Normal Coronary Arteries Group Research Articles

Relation of epicardial fat thickness and brachial flow-mediated vasodilation with coronary artery disease

ObjectiveThe purpose of this study is to investigate the presence of a statistical association between epicardial fat thickness (EFT) and coronary artery disease (CAD) and between flow-mediated vasodilation (FMD) and CAD. MethodsWe measured the EFT and FMD in 64 subjects with suspected stable angina pectoris. The patients were separated into two groups according to their coronary angiography results: 34 patients with CAD and 30 patients with normal coronary arteries (NCA). ResultsEFT was significantly higher in the patients with CAD than the NCA group (6.43±0.90mm vs. 5.35±0.75mm, p<0.001) while FMD was significantly lower in the patients with CAD than those in the NCA group (6.41±2.51% vs. 8.33±3.45%, p=0.015). No significant correlation was found between EFT and FMD. After adjustment for EFT, FMD, age, sex, ejection fraction, glucose, and low-density lipoprotein cholesterol through multivariate logistic regression analysis, EFT (odds ratio: 6.325, 95% confidence interval 2.289–17.476, p<0.001) and age (odds ratio: 1.093, 95% confidence interval 1.008–1.185, p=0.032) remained significant predictors of CAD. A cut-off value of EFT≥5.8mm predicted the presence of CAD with 77% sensitivity and 70% specificity. ConclusionAn echocardiographic EFT assessment is independently associated with the presence of CAD. Thus, EFT may be helpful in cardiometabolic risk stratification and therapeutic interventions.

Increased YKL-40 levels in patients with isolated coronary artery ectasia: an observational study

YKL-40, a new biomarker of localized inflammation, is secreted by macrophages within the atherosclerotic plaques. Coronary artery ectasia (CAE) is a clinical entity with unclear etiopathogenesis. Some studies have revealed that CAE may be a form of atherosclerosis that has more localized and intense inflammatory properties than atherosclerosis. The goal of this study was to investigate YKL-40 and C-reactive protein (CRP) levels in patients with isolated CAE compared to patients with normal coronary arteries (NCA) and coronary artery disease (CAD). Our study has an observational and cross-sectional design. Forty-nine patients with isolated CAE (mean age: 60±10 years), 30 age-and gender-matched control participants with NCA (30 patients, mean age: 58±12 years) and 30 patients with CAD (mean age: 61±10 years), were included in the study. The relationship between YKL-40, CRP levels and the presence of CAE was investigated. Univariate and multiple logistic regression analysis were used for analysis of independent variables to predict CAE. Serum YKL-40 levels were significantly different among study groups (NCA: 110±53 μg/L, CAE: 144±68 and CAD: 180±117, p=0.005). CAD group and CAE group had significantly higher YKL-40 levels than NCA group (p=0.004 and p=0.015, respectively). CRP was not significantly different between three groups. In addition, there were no any statistically significant differences, with respect to age, gender, the presence of hypertension or diabetes mellitus, and the smoking status (p>0.05). Logistic regression analysis revealed only YKL-40 level as the determinant of CAE (OR: 1.010, 95% CI: 1.001-1.019, p=0.027). YKL-40 levels in patients with isolated CAE compared to patients with NCA were found significantly high and only YKL-40 level was established as the determinant of CAE. We believe that further studies are needed to clarify the possible causative roles of YKL-40 in patients with isolated CAE.

Evaluation of Circulation Disorder in Coronary Slow Flow by Fundus Fluorescein Angiography

Coronary slow flow (CSF) may be a reflection of a systemic slow-flow phenomenon in the coronary arterial tree. In this study, the CSF group consisted of 24 men (77.4%) and 7 women (22.5%). An age- and gender-matched normal coronary artery (control) group was composed of 21 men (72.4%) and 8 women (27.5%). Retinal arteriovenous circulation time was measured using fundus fluorescein angiography as a part of the microcirculation and the circulation time between the antecubital vein and the retina as a part of the systemic circulation in patients with CSF and controls with normal coronary arteries. The mean arm-retina circulation time was 19.0 ± 5.7 seconds in the CSF group and 14.1 ± 3.1 seconds in the control group (p <0.001). The mean retinal arteriovenous passage time was 2.6 ± 0.9 seconds in the CSF group and 2.1 ± 0.7 seconds in the control group (p= 0.001). Strikingly, retinal findings of chronic central serous retinopathy were observed in 3 patients in the CSF group. In conclusion, CSF may indeed be a part of a systemic slow-flow phenomenon. The association of central serous retinopathy with this condition suggests that corticosteroids and the sympathetic system may play important roles in the pathogenesis of the disease by causing or contributing to increases in microvascular resistance and tonus.

No relevant association between coronary artery ectasia and mean platelet volume, gamma-glutamyltransferase and uric acid levels

In this study, we aimed to investigate whether there is an association between mean platelet volume (MPV), gamma-glutamyltransferase (GGT) and uric acid and coronary artery ectasia (CAE) in a large patient population. A total of 406 patients (245 male, 161 female; mean age: 55±9 years) were selected retrospectively as the study population from among 3265 individuals who underwent coronary angiography between August 2011 and December 2012. Information regarding blood tests of the patients obtained during hospitalization was extracted from the institute electronic database. MPV, GGT and uric acid levels were significantly higher in subjects with stenotic coronary artery disease (CAD) and in subjects with both CAD and CAE compared with subjects with isolated CAE and subjects with normal coronary arteries (NCA). There were no significant differences between the isolated CAE and NCA groups in terms of MPV (8.6±1.2 fL vs. 8.6±1.1, respectively, p=0.993), serum GGT (33±15 U/L vs. 30±15 U/L, respectively, p=0.723) and uric acid levels (5.4±1.6 mg/dl vs. 5.2±1.7 mg/dl, respectively, p=0.845). Unlike previous studies, our study failed to demonstrate any association between CAE and MPV, uric acid and GGT levels.

Increased circulating soluble CD40 levels in patients with slow coronary flow phenomenon: an observational study

Slow coronary flow (SCF) is an angiographic finding characterized with delayed opacification of epicardial coronary arteries without obstructive coronary disease. CD40/CD40 ligand (CD40L) signaling seems closely related to atherosclerosis due to increased inflammation and prothrombotic state. We investigated whether soluble CD40 (sCD40), an indirect marker of CD40/CD40L dyad, is related to SCF. The present study was cross-sectional and observational, consisting of seventy individuals who underwent coronary angiography with suspicion of CAD and had angiographically normal coronary arteries of varying coronary flow rates. The relationship between sCD40, C-reactive protein (CRP) and SCF phenomenon was investigated. Fifty patients with isolated SCF (mean age: 56±10 years) and 20 age- and gender-matched control participants with normal coronary flow (NCF) and normal coronary arteries (NCA), (mean age: 55±10 years) were included in the study. We used logistic regression analysis to determine the predictors of SCF. The clinical characteristics were not statistically significant different between SCF and NCA group. Serum CRP levels were also similar between two groups. Serum sCD40 level was significantly higher in the SCF group compared to control group (74±31 vs. 59±16 pg/mL, p=0.014). In multiple regression analyses, mean coronary diameter strongly (OR: 7.358, 95% CI: 1.990-27.20, p=0.003) and sCD40 (OR: 1.044, 95% CI: 1.006-1.084, p=0.023) weakly predicted SCF. This study revealed, significantly increased serum sCD40 levels in patients with SCF. Although we cannot conclude the underlying pathological process of SCF, we believe that these findings may be pivotal for further studies searching the specific roles of CD40/CD40L signaling on SCF phenomenon in coronary vasculature.

The degree of premature hair graying as an independent risk marker for coronary artery disease: a predictor of biological age rather than chronological age

Age is the most important and uncorrectable coronary risk factor at the moment. The concept of measuring aging biologically rather than only chronologically may be of importance in clinical practice. Hair graying is the most apparent sign of biological aging in humans, yet its mechanism is largely unknown. Today, it is known that cardiovascular risk factors (CVRFs), especially in combination, cause premature atherosclerosis. In our opinion, premature hair graying or whitening may represent early atherosclerotic changes as a surrogate of host response to the CVRFs. In this study, we planned to investigate the relationship of hair graying with CVRFs and coronary atherosclerotic burden in order to determine whether it is an independent marker for coronary artery disease (CAD). The current study has a cross-sectional observational design. Two hundred and thirteen men who underwent coronary angiography with a suspicion of CAD were enrolled in the study. The patients were evaluated in terms of age, demographical properties and the CVRFs. Hair whitening score (HWS) was defined according to extent of gray/white hairs (1: pure black; 2: black>white; 3: black=white; 4: white>black; 5: pure white). Coronary atherosclerotic burden was assessed by the Gensini score. Analyses were performed in age-matched normal coronary arteries (NCA) and CAD groups. Linear and logistic regression analyses were used for the multivariate analyses of independent variables associated with hair greying. The CVRFs were higher in CAD group. Hair whitening score (2.7 ± 1.3 vs. 3.3 ± 1.2, p=0.002), hair losing score (1.2 ± 0.9 vs. 1.5 ± 1.0, p=0.038) and xanthelasma rate (24% vs. 45%, p=0.013) were also significantly different between NCA and CAD groups. Age (p<0001), Gensini score (p<0.001) and coronary severity score (p=0.001) were higher in the categories of increased HWS. In multiple logistic regression analysis, only diabetes mellitus (OR: 3.240, 95% CI: [1.017-10.319], p=0.047), low-density lipoprotein cholesterol, (OR: 1.014, 95%CI: [1.001-1.027], p=0.029) and HWS (OR: 1.513, 95% CI: [1.054-2.173], p=0.025) were independently related to presence of CAD. Age (p<0.001), family history of CAD (p=0.004), hyperlipidemia (p=0.02) and serum creatinine levels (p=0.019) were found as independent predictors of hair graying. In our study, we found that the degree of gray/white hairs is related to extent of CAD. Our findings also suggested that hair graying is a risk marker for CAD independent of age and other traditional risk factors. Biological age may be important in determining total risk of patients. During assessment of cumulative CVRF effects on human body, presence of biological aging signs may be useful in identifying individuals with increased risk of cardiovascular disease.

Abstract 396: Serum Osteoprotegerin (OPG) Differs Significantly in Patients with Calcified Aortic Valve Stenosis in Relation to the Presence of Coronary Atherosclerosis

Background. We concentrated on OPG/RANKL in patients with symptomatic calcified AoS of the trileaflet valve, who were being considered for aortic valve replacement (AVR). Methods. Serum levels of cytokines were measured in: Group A (N = 101) patients with AoS and normal coronary arteries (assessed using coronary angiography), Group B (N = 105) patients with AoS and significant (stenosis &gt; 50%) coronary atherosclerosis. Control groups consisted of patients without AoS and with normal coronary arteries (group C, N = 39) or with significant coronary atherosclerosis (Group D, N = 30). Results. Values of OPG were significantly higher in patients with AoS and normal coronary arteries compared to controls with normal coronary arteries and without AoS. No difference was observed between levels of OPG in patients with AoS and CAD and control group of patients with CAD and without AoS. Multivariable analyses underscored these results (table). Serum levels of RANKL did not differ significantly between groups A vs. C. Serum OPG did not change significantly in patients after AVR (Group A). The difference in serum concentration of OPG in patients after AVR and CABG (Group B) was significant (p&lt;0.001). Conclusion. Serum OPG differs significantly in patients with calcified aortic stenosis in relation to the presence of significant coronary atherosclerosis. Our results suggest that OPG plays and important role in pathomechanism of calcified aortic valve disease in patients without coronary atherosclerosis

Coronary Microvascular Function and Cortical Pain Processing in Patients With Silent Positive Exercise Testing and Normal Coronary Arteries

ST-segment depression during exercise stress testing in asymptomatic subjects showing normal coronary arteries is considered a "false-positive" result. Coronary microvascular dysfunction, however, might be a possible cause of ST-segment depression in these cases. We assessed the coronary blood flow response to adenosine and to cold pressor test in the left anterior descending artery, using transthoracic Doppler echocardiography in 14 asymptomatic subjects with exercise-induced ST-segment depression and normal coronary arteries (group 1), 14 patients with microvascular angina (group 2), and 14 healthy subjects (group 3). Flow-mediated dilation was assessed in the brachial artery. Central pain processing was assessed using cortical laser evoked potentials during chest and right hand stimulation with 3 sequences of painful stimuli. The coronary blood flow response to adenosine was 1.8 ± 0.4, 1.9 ± 0.5, and 3.1 ± 0.9 in groups 1, 2, and 3, respectively (p <0.001). The corresponding coronary blood flow responses to the cold pressor test were 1.74 ± 0.4, 1.53 ± 0.3, and 2.3 ± 0.6 (p <0.001). The flow-mediated dilation was 5.5 ± 2.3%, 4.6 ± 2.4%, and 9.8 ± 1.2% in the 3 groups, respectively (p <0.001). The laser evoked potential N2/P2 wave amplitude decreased throughout the 3 sequences of stimulation in groups 1 and 3 but not in group 2 (chest, -19 ± 22%, +11 ± 42% and -36 ± 12%, p <0.001; right hand, -22 ± 25%, +12 ± 43% and -30 ± 20%, p = 0.009; in groups 1, 2, and 3). In conclusion, exercise stress test-induced ST-segment depression in asymptomatic subjects with normal coronary arteries cannot be considered as a simple false-positive result, because it can be related to coronary microvascular dysfunction. The different symptomatic state compared to patients with microvascular angina can, at least in part, be explained by differences in cortical processing of neural pain stimuli.

PP-018 THE ASSOCIATION BETWEEN SOLUBLE LECTIN-LIKE OXIDIZED LOW-DENSITY LIPOPROTEIN RECEPTOR-1 LEVELS AND PATIENTS WITH ISOLATED CORONARY ARTERY ECTASIA

Some evidence suggests that chronic inflammation plays a critical role in the development and progression of coronary artery ectasia. Lectin-like oxidized low-density lipoprotein receptor-1 is involved in multiple phases of vascular dysfunction, including endothelial dysfunction, atherogenesis, initiation of plaque rupture, and restenosis. The objectives was to study the purpose of the current study was to determine whether soluble lectin-like oxidized low-density lipoprotein receptor-1 is associated with isolated coronary artery ectasia patients. Forty-six patients with isolated coronary artery ectasia without stenosis and 46 control subjects with angiographically normal coronary arteries were included in this study. Lectin-like oxidized low-density lipoprotein receptor-1 levels were measured in serum by sandwich enzyme-linked immunosorbent assay. Baseline characteristics of the two groups were similar. Plasma levels of lectin-like oxidized low-density lipoprotein receptor-1 were significantly higher in the coronary artery ectasia group than normal coronary artery group (1.7 ± 0.8 ng/ml vs. 1.1 ± 0.3 ng/ml, P < 0.001, respectively). No correlation was found between plasma soluble lectin-like oxidized low-density lipoprotein receptor-1 levels and different types of ectasia in patients with coronary artery ectasia. In this study, we found significantly higher levels of soluble lectin-like oxidized low-density lipoprotein receptor-1 in coronary artery ectasia patients when compared to control subjects with normal coronary arteries, suggesting that soluble lectin-like oxidized low-density lipoprotein receptor-1 may be involved in the pathogenesis of coronary artery ectasia.

The association between soluble lectin-like oxidized low-density lipoprotein receptor-1 levels and patients with isolated coronary artery ectasia

Some evidence suggests that chronic inflammation plays a critical role in the development and progression of coronary artery ectasia. Lectin-like oxidized low-density lipoprotein receptor-1 is involved in multiple phases of vascular dysfunction, including endothelial dysfunction, atherogenesis, initiation of plaque rupture, and restenosis. The objectives was to study the purpose of the current study was to determine whether soluble lectin-like oxidized low-density lipoprotein receptor-1 is associated with isolated coronary artery ectasia patients. Forty-six patients with isolated coronary artery ectasia without stenosis and 46 control subjects with angiographically normal coronary arteries were included in this study. Lectin-like oxidized low-density lipoprotein receptor-1 levels were measured in serum by sandwich enzyme-linked immunosorbent assay. Baseline characteristics of the two groups were similar. Plasma levels of lectin-like oxidized low-density lipoprotein receptor-1 were significantly higher in the coronary artery ectasia group than normal coronary artery group (1.7±0.8ng/ml vs. 1.1±0.3ng/ml, P<0.001, respectively). No correlation was found between plasma soluble lectin-like oxidized low-density lipoprotein receptor-1 levels and different types of ectasia in patients with coronary artery ectasia. In this study, we found significantly higher levels of soluble lectin-like oxidized low-density lipoprotein receptor-1 in coronary artery ectasia patients when compared to control subjects with normal coronary arteries, suggesting that soluble lectin-like oxidized low-density lipoprotein receptor-1 may be involved in the pathogenesis of coronary artery ectasia.

The Predictive Value of Flow‐Mediated Dilation and Carotid Artery Intima‐Media Thickness for Occult Coronary Artery Disease

Multidetector row computed tomography (MDCT) is an attractive noninvasive alternative to assess overall coronary artery disease (CAD) burden and may reveal coronary plaques, which may be underestimated by conventional coronary angiography. The aim of this study was to determine whether brachial artery flow-mediated dilation (FMD) and carotid artery intima-media thickness (CIMT) might accurately predict patients with occult coronary plaques whose conventional coronary angiographies revealed normal coronary arteries (NCA). Thirty-five patients with angiographically NCA were consecutively recruited into the study. They underwent MDCT and were divided into NCA group (18 patients; 8 male; 47 ± 9 years) and occult CAD group (17 patients; 11 male; 50 ± 10 years) according to presence of coronary plaque. Nineteen consecutive patients with evident CAD (16 male; 54 ± 7 years) and 19 healthy subjects (10 male; 50 ± 6 years) were included as control groups. FMD and CIMT were measured by brachial and carotid artery ultrasonography. Occult CAD group had significantly lower FMD and insignificantly higher CIMT than NCA group whereas they had significantly higher FMD and insignificantly lower CIMT than evident CAD group. NCA group had significantly lower CIMT than evident CAD group. Receiver operating characteristic curve analysis demonstrated FMD < 8% (sensitivity: 94.4%; specificity: 73.0%; PPV: 77.3%; NPV: 93.1%) and CIMT ≥ 0.65 cm (sensitivity: 72.2%; specificity: 62.2%; PPV: 65.0%; NPV: 69.7%) could predict patients with CAD. FMD and CIMT were independent predictors of CAD (P < 0.001; OR: 45.630; 95%CI: 5.38-386.983 and P = 0.015; OR: 14.226; 95%CI: 1.666-121.467, respectively). FMD and CIMT might predict patients with occult CAD and be helpful in selecting patients for MDCT.

Increased plasminogen activator inhibitor-1 levels in patients with isolated coronary artery ectasia

Isolated coronary artery ectasia (ICAE) is defined as the ectasia of the coronary arteries without concomitant coronary artery stenosis. The etiology and the clinical course of ICAE are still not clear. Increased levels of plasminogen activator inhibitor-1 (PAI-1) inhibit vasa vasorum, leading to diminished vessel wall supply and thus contributes to aortic aneurysm expansion. Whether the same process has role in coronary artery ectasia is not known. The aim of this study is to investigate the association between PAI-1 and coronary artery ectasia in patients without concomitant obstructive coronary artery disease. Among 2830 patients who underwent coronary angiography between March 2010 and 2011, 55 patients (40 male, 15 female, mean age 60±8years) with ICAE, formed our study group. 27 patients with similar patient characteristics, with angiographically proven normal coronary arteries, were enrolled as the control group. The basal characteristics were similar between two groups. PAI-1 levels were statistically higher in the ICAE group compared to the control group (104.13±56.65 and 63.39±35.01ng/dl, respectively) (P=0.008). A significant positive correlation between CAE and PAI-1 (r=0.358, P=0.007) was also demonstrated. Serum high sensitive C reactive protein (hsCRP) levels did not differ between two groups (P>0.05). The plasma PAI-1 levels were significantly higher in ICAE patients compared to normal coronary artery group. Increased PAI-1 levels may diminish vasa vasorum by antiangiogenic activity leading to coronary ectasia.

Paraoxonase and arylesterase activities in stent restenosis in bare metal stent

The serum paraoxonase and arylesterase activities are related to coronary artery diseases. However, there are a few data about the association of paraoxonase and arylesterase activities with in-stent restenosis (ISR). The aim of this study was to evaluate the relationship between paraoxonase and arylesterase activities and ISR in patients with bare metal stent (BMS). Thirty-one patients with normal coronary artery (group 1) and 60 with BMS were enrolled in this observational study. According to the ISR, the patients were classified as group 2, without the ISR (n=29) and group 3, with the ISR (n=31). Serum paraoxonase and arylesterase activities were measured spectrophotometrically. The paraoxonase and arylesterase activities were lower in patients with BMS than in the individuals with normal coronary artery (P < 0.001 and P = 0.001, respectively). The enzyme activities were also higher in patients without ISR than with ISR (both of P < 0.001). In bivariate correlation analyses in patients with BMS, ISR shows significant positive correlations with the presence of hypertension and hyperlipidemia, type C lesion, and stent length, but shows negative correlations with type A lesion stent diameter, high-density lipoprotein cholesterol, and paraoxonase and arylesterase activities. In regression analysis, ISR is independently associated with paraoxonase and arylesterase activities (β = -0.216, P = 0.038 and β = -0.452, P < 0.001, respectively), type A lesion (β = -0.251, P = 0.013), and stent diameter (β = -0.192, P = 0.024) in patients with BMS. Our study shows that decreased paraoxonase and arylesterase activities play a significant role in ethiopathogenesis ISR in patients with BMS.

049 The influence of left ventricular systolic function and clinical status of ischemia on plasma levels of metalloproteinases -9 and -7 and their inhibitors in patients with coronary artery disease

To describe the enzymatic profile of plasma matrix metalloproteinases (MMP7 and MMP9) and their tissue inhibitors (TIMP1 and TIMP2) in different categories of patients (pts.) with coronary artery disease (CAD), and their relationship with clinical status, left ventricular (LV) function and remodelling. Total MMP7, active fraction of MMP9, TIMP1 and TIMP2 were determined in 68 consecutive pts with confirmed CAD (Group A, 56.6 ± 9.9 years, 75% men) and compared with a control group of 23 pts. with normal coronary arteries (Group B, 58.1 ± 10.7 years, 56.5% men). LVEF was calculated by Simpson's method. We calculated global longitudinal (L), circumferential (C) and radial (R) strain (S) and strain rate (SR) values as the average of segmental values by 2D strain analyses. The active form of MMP9 differed significantly between group A and B, as did the MMP9/TIMP1 and MMP9/TIMP2 ratios (8.78 ± 10.0 ng/ml vs 3.33 ± 4.0 ng/ml p = 0.016; 5.43 ± 3.4 v 0.85 ± 0.9, p = 0.039 and 11.60 ± 5.2 v 3.71 ± 1.0, p = 0.022, respectively). Group A included 35 pts. with acute coronary syndromes (ACS) and 33 pts. with stable angina (SA), with similar profile of LVEF and number of coronary arteries involved. The were no significant differences in MMP9, MMP9/TIMP1 and MMP/TIMP2 ratio between normal and SA group, but only between normal and ACS group (p = 0.02 for MMP9). In group A, only MMP7, TIMP1/MMP7 and TIMP2/MMP7 ratio corellated with markers of systolic function: LVEF (p<0.05 for all), and global LS (r = 0.31, r = 0.40, r = 0.23, p = 0.023, respectively, p<0.05 for all). There were no significant correlations between MMP or TIMP and global C and R-S or SR. There were no significant changes in extracellular matrix markers in pts. with chronic stable ischemia vs normals. Only active form of MMP9 and its ratio with TIMP differed significantly in ACS. Total MMP7 and its ratio with TIMP correlated with parameters of LV systolic function even in pts. with normal LVEF.

Aortic distensibility associates with increased ascending thoracic aorta diameter and left ventricular diastolic dysfunction in patients with coronary artery ectasia

Coronary artery ectasia is usually linked to coronary atherosclerosis. Its primary defect is a destruction of vascular media, which leads to coronary dilatation. The aim of the present study is to evaluate whether ascending aorta present anatomical and functional wall changes in patients with coronary ectasia compared with patients without ectasia. Forty patients with known coronary ectasia (group A) underwent echocardiography in order to study aortic lumen diameter and wall properties (distensibility and stiffness index). Twenty-five patients with coronary artery disease (group B) and 40 individuals with normal coronary arteries (group C) served as control groups. Both ascending aorta diameter and ascending aorta index were significantly increased in group A compared with groups B and C (P < 0.05 and P < 0.001, respectively). Furthermore, in patients with ectatic coronary arteries ascending aorta index, systolic blood pressure and diastolic dysfunction independently associate with aortic distensibility. In patients with coronary artery ectasia, ascending aortic diameter could be enlarged while aortic stiffness is related to diastolic dysfunction. We suggest that coronary ectasia is not an isolated lesion but a reflection of a generalized vascular media defect, and should not be recognized as a benign entity.

Elevation of the serum total and free prostate specific antigen levels after stent implantation in patients with coronary artery disease.

Prostate specific antigen (PSA) is the most important biochemical marker in the diagnosis and follow-up of patients with prostate cancer. In recent years, a relationship between PSA levels and cardiovascular conditions has been described. However, no study has investigated the PSA levels after coronary stenting. To investigate the impact of coronary stent implantation on serum total PSA (tPSA) and free PSA (fPSA) levels. This study involved 60 men who underwent coronary angiography for suspected coronary artery disease. Of these, 25 were diagnosed as having angiographically normal coronary arteries (Group 1) and 35 underwent coronary stent implantation (Group 2). Serum tPSA and fPSA levels and f/tPSA ratios were determined in all patients immediately before the intervention and 24 hours and 30 days after the procedure. In Group 1, there was no statistically significant change in the values of tPSA, fPSA and f/tPSA ratio before and after coronary angiography (p >0.05). In Group 2, tPSA and fPSA values 24 hours after stent implantation were significantly higher than the values at the baseline (p <0.01), whereas f/tPSA ratio did not change (p >0.05). Compared with the baseline, there was no statistically significantly difference in the PSA values 30 days after stent implantation (p >0.05). This study demonstrated that serum tPSA and fPSA levels are increased after coronary stent implantation, but f/tPSA ratio is not affected. The findings suggest that serum tPSA and fPSA levels should not be used for the diagnosis of prostate cancer during the first 30 days after coronary stenting.

Elevation of the serum total and free prostate specific antigen levels after stent implantation in patients with coronary artery disease.

Prostate specific antigen (PSA) is the most important biochemical marker in the diagnosis and follow-up of patients with prostate cancer. In recent years, a relationship between PSA levels and cardiovascular conditions has been described. However, no study has investigated the PSA levels after coronary stenting. To investigate the impact of coronary stent implantation on serum total PSA (tPSA) and free PSA (fPSA) levels. This study involved 60 men who underwent coronary angiography for suspected coronary artery disease. Of these, 25 were diagnosed as having angiographically normal coronary arteries (Group 1) and 35 underwent coronary stent implantation (Group 2). Serum tPSA and fPSA levels and f/tPSA ratios were determined in all patients immediately before the intervention and 24 hours and 30 days after the procedure. In Group 1, there was no statistically significant change in the values of tPSA, fPSA and f/tPSA ratio before and after coronary angiography (p >0.05). In Group 2, tPSA and fPSA values 24 hours after stent implantation were significantly higher than the values at the baseline (p <0.01), whereas f/tPSA ratio did not change (p >0.05). Compared with the baseline, there was no statistically significantly difference in the PSA values 30 days after stent implantation (p >0.05). This study demonstrated that serum tPSA and fPSA levels are increased after coronary stent implantation, but f/tPSA ratio is not affected. The findings suggest that serum tPSA and fPSA levels should not be used for the diagnosis of prostate cancer during the first 30 days after coronary stenting.

Elevation of the serum total and free prostate specific antigen levels after stent implantation in patients with coronary artery disease.

Prostate specific antigen (PSA) is the most important biochemical marker in the diagnosis and follow-up of patients with prostate cancer. In recent years, a relationship between PSA levels and cardiovascular conditions has been described. However, no study has investigated the PSA levels after coronary stenting. To investigate the impact of coronary stent implantation on serum total PSA (tPSA) and free PSA (fPSA) levels. This study involved 60 men who underwent coronary angiography for suspected coronary artery disease. Of these, 25 were diagnosed as having angiographically normal coronary arteries (Group 1) and 35 underwent coronary stent implantation (Group 2). Serum tPSA and fPSA levels and f/tPSA ratios were determined in all patients immediately before the intervention and 24 hours and 30 days after the procedure. In Group 1, there was no statistically significant change in the values of tPSA, fPSA and f/tPSA ratio before and after coronary angiography (p >0.05). In Group 2, tPSA and fPSA values 24 hours after stent implantation were significantly higher than the values at the baseline (p <0.01), whereas f/tPSA ratio did not change (p >0.05). Compared with the baseline, there was no statistically significantly difference in the PSA values 30 days after stent implantation (p >0.05). This study demonstrated that serum tPSA and fPSA levels are increased after coronary stent implantation, but f/tPSA ratio is not affected. The findings suggest that serum tPSA and fPSA levels should not be used for the diagnosis of prostate cancer during the first 30 days after coronary stenting.

Increased plasma osteoprotegerin levels are associated with the presence and severity of acute coronary syndrome

Objective — The objective of this study was to explore the relationship between increased plasma osteoprotegerin (OPG) levels and acute coronary syndrome (ACS).Methods — Plasma OPG levels from 85 subjects undergoing coronary artery angiography in three different groups, including ACS (n = 45), stable angia pectoris (SAP) (n = 20) and normal coronary artery (NCA) (n = 20), were detected by ELISA.Twenty-two ascending aorta specimens were surgically taken from 8 ACS, 7 SAP and 7 NCA patients, and OPG mRNA expression in the specimens was detected by RT-PCR. In addition, 10 coronary artery sections each were selected from autopsy archives for the presence of vulnerable atherosclerosis plaques (VP), stable plaques (SP) or no plaques (NP) and OPG protein expression in the sections was detected by immunohistochemistry.Results — Plasma OPG concentrations in the ACS group were significantly higher than those in the SAP or NCA group. The levels of plasma OPG in the 1-, 2- and 3-vessel disease subgroups of ACS were increasingly higher (P< 0.05 or 0.01). Multiple logistic regression analyses revealed a significant independent relation between plasma OPG concentration and the presence of ACS (P= 0.032, odd ratio = 1.006). Ascending aorta specimens from the ACS group had a greater OPG mRNA expression than those from the NCA or SAP group (P < 0.01). Sections with VP had a markedly higher OPG expression than sections with SP or NP (P < 0.05 and P< 0.01, respectively).Conclusions — Increased plasma osteoprotegerin levels are associated with the presence and severity of acute coronary syndrome.

Relationship between total and differential leukocyte counts and isolated coronary artery ectasia

Coronary artery ectasia (CAE) is a clinical entity characterized by localized or diffuse dilatation of more than or equal to 1.5 times that of the normal adjacent segments of vessels. Although the etiopathogenesis is not clearly understood, some studies have shown that CAE may be a form of atherosclerosis and has more potent inflammatory properties. Leukocytes have a crucial role in the development of inflammatory processes. We aimed to investigate a possible relationship between leukocytes and the coronary ectatic process without coronary artery disease (CAD) and to compare it with the inflammatory atherosclerotic process related to leukocytes. The study population consisted of 371 patients. We divided the patients into three groups: 42 patients with isolated CAE as group I, 279 patients with CAD as group II, and 50 control participants with normal coronary arteries (NCA) as group III. The counts of total leukocytes (7348+/-1898, 7569+/-1619, and 6770+/-1748 cells/mm, P=0.002), neutrophils (4260+/-2169, 4529+/-1380, and 4040+/-1649 cells/mm, P=0.037) and monocytes (630+/-216, 583+/-198, and 480+/-140 cells/mm, P<0.001) were significantly different among the CAE, CAD, and NCA groups, respectively. The CAE group also had significantly higher leukocyte and subtype counts than the nonobstructive CAD subgroup and NCA group. This study demonstrates that total and differential leukocyte counts, which play an important role in inflammation, are increased in patients with isolated CAE. In conclusion, this study's findings show that leukocytes may play an important role in the development of CAE independently of the atherosclerotic process.