsCRP.
Biochemical measurements
Coronary angiography was performed via a femoral approach using the standard Judkins technique, with a monoplane cineangiography system. Coronary angiograms were recorded in right and left oblique planes using cranial and caudal angulations, with a rate of 30 frames/s. During the coronary angiography procedures, iopromide (Ultravist 370, Schering AG, Berlin, Germany) was used as the contrast agent for all study participants. The patients were evaluated for the presence of CSF during coronary angiography. Coronary blood flow rates were measured quantitatively, using the thrombolysis in myocardial infarction (TIMI) frame count method (TFC), by two experienced interventional cardiologists who were totally blinded to the study [20]. The intraand interobserver coefficients of variation were 4.8 and 7.6 %, respectively. This method notes the number of cine frames required for the contrast agent to reach standard distal coronary landmarks in the left anterior descending (LAD), left circumflex (LCX), and right coronary (RCA) arteries. The initial frame count is defined as the frame in which concentrated dye occupies the full width of the proximal coronary artery lumen, touching both borders of the lumen, and having forward motion distal to the artery. The final frame is designated when the leading edge of the contrast column first reaches the distal end. Predefined distal landmarks are the distal bifurcation for the LAD, commonly referred to as the “mous-
Blood samples were drawn by venipuncture, using the vacutainer system from Becton Dickinson (Franklin Lakes, N.J.), into tubes containing anticoagulant EDTA. Samples were collected between 8:00 and 10:00 a.m. after a 12-h overnight fast from the antecubital vein, with the patient in a sitting position. The serum was obtained by centrifugation at 3,000 rpm at 4 °C for 15 min. Obtained sera were stored at − 80 °C until analysis. All routine biochemical and hematological parameters were measured on the day of blood draw. Biochemical parameters, including fasting blood glucose, creatinine, total cholesterol, high-density lipoprotein (HDL) cholesterol, LDL cholesterol, and TG, were measured using an Abbott Diagnostics C8000i (Abbott, Germany) auto-analyzer with commercial kits. The LDL cholesterol was assayed by applying Friedewald’s formula for samples with TG ≤ 400 mg/dl. Hematological parameters were obtained using the Coulter LH 780 Hematology Analyzer (Beckman Coulter Ireland, Inc., Mervue, Galway, Ireland). The neutrophil–lymphocyte ratio (NLR) was calculated from the differential count by dividing the absolute neutrophil count by the absolute lymphocyte count. Serum visfatin levels were measured with a commercially available kit using an enzyme-linked immunosorbent assay (ELISA) method (Human visfatin ELISA kit, catalogue no. SK00121-01, Avis-
Coronary angiography procedure and determination of coronary slow flow
Abstract · Zusammenfassung tache,” “pitchfork,” or “whale’s tail,” the distal bifurcation of the segment with the longest total distance for the LCX, and the first branch of the posterolateral artery for the RCA. The LAD artery is usually longer than the other major coronary arteries, so the TFC for this vessel is often higher. The corrected TIMI frame count (CTFC) for the LAD was obtained by dividing the TFC by 1.7. The mean TFC for each patient and control subject was calculated by totaling the TFC for the LAD, LCX, and RCA and then dividing by 3. The standard corrected mean values for normal visualization of the coronary arteries are 36.2 ± 2.6 frames for the LAD, 22.2 ± 4.1 frames for the LCX, and 20.4 ± 3 frames for the RCA [20]. The standard corrected mean value (cTFC) for the LAD coronary artery is 21.1 ± 1.5 frames. All study participants with a TFC that exceeded the previously published range for the particular vessel by more than 2 standard deviations (SDs) were considered to have CSF. In our study, values obtained above these thresholds in any of the three coronary arteries (not all three) were considered to be indicative of CSF.
Statistical analysis Continuous, normally distributed variables are presented as mean ± SD. Categorical variables are presented as frequencies and/or percentages. The Kolmogorov–Smirnov test was used to evaluate whether the continuous variables were normally distributed. Student’s t test was used for the comparison of normally distributed continuous numerical variables, the Mann–Whitney U test was used for non-normally distributed numerical variables, and the χ2test was used for comparing categorical variables between the two groups. Any correlation between data was tested by Spearman or Pearson correlation analysis. A receiver operating characteristic (ROC) analysis was performed to investigate the diagnostic value of serum visfatin and hsCRP levels in discriminating patients with CSF in at least one of the coronary arteries from patients without CSF. A logistic regression analysis was performed to detect the independent predictors of angiographically confirmed CSF. The covariates that signifi-
Herz DOI 10.1007/s00059-015-4313-4 © Urban & Vogel 2015 H.A. Cakmak · S. Aslan · A.A. Yalcin · I.F. Akturk · B. Yalcin · F. Uzun · D. Ozturk · M. Erturk · M. Gul
Relationship between serum visfatin levels and coronary slow-flow phenomenon Abstract Background. Increased levels of visfatin, a novel adipocytokine, are reported in atherosclerosis, obesity, and type 2 diabetes. The aim of the present study was to investigate the relationship between coronary slow flow (CSF) and visfatin in patients undergoing elective coronary angiography for suspected coronary artery disease. Patients and methods. A total of 140 recruited participants (90 patients with CSF and 50 controls) were divided into two groups according to their coronary flow rates. Coronary flow was quantified by thrombolysis in myocardial infarction (TIMI) frame count (TFC). Results. Serum visfatin levels were higher in the CSF group than in the control group (3.29 ± 1.11 vs. 2.70 ± 1.08 ng/ml, p = 0.003).
A significant correlation was found between TFC and visfatin (r = 0.535, p
