Atherogenic Index of Plasma Predicts Obstructive Coronary Artery Disease in Patients with Stable Angina Pectoris.

AIMS: Chronic coronary syndrome is associated with several risk factors, such as dyslipidemia and hypertension. The atherogenic index of plasma (AIP) has been demonstrated to be a biochemical risk factor for coronary artery disease (CAD). This study aimed to determine whether the AIP is an effective parameter for estimating obstructive CAD. METHODS AND RESULTS: A total of 345 patients (with a mean age of 62.2 ± 10.3; 63% male) who underwent coronary angiography were included in this study. Obstructive CAD is defined as having one or more vessels with a stenosis level of ≥50%. Depending on the presence of obstructive CAD, all patients were divided into two groups. The mean AIP value was found to be 0.538 ± 0.26 in the study group. The AIP values were significantly higher in the obstructive coronary artery group (AIP; 0.49 ± 0.26 vs. 0.58 ± 0.27, p = 0.002). According to a univariable analysis, AIP values were significantly associated with obstructive coronary artery disease [OR: 3.74 (CI 95% 1.62-8.64), p = 0.020]. The AIP was further adjusted for confounding risk factors in three multivariable analysis models and, all three models showed a significant association. According to an ROC analysis, 0.49 is the cut-off value for AIP, and a value above 0.49 indicates 50% coronary artpery stenosis. CONCLUSIONS: The AIP may be used in the assessment of cardiovascular risk for patients with stable angina pectoris, and it may also be used to estimate obstructive CAD.

Impact of serum erythropoietin level on collateral vessel development in patients with coronary artery disease.

OBJECTIVE: Experimental data have shown that Erythropoietin (EPO) stimulates angiogenesis and neovascularization which may result in improved collateral development. The aim of this study was to investigate the association between serum EPO levels and the extent of coronary collaterals. Patient characteristics possibly related with coronary collaterals were also sought. METHODS: A total of 256 patients with high grade coronary stenosis or occlusion were evaluated for the extent of coronary collaterals using Rentrop classification. Patients with grade 0 or 1 collaterals were grouped as poor collaterals, while grade 2 or 3 collaterals were grouped as good collaterals. RESULTS: Mean age of the study population was 63 years, 77% were males. Subjects with good collaterals were significantly more likely to have anemia (p=0.038) and stable angina pectoris as clinical presentation (p=0.40). Serum EPO levels were not different among good and poor collateral groups (10.4±9.4 mU/mL vs. 9.7±11 mU/mL, p=0.397). The prevalence of all other cardiovascular risk factors, medications, and angiographic characteristics were similar between the two groups. After adjusting for age, gender, and clinical presentation with stable angina pectoris, presence of anemia persisted to be a significant correlate of the good collateral formation (OR: 1.95; 95%; CI: 1.07-3.54, p=0.029). CONCLUSION: There has been conflicting results from trials studying the effects of serum EPO on coronary collateral development. The present study, with the largest patient population studying this topic, suggests that presence of anemia, but not serum EPO level, is associated with good collateral development.

Assessment of efficacy of single dose acetylsalicylic acid over a 24-hour period.

OBJECTIVE: Acetylsalicylic acid (ASA) has a half-life of less than 30 minutes in the human body. This study aimed to test whether the effects of a single dose of ASA wane over a 24-hour period due to the daily release of new reactive blood platelets into the bloodstream. METHODS: The study included 30 patients (10 female and 20 male, mean age: 62.8±9.0). Each took a single dose of 300 mg enteric coated ASA orally. Platelet aggregation was determined using VerifyNow® Aspirin kits immediately prior to intake, and at 12 and 24 hours following intake. Laboratory parameters such as serum CRP and CBC were also examined before ASA intake. Patients were included irrespective of routine ASA and/or clopidogrel use. RESULTS: Aspirin reaction unit (ARU) values were lower than 550 at 24 hours after drug intake in 26 (86.7%) patients. Values lower than 550 indicate therapeutic range of ASA on platelet function. Two (6.7%) patients were found to be responsive to ASA at 12 hours after intake, but unresponsive at 24 hours. Aspirin resistance was found in another 2 (6.7%) patients. CONCLUSION: Although ASA was found to be effective on platelet inhibition over a 24-hour period in most of the patients, there was a considerable number who were resistant to ASA, and who had developed unresponsiveness to ASA by the end of 24 hours. There is evidence in the literature regarding the clinical importance of ASA resistance, but the importance of loss ASA's effectiveness during a day warrants further studies.

The relationship between coronary collateral artery development and inflammatory markers.

OBJECTIVE: This study aims to show the effect of myeloperoxidase (MPO), hsCRP, TNF-alpha values and leukocyte count on the development of coronary collateral arteries in patients with severely diseased coronary arteries. METHODS: Current study is an observational cross-sectional study. In the study, 295 patients who had functional obstruction or total coronary occlusion at least 1 month on their angiograms were included. We divided the study population into two groups according to their collateral grade as good collateral (Group 1) (169 patients) and poor collateral (Group 2) (126 patients). Multiple logistic regression analysis was used for independent variables associated with the coronary collateral grade. RESULTS: History of stable angina pectoris was statistically more prevalent in good collateral group (61.5% and 48.4%, p=0.025). Furthermore, MPO activation was higher in good collateral group and the difference was statistically significant (3.7 U/mL and 3.0 U/mL p=0.001). In multiple logistic regression analysis, stable angina pectoris [OR 1.7, 95% CI (1.05-2.8), p=0.03] and high MPO levels [OR 2.7, 95% CI (1.7-4.3), p<0.001] were found to be independent predictors of good collateral development. CONCLUSION: We think that proinflammatory enzymes and cytokines released from these cells rather than inflammatory cells themselves may play an important role on the collateral development.

Effect of hypertension on coronary remodeling patterns in angiographically normal or minimally atherosclerotic coronary arteries: an intravascular ultrasound study.

Whether there is any particular role of hypertension in remodeling process has not been completely understood yet. The aim of this study was to assess the association between hypertension and remodeling patterns in normal or minimally atherosclerotic coronary arteries. Seventy-nine patients who were free of significant coronary atherosclerosis were divided into two groups according to the absence (n = 39) or presence (n = 40) of hypertension; and standard intravascular ultrasound examination was performed in 145 segments. To determine the remodeling pattern in early atherosclerotic process, patients were also analyzed according to the level of plaque burden at the lesion site after the analysis of remodeling patterns. Positive remodeling was more prevalent in the hypertensive group (52.5% vs. 12.8%; P < .001) whereas negative remodeling was more common in diabetic patients (53.6% vs. 27.4%; P = .03). Mean remodeling index was 1.04 for hypertensives and 0.96 for normotensives (P = .03). There were no correlations between remodeling patterns and other risk factors such as age, family history, and hypercholesterolemia. Early atherosclerotic lesions (< 30%) exhibited more negative remodeling characteristics while intermediate pattern was observed more frequently in patients with high plaque burden (P = .006 and .02, respectively). Positive remodeling showed no association in this context (P = .07). This study demonstrated that minimal atherosclerotic lesions in hypertensives had a tendency for compensatory arterial enlargement. Positive remodeling may result from local adaptive processes within vessel wall or hemodynamic effects of blood pressure itself.

Intracoronary versus intravenous high-dose bolus plus maintenance administration of tirofiban in patients undergoing primary percutaneous coronary intervention for acute ST elevation myocardial infarction.

We aimed to examine whether intracoronary high-dose bolus of tirofiban plus maintenance would result in improved clinical outcome in STEMI patients undergoing primary PCI in this pilot trial. A total of 56 patients were enrolled to receive either intracoronary high-dose bolus plus maintenance (n = 34) or intravenous high-dose bolus plus maintenance (n = 22) of tirofiban. Pre and post intervention TIMI flow grades, myocardial blush grades, peak CKMB and troponin levels, time to peak CKMB and troponin, time to 50% ST resolution and major composite adverse cardiac event rates at 30 days were recorded. Although incidence of major adverse cardiac events was not different, post intervention TIMI flow and TIMI blush grades, peak CKMB and troponin levels, and time to peak CKMB and time to peak troponin were significantly different, favoring intracoronary strategy. In conclusion, this regimen improved myocardial reperfusion and coronary flow, and reduced myocardial necrosis, but failed to improve clinical outcomes at 30 days.

Anticalcifying nanoparticle antibody titer is an independent risk factor for coronary artery calcification.

BACKGROUND: Calcium phosphate deposition is present even in the early phases of the atherosclerotic plaque formation. Calcifying nanoparticles (CNPs), previously known as nanobacteria, have emerged as a potential causative agent for pathological calcification in human vasculature. This study investigates the relationship between the anti-CNPs antibody titers and the extent of coronary calcification. METHODS: A total of 197 consecutive patients undergoing multidetector computed tomography were enrolled in this study. The patients with coronary artery calcification (CAC; n=103) were included in the CAC group, and those without calcification (n=94) were determined as controls. The commercially available enzyme-linked immunosorbent assay kits were used to detect IgG antibodies against CNPs in serum samples. RESULTS: Mean titers of anti-CNPs antibodies were higher in individuals with CAC than in the control group (0.4 ± 0.4 vs. 0.19 ± 0.21U; P<0.0001). Multivariate logistic regression analysis revealed that high anti-CNPs antibody levels were an independent correlate of CAC in addition to conventional risk factors such as age, hypertension, diabetes mellitus, and low levels of high-density lipoprotein cholesterol. When the CAC scores were subcategorized: score 0, 1-100, 101-400, and more than 400, they still correlated significantly with the anti-CNPs antibody, especially in the group having CAC scores greater than 400 (P<0.0001). CONCLUSION: Anti-CNPs antibodies are an independent risk factor for CAC and the antibody levels correlate with CAC scores.

Association between antibodies against calcifying nanoparticles and mitral annular calcification.

BACKGROUND AND AIM OF THE STUDY: Mechanisms leading to vascular and tissue calcification are not yet fully understood. Previously, an association has been demonstrated between a controversial calcifying nanoparticle (CNP; also known as 'nanobacteria') and vascular calcification and kidney stone formation. The study aim was to evaluate a possible association between mitral annular calcification (MAC) and CNP infection. METHODS: A total of 93 patients with MAC, detected using echocardiography, and 94 asymptomatic subjects without valvular and coronary artery calcification, were enrolled in the study. The serum levels of anti-CNP-antibodies were monitored in all subjects. RESULTS: Patients with MAC were generally older and had a higher prevalence of systemic hypertension, diabetes mellitus, and dyslipidemia. The anti-CNP-antibody titers, which were significantly associated with MAC (p < 0.0001), were increased with older age and MAC thickness, but decreased in line with serum levels of HDL-cholesterol (p < 0.0001). In order to provide a cut-off point for anti-CNP-antibodies when detecting MAC, a receiver operating characteristic curve was created. Serum CNP-antibody levels above 0.19 units/ml showed a sensitivity of 73%, a specificity of 72%, and positive and negative predictive values of 72% and 73%, respectively. Multivariate logistic regression analysis revealed that increasing age, systemic hypertension, diabetes, HDL-cholesterol levels and high anti-CNP titers were risk factors that were independently associated with calcification in the mitral annuli. CONCLUSION: The study results suggested that CNP might play an important role in the pathogenesis of MAC.

Prediction of subclinical left ventricular dysfunction with longitudinal two-dimensional strain and strain rate imaging in patients with mitral stenosis.

Longitudinal two-dimensional strain deformation is a novel technique which evaluates global and regional left ventricular (LV) function with high reproducibility. The aim of the study was to investigate the global and regional systolic function using this method in patients with pure mitral stenosis (MS). Conventional echocardiography and longitudinal two-dimensional strain analysis were performed in 60 patients (41 +/- 5 years, 48 women) with mild to moderate MS (mitral valve area: 1.9 +/- 0.5 cm(2)), and 52 healthy controls (40 +/- 7 years, 37 women). For strain analysis standard apical views were obtained, and by using a software system peak systolic strain and strain rate were calculated off-line in each segment. In all, 88% of the segments could be optimally tracked by the software system. Despite normal LV systolic function as assessed by ejection fraction (66 +/- 8%), mean global longitudinal strain (GLS) and global longitudinal strain rate (GLSR) were significantly reduced in patients with isolated MS (GLS -17 +/- 3.3 vs. -19 +/- 2.5%, P = 0.006 and GLSR -1.3 +/- 0.3 vs. -1.5 +/- 0.3 s(-1), P < 0.0001). Regional analysis demonstrated that patients with MS had a significantly reduced longitudinal peak strain and strain rate in all basal, and some mid (inferior, anteroseptal, interventricular septum) segments of the left ventricle. For other segments longitudinal peak strain and strain rate values were similar among the groups. Evaluation of LV systolic function by longitudinal two-dimensional strain deformation identified early abnormalities in MS patients who had apparently normal standard systolic function.

Two-dimensional longitudinal strain and strain rate imaging for assessing the right ventricular function in patients with mitral stenosis.

BACKGROUND: Longitudinal two-dimensional strain (L2DS) deformation is a novel technique that evaluates global and regional right ventricular (RV) function. The aim of the study was to investigate the systolic function of RV by using this method in patients with pure mitral stenosis (MS). METHODS: Conventional echocardiography and L2DS analysis were performed in 45 MS patients and 21 healthy controls. For strain analysis apical four-chamber views were obtained and by using a software system, peak systolic strain and strain rates were calculated off-line in each segment. RESULTS: The mean global longitudinal strain (GLS) of the whole RV (-20 + or - 7 vs. -24 + or - 6%, P= 0.02) and mean GLS of the septum (-19 + or - 7 vs. -23 + or - 5%, P = 0.03) were significantly reduced in the MS patients. Compared with the control group no significant change was determined in the mean GLS of the RV free wall (RVFW). While the mean global longitudinal strain rates (GLSR) of the entire RV and RVFW were similar between the groups, a significant difference in the mean GLSR of the septum (-1.2 + or - 0.4 vs. -1.5 + or - 0.3 s(-1), P= 0.005) was determined in the patients with MS. A regional analysis demonstrated that MS patients had significantly reduced strain and strain rates in the basal and mid-segments of the septum, whereas only lower strain values in the basal RVFW. CONCLUSIONS: RV systolic function evaluated by L2DS analysis in patients with MS has shown decreased global and segmental systolic functions. (ECHOCARDIOGRAPHY 2010;27:525-533).

Facilitation of radial artery cannulation by periradial subcutaneous administration of nitroglycerin.

PURPOSE: To determine whether subcutaneous administration of nitroglycerin mixed with local anesthetic agent results in effective vasodilation of the radial artery, and whether this technique improves access time and decreases complications. MATERIALS AND METHODS: This prospective study consisted of two consecutive investigations. In the first (n = 30), only local anesthetic agent (prilocaine 2%) was injected into one arm, and local anesthetic agent plus 500 microg nitroglycerin was injected into the other arm. Radial artery diameters before and after injections were measured by ultrasonography. In the second, 33 patients received local anesthetic agent (prilocaine 2%) plus 500 microg nitroglycerin (group A) and 30 received only local anesthetic agent (group B) to determine whether the addition of nitroglycerin would improve radial artery access time, duration of angiography, perception of arterial pulse (ie, pulse score), number of punctures before successful cannulation, and complication rates. RESULTS: In the first investigation, radial artery diameter increased significantly in the nitroglycerin-treated arm (2.3 mm +/- 0.4 vs 2.9 mm +/- 0.5; P = .05). In the second, there were no significant differences between groups with respect to age, sex, duration of angiography, and number of punctures before cannulation. However, the pulse score increased and radial artery access time improved significantly after addition of nitroglycerin (79% vs 10% [P < .001] and 75 sec +/- 47 vs 132 sec +/- 100 [P = .005], respectively). Radial artery spasm and thrombosis were less frequently observed in group A, albeit to an insignificant extent (P = .39 and P = .49, respectively). CONCLUSIONS: Subcutaneous administration of nitroglycerin significantly increased radial artery diameter, which can lead to facilitation of catheterization of the radial artery for arteriography and interventions.

The relation between endothelial dependent flow mediated dilation of the brachial artery and coronary collateral development - a cross sectional study.

BACKGROUND: Endothelial dysfunction is thought to be a potential mechanism for the decreased presence of coronary collaterals. The aim of the study was to investigate the association between systemic endothelial function and the extent of coronary collaterals. METHODS: We investigated the association between endothelial function assessed via flow mediated dilation (FMD) of the brachial artery following reactive hyperemia and the extent of coronary collaterals graded from 0 to 3 according to Rentrop classification in a cohort of 171 consecutive patients who had high grade coronary stenosis or occlusion on their angiograms. RESULTS: Mean age was 61 years and 75% were males. Of the 171 patients 88 (51%) had well developed collaterals (grades of 2 or 3) whereas 83 (49%) had impaired collateral development (grades of 0 or 1). Patients with poor collaterals were significantly more likely to have diabetes (p = 0.001), but less likely to have used statins (p = 0.083). FMD measurements were not significantly different among good and poor collateral groups (11.5 +/- 5.6 vs. 10.4 +/- 6.2% respectively, p = 0.214). Nitroglycerin mediated dilation was also similar (13.4 +/- 5.9 vs. 12.8 +/- 6.5%, p = 0.521). CONCLUSION: No significant association was found between the extent of angiographically visible coronary collaterals and systemic endothelial function assessed by FMD of the brachial artery.

The impact of the distance between the atrial electrode and the atrial wall on atrial undersensing in patients with VDD pacemakers: long-term follow-up.

AIM: Atrial undersensing (AUS) in single-lead VDD pacemakers may be due to diminished P-wave amplitude secondary to local inflammation beneath the electrodes closer to atrial wall. The aim of this study was to assess the potential effect of distance between atrial electrode and atrial wall on immediate and long-term atrial sensing stability in VDD systems. METHODS: A total of 275 patients with normal sinus node function who received VDD pacemakers were enrolled into the study and were followed up for a median duration of 33 months. During each control visit, a standard 12-lead electrocardiogram (ECG) was obtained and standard pacemaker function assessment was performed including testing for pacing threshold and atrioventricular synchrony. The distance between atrial electrode and atrial wall was measured from chest X-ray. RESULTS: Of the 275 patients, AUS was detected in 59 patients. Univariate predictors of AUS were use of closely spaced bipolar ring atrial electrode (CSBR) (P = 0.01), wider atrial ring-spacing (P = 0.03), and atrial sensitivity programmed to a higher level (P = 0.001). Use of CSBR (P = 0.04) and atrial sensitivity > or =0.3 mV (P = 0.02) were observed to be the independent predictors for AUS. When the distance between atrial electrode and atrial wall was <7 mm, AUS was less with diagonally arranged bipolar ring electrodes (DABR) than it was with CSBRs (P = 0.02). CONCLUSIONS: The distance between atrial electrode and atrial wall does not appear to affect AUS incidence in VDD pacemakers. For VDD electrodes closer to atrial wall, AUS was significantly less likely in DABR-type electrodes.

Total blush score: a new index for the assessment of microvascular perfusion in idiopathic dilated cardiomyopathy.

BACKGROUND: The aim of this study was to evaluate tissue-level perfusion in patients with idiopathic dilated cardiomyopathy (IDC), using the myocardial blush grade technique. METHOD: The study population consisted of 26 prospectively enrolled IDC patients (15 women and 11 men; mean age, 59+/-8.8 years) and 26 control subjects (11 women and 15 men; mean age, 54.9+/-10.6 years), whose angiographic films were technically adequate for myocardial blush grade analysis. After grading, we measured total blush score (TBS) for both groups. TBS was determined as the sum of the blush grades of each coronary territory. RESULTS: A total of 156 coronary territories in both groups were assessed. Average of TBS was significantly lower in patients with IDC than in control group (7.6+/-1.2 vs. 8.8+/-0.4; P<0.0001). The TBS significantly and inversely correlated with New York Heart Association class, heart rate, left ventricular end-systolic dimension, and left ventricular end-diastolic pressure, and positively correlated with left ventricular ejection fraction (r=-0.76, P<0.001; r=-0.61, P=0.001; r=-0.77, P<0.0001; r=-0.68, P<0.0001; and r=0.67, P<0.0001, respectively). CONCLUSION: In IDC, decreased TBS might be assumed to be a surrogate marker for a diseased microvascular network in the catheterization laboratory. The relationship between reduced TBS and IDC severity suggests that this index might have prognostic significance.

Angiographic restenosis in ephesos coronary stents: experience from a large medical center in Ankara, Turkey.

Coronary stent restenosis, which emerges in late periods after implantation, has not been completely abolished. Our aim was to investigate the restenosis rates of Ephesos coronary stents. In all, 96 patients (66 men) with 135 Ephesos coronary stents were included. Control angiograms were performed after 160 +/- 60 days. Quantitative coronary analysis was performed during the procedure and control angiogram. The stents were divided into 2 groups according to the presence or absence of restenosis. Groups were compared with clinical and angiographic variables. Restenosis was observed in 31 (23%) of 135 stents. Preprocedure percent diameter stenosis was higher (P = .02), whereas minimum lumen diameter ( P = .02), mean age (P < .001), and hypertension incidence ( P = .043) was less, and there was a trend toward smaller stent size ( P = .054) in the restenosis group. By multivariate analysis, age <50 years (P < .001) and stent size <3.0 mm (P = .016) were independent predictors of restenosis. Ephesos coronary stents seems to have acceptable restenosis rates.

The association of elevated white blood cell count and C-reactive protein with endothelial dysfunction in cardiac syndrome X.

BACKGROUND: The aim of the study is to evaluate the association of inflammatory markers with endothelial function in syndrome X. METHODS: The study population consisted of 59 prospectively enrolled patients (28 women and 31 men; mean age, 50.29 +/- 6.48 years) and 51 healty control subjects (18 women and 33 men; mean age, 51.04 +/- 7.25 years). High-sensitive CRP (hs-CRP), white blood cell (WBC) count and its subtypes [neutrophil (N), lymphocyte (L) and monocyte (M)] were measured in each subject. Endothelial function was assessed with the brachial artery flow-mediated dilatation (FMD) technique. RESULTS: WBC counts and hs-CRP levels were significantly higher in patients who had syndrome X than in control subjects (7.53 +/- 1.52 x 10(9) cells/L versus 6.21 +/- 1.17 x 10(9) cells/L, P = 0.0001, and 3.11 +/- 0.63 mg/L versus 2.68 +/- 0.76 mg/L, P = 0.002, respectively). Neutrophil count and N/L ratio was significantly increased in syndrome X when compared with the control subjects (5.14 +/- 1.10 x 10(9) cells/L versus 4.11 +/- 0.76 x 10(9) cells/L, P = 0.0001 and 2.75 +/- 1.06 versus 2.37 +/- 0.65, P = 0.02, repectively). Other subtype counts were similar between the groups. FMD was impaired significantly in patients who had syndrome X in comparison with the control subjects (5.71 +/- 4.08% versus 16.02 +/- 4.13%, P = 0.0001). There was a significant correlation between hs-CRP levels and FMD measurements (r = -0.44; P = 0.0001). Furthermore, the correlation between WBC count and FMD measurements were also significant (r = -0.48; P = 0.0001). CONCLUSIONS: The present study showed that hs-CRP and WBC count were higher in patients with syndrome X than in control subjects. Furthermore, endothelial function was impaired significantly in patients with syndrome X.The increased levels of hs-CRP and WBC count may suggest that these markers may be used in clinical practice for the assessment of the inflammatory status of the endothelium in syndrome X.

The effect of high-dose aspirin pre-treatment on the incidence of myonecrosis following elective coronary stenting.

BACKGROUND: Inadequate platelet response to aspirin is associated with increased incidence of peri-procedural myonecrosis. Antiplatelet activity of aspirin can be improved by increasing the dose. High-dose aspirin pre-treatment, therefore, may reduce the incidence of myonecrosis post stenting. METHODS AND RESULTS: Two-hundred patients taking 75-325 mg daily doses of aspirin for at least 2 weeks were randomized for addition or no addition of 500 mg aspirin before elective coronary stenting (aspirin 500 group, n=100 and control group, n=100). Primary endpoint was the occurrence of peri-procedural myonecrosis defined as creatine kinase-myocardial band (CK-MB) elevation of >1x upper limits of normal (ULN). Aspirin 500 patients were significantly younger and more likely to have family history of coronary artery disease, but less likely to have received statins than controls. Elevation of CK-MB was observed in 29% of aspirin 500 patients and 15% of controls (p=0.017). The incidence of non-Q wave myocardial infarction (CK-MB elevation of >3xULN) tended to be higher in the aspirin 500 group than in the control group (5% versus 0%, p=0.059). Multivariate analysis identified baseline aspirin dose (OR: 1.006; 95% CI: 1.002-1.010; p=0.004), aspirin 500 mg treatment (OR: 2.5; 95% CI: 1.2-5.5; p=0.021) and baseline CK-MB level (OR: 1.4; 95% CI: 1.1-1.7; p=0.012) as independent predictors of CK-MB elevation after coronary stenting. CONCLUSION: For patients taking daily low-dose aspirin therapy, supplementation with high-dose aspirin before elective coronary stenting does not reduce, but may increase the incidence of peri-procedural myonecrosis.

Erectile dysfunction may predict coronary artery disease: relationship between coronary artery calcium scoring and erectile dysfunction severity.

OBJECTIVES: The aim of this prospective study is to evaluate patients with erectile dysfunction (ED) in terms of coronary artery calcium (CAC) levels assessed by multidetector computed tomography (MDCT) and to find out if ED severity may predict coronary heart disease risk. PATIENTS AND METHOD: Sixty men with a mean age of 55.7 (41-77) years with ED and 23 men with a mean age of 53.2 (39-76) years without ED, who admitted to our clinic between January 2005 and December 2005, were included in the study. All patients answered the standard International Index of Erectile Function (IIEF) forms, and were classified into four groups as mild, moderate, severe ED and no ED. CAC levels were assessed by MDCT protocol. CAC levels and IIEF scores were analyzed within each group. RESULTS: Pearson correlation test demonstrated significant negative correlation between IIEF score and CAC score (r= -497; P<0.0001). CAC scores increased significantly with regard to IIEF scores decrease: IIEF 1-10 (n=18), mean CAC: 557.7; IIEF 11-16 (n=13), mean CAC: 541.3; IIEF 17-25 (n=29), mean CAC: 84.6; and IIEF >or= 26 [n=23 (Control group)], mean CAC: 10.1. The difference between the mean CAC scores of these four groups was statistically significant (P<0.0001). When we took the cut-off value for IIEF score 26 we observed significantly higher CAC scores at the group of IIEF <26 (mean 325.5 vs 10.1; P<0.0001). CONCLUSION: We observed positive correlation with ED severity and CAC levels. Therefore, we think that detection and quantification of preclinical coronary artery disease by CAC scoring with a non-invasive method might have a great potential for early cardiac preventive measures.

Glu298Asp polymorphism of the eNOS gene is associated with coronary collateral development.

OBJECTIVE: We examined the endothelial nitric oxide (eNOS) gene Glu298Asp polymorphism to assess its possible association with the extent of coronary collaterals. METHODS: A total of 473 consecutive patients who had high grade coronary stenosis or occlusion were evaluated for the extent of coronary collaterals by using Rentrop classification. Patients with grade 0 or 1 collaterals were identified as having poor collaterals. The relation between collateral status and eNOS Glu298Asp polymorphism was studied by multivariate logistic regression analysis. RESULTS: Subjects with poor collaterals were more likely to have diabetes mellitus (p<0.001) and unstable angina pectoris as clinical presentation (p=0.014) and more likely to carry Asp298 variant (p=0.02) but they were less likely to have received statins (p=0.031). Multivariate analysis demonstrated that Asp298 allele carriers were 1.7 times more likely to have poor collaterals than patients with GluGlu genotype (95% CI: 1.09-2.69, p=0.024). There was a significant interaction between diabetes mellitus and eNOS Glu298Asp polymorphism in the analysis of collateral development. Among 145 diabetic patients Asp298 allele was the only predictor of poor collateral development with OR of 5.38 (95% CI: 2.41-11.98, p<0.001). Once diabetic patients were excluded from the analysis Asp298 allele was no longer a significant correlate of poor collateral formation. CONCLUSIONS: The present study suggests that the Asp298 allele of the eNOS gene is significantly associated with impaired collateral development, especially in patients with diabetes mellitus. Treatment strategies that modulate eNOS activity and/or NO production may improve coronary collateral development.