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Aysun Erdem,1 Ufuk Sadik Ceylan,1 Aycan Esen,1 Ertugrul Zencirci,2 Birol Topcu,3 Kivilcim Ozden,1 Selcuk Yazici,1 Sait Terzi,1 Ayse Emre,1 Kemal Yesilcimen1 1Department of Cardiology, Siyami Ersek Thoracic and Cardiovascular Surgery Training and Research Hospital, Istanbul, Turkey; 2Department of Cardiology, Acibadem Hospital Maslak, Istanbul, Turkey; 3Department of Biostatistics, Faculty of Medicine, Namik Kemal University, Tekirdag, Turkey Background: Red cell distribution width (RDW) is a quantitative measurement and shows heterogeneity of red blood cell size in peripheral blood. RDW has recently been associated with cardiovascular events and cardiovascular diseases, and it is a novel predictor of mortality. In this study, we aimed to evaluate the clinical usefulness of measuring RDW in patients with coronary stent thrombosis.Patients and methods: We retrospectively reviewed 3,925 consecutive patients who presented with acute coronary syndrome and who underwent coronary angiography at the Siyami Ersek Hospital between May 2011 and December 2013. Of the 3,925 patients, 73 patients (55 males, mean age 59±11 years, 55 with ST elevated myocardial infarction) with stent thrombosis formed group 1. Another 54 consecutive patients who presented with acute coronary syndrome (without coronary stent thrombosis, 22 patients with ST elevated myocardial infarction, 44 males, mean age 54±2 years) and underwent percutaneous coronary intervention in May 2011 formed group 2. Data were collected from all groups for 2 years. The RDW values were calculated from patients 1 month later at follow-up. Syntax scores were calculated for all the patients. The patients were also divided as low syntax score group and moderate–high syntax score group.Results: The patients in group 1 with stent thrombosis had significantly higher RDW level (13.85) than the patients in group 2 without stent thrombosis (12) (P

Background: Nitric oxide plays an important role in the regulation of basal vascular tone and cardiac myocyte function. We investigated the NOS3-786T>C polymorphism in chronic heart failure (CHF) and its effects on long-term mortality., Methods: Ninety-one patients with CHF who were referred to the Department of Cardiology of Siyami Ersek Cardiovascular and Thoracic Surgery Center for cardiopulmonary exercise testing between April 2001 and January 2004 and 30 controls were enrolled in this study. Patient were followed prospectively for a period of 1 to 12 years., Results: Patients and controls were divided into three groups: TT, TC and CC, according to their NOS3-786T>C polymorphism. We noted that there was no significant difference in the genotype distribution between patients and controls. There was also no significant difference in endothelial nitric oxide synthase (eNOS) gene polymorphism between ischemic HF and nonischemic HF. During the follow-up period, 61 (67%) deaths occurred. The nonsurvivor group had lower left ventricular ejection fraction (LVEF) (p = 0.01), reduced peak oxygen consumption (p = 0.04) and were of older age (p = 0.001). Age, LVEF, peak oxygen consumption and genotype were found to be predictors of mortality (p < 0.05). Additionally, mortality was significantly increased in -786CC genotype patients compared to TT genotype patients (hazard ratio = 2.2; p = 0.03). By multivariate analysis, age and eNOS genotype were determined to be significant independent predictors of death. Additionally, Kaplan-Meier analysis confirmed that homozygote -786C genotype was associated with an increased risk of death (χ2 = 4.6, p = 0.03)., Conclusions: Our findings showed that the NOS3-786T>C polymorphism was associated with an increased risk of mortality in patients with CHF.

Stent thrombosis (ST) is considered as a multifactorial problem which is mostly occurs due to clopidogrel resistance. It may be due to some CYP450 enzyme deficiencies which play role in clopidogrel metabolism. Therefore the aim of this study is to detect the mutations in CYP2C19 and CYP2C9 genes which may cause ST, and to investigate the relation between other risk factors and ST. 50 individuals who have stent thrombosis and 50 individuals who haven't got any complication were enrolled as patient and control group respectively. *2,*3,*4,*5,*17 mutations in CYP2C19 gene and *2 ve *3 mutations in CYP2C9 gene were investigated with RT-PCR. Clopidogrel and aspirin resistance were investigated with multiple electrode platelet aggregometry. Results were evaluated statistically. CYP2C19*2 mutation was found statistically higher in patients (% 18), whereas CYP2C19*17 was found statistically higher in controls (% 36)(p&lt;0.05). Additionally, it was found that patients who have clopidogrel and/or aspirin resistance also have CYP2C19*1/*2 or CYPC19*2/*2 genotype. These relations were also found statistically significant. (p=0,000005 for clopidogrel resistance and p=0,000059 for aspirin resistance). In conclusion, it was suggested that there is a relation between CYP2C19*2 mutations and ST due to clopidogrel resistance, and CYP2C19*17 may have a protective role in this process. The use of novel and more potent drug or high clopidogrel maintenance dosing before stent implantation may be beneficial treatment options for antiplatelet therapy in CYP2C19*2 carriers.

Limited data exist on the role of nonalcoholic fatty liver disease (FLD) as a potential independent risk factor in the setting of acute coronary syndromes. The aim of this study was to evaluate the impact of FLD on myocardial perfusion and inhospital major adverse cardiac events (MACE) in the setting of ST-elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (PCI). We examined 186 consecutive nondiabetic patients (mean age 58 ± 11 years and 76% men) who underwent primary PCI for STEMI by ultrasound within 72 hours of admission. FLD was graded according to a semiquantitative severity score as mild (score <3) or moderate to severe (score ≥3). Myocardial perfusion was determined by measuring myocardial blush grade (MBG) and ST-segment resolution (STR) analysis. Patients were divided into 2 groups according to FLD score (<3 or ≥3). There were no differences with regard to postprocedural Thrombolysis In Myocardial Infarction 3 flow grade between the 2 groups (89% vs 83%, p = 0.201). Patients with FLD score ≥3 were more likely to have absent myocardial perfusion (MBG 0/1, 37% vs 12%, p <0.0001), absent STR (27% vs 9%, p = 0.001), and higher inhospital MACE rate (31% vs 8%, p <0.0001). By multivariate analysis, FLD ≥3 score was found to be an independent predictor of absent MBG 0/1 (odds ratio [OR] 2.856, 95% confidence interval [CI] 1.214 to 6.225, p = 0.033), absent STR (OR 2.862, 95% CI 1.242 to 6.342, p = 0.031), and inhospital MACE (OR 2.454, 95% CI 1.072 to 4.872, p = 0.048). In conclusion, we found that despite similar high rates of Thrombolysis In Myocardial Infarction 3 after primary PCI, patients with FLD score ≥3 are more likely to have impaired myocardial perfusion which may contribute to adverse inhospital outcome., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Background: Demographic and clinical characteristics and angiographic findings of Turkish patients with coronary artery fistula have been investigated in this study and diagnostic tests and treatment methods used in these patients have also been evaluated in detail., Methods: We have examined the cardiac catheterization laboratory database retrospectively between March 2006 and July 2010. Among 49,567 patients, we have noted 60 patients diagnosed as coronary artery fistula. After coronary angiographic images were evaluated by two invasive cardiologists, 54 patients who had clear evidence of vessel of origin and drainage were included in the study., Results: A total of 54 (0.1%) patients with coronary artery fistula were noted. Mean age was 56.7 ± 10.7 years; 42 out of 54 patients had accompanying cardiac disorders. Patients complaints were directly associated with the presence of the fistula. Chest pain was the admission symptom in all of the patients with isolated coronary artery fistula. Six patients had coexistent congenital anomalies. Myocardial infarction with ST segment elevation occurred in 11 of the patients. In contrast to the previous reports, the most common artery of origin of the fistula was left anterior descending artery (50.8%) and pulmonary artery was found to be the most frequent region of the fistula drainage by 53.7%., Conclusions: Our findings suggest that large fistulas originating from the proximal segments of coronary arteries may increase the likelihood of atherosclerosis and myocardial infarction even in asymptomatic patients with no evidence of ischemia in noninvasive tests and no dilatation of cardiac chambers, and should therefore be closed.

Background: Large artery stiffness is a major determinant of pulse pressure (PP), and PP at baseline has been associated with future coronary events., Objective: To evaluate the impact of the metabolic syndrome on aortic PP and ascending aortic pulsatility (AP) in patients with angiographically normal coronary arteries., Methods: Forty-two patients with the metabolic syndrome and 40 age matched control subjects without the metabolic syndrome were included in the study. All subjects had normal coronary arteries. Diagnosis of the metabolic syndrome was based on the International Diabetes Federation guidelines published in 2005. Ascending AP was estimated as the ratio of aortic PP to mean blood pressure., Results: Aortic PP (59+/-12 mmHg versus 43+/-10 mmHg; P<0.001) and ascending AP (0.54+/-0.10 versus 0.48+/-0.10; P<0.001) were significantly higher in the metabolic syndrome group. Multiple regression analysis revealed statistically independent relationships between ascending AP and fasting blood glucose, waist circumference and systolic blood pressure (model R2=0.408; P<0.001). The metabolic syndrome, as a whole, was also independently associated with both ascending AP (P<0.01) and aortic PP (P<0.01)., Conclusion: The data showed that the metabolic syndrome is independently associated with increased aortic PP and ascending AP in patients with normal coronary arteries, suggesting aortic stiffness as one of the possible mechanisms underlying the excess cardiovascular risk associated with the metabolic syndrome.

Background: Cardiac valve calcification is a frequent finding in chronic haemodialysis patients. Left ventricular hypertrophy (LVH) is a significant predictor of cardiovascular mortality in patients with end-stage renal disease. We evaluated the influence of aortic valve sclerosis (AVS) on the development of LVH in chronic haemodialysis patients., Methods: A total of 82 consecutive patients (52 male, mean age 48 +/- 12 years) undergoing chronic haemodialysis treatment for > 1 year were subjected to echocardiography for the screening of AVS and the assessment of transaortic flow velocity and the left ventricular mass index (LVMI). The absence (group 1, n = 42) and presence of AVS (group 2, n = 40) was established. The average values of systolic, diastolic and pulse pressure were obtained. Plasma calcium, phosphorus, intact parathyroid hormone, C-reactive protein, haemoglobin and lipid levels were also measured., Results: LVH was detected in 59 (72%) of the study patients. The LVMI was higher in the AVS group (171 +/- 39 vs. 132 +/- 41 g/m2, p < 0.001). Patients with AVS also had higher transaortic flow velocities (1.64 +/- 0.36 vs. 1.21 +/- 0.21 m/s, p < 0.01) and maximal pressure gradients (10.8 +/- 7.1 vs. 5.9 +/- 3.4 mmHg, p < 0.01). The LVMI showed a direct correlation with transaortic flow velocity in the AVS group (r = 0.60, p < 0.01). Stepwise linear regression analysis revealed transaortic flow velocity (p = 0.02), pulse pressure (p = 0.01) and haemoglobin levels (inverse relationship) (p = 0.02) to be independent predictors of the LVMI., Conclusion: These data suggest that AVS is strongly and independently interrelated with LVH in chronic haemodialysis patients. The underlying mechanism might be the valve resistance to left ventricular outflow, as shown by increased transaortic flow velocities and maximal pressure gradients in AVS patients.

Left ventricular (LV) systolic and diastolic parameters derived from Doppler echocardiography have been used widely to predict functional capacity but diastolic filling is affected by various factors. Tissue Doppler imaging (TDI) that records systolic and diastolic velocities within the myocardium and at the corners of the mitral annulus, has been shown to provide additional information about regional and global LV function. The goal of this study was to examine whether TDI-derived parameters add incremental value to other standard Doppler echocardiographic measurements in predicting exercise capacity. The study enrolled 59 consecutive patients with stable congestive heart failure (CHF). The etiology of heart failure was coronary artery disease in 42 patients and dilated cardiomyopathy in 17. Twenty-three age-matched healthy subjects were recruited as controls. Conventional echocardiographs and TDI were obtained. Early (Ea) and late (Aa) diastolic and systolic (Sa) mitral annulus velocities, the Ea/Aa and E/Ea ratios, were measured by pulsed wave TDI placed at the septal side of the mitral annulus and results were compared with results of cardiopulmonary exercise testing. Systolic and early diastolic velocities of mitral annulus were decreased and the E/Ea ratio was increased in the restrictive group as compared to controls (P = 0.02, P = 0.03, P < 0.001, respectively) but there was no significant difference in late diastolic velocity and the Ea/Aa ratio between the restrictive group and controls. The average peak VO2 of the patients were 14.9 +/- 4.9 ml/min per kg. Achieved peak VO2 of the patients with E/Ea ratio 7.5 (P < 0.001). Interestingly, the patients with the nonrestrictive pattern and E/Ea ratio >7.5 had reduced exercise capacity, as did the group with restrictive LV filling patterns (12.8 +/- 3.3 vs 12.9 +/- 4.0 ml/min per kg, P = 0.9). Similarly, there was no significant difference in the mean exercise capacity between the patients with a nonrestrictive pattern vs restrictive pattern with E/Ea ratio 7.5 was used, 21 out of 24 patients in the reduced exercise capacity group were identified with 16 false positives in the preserved exercise capacity group (P = 0.001). Mitral annular systolic and diastolic velocities of TDI were associated with cardiopulmonary exercise capacity in patients with LV systolic dysfunction. Index of the E/Ea ratio was found to be the most powerful predictor of peak oxygen uptake.

Background: Elevated plasma homocysteine (Hcy) concentrations are associated with an increased risk of vascular disease. Hcy is known to inhibit endothelial cell proliferation in vitro. The purpose of the present study was to investigate the role of plasma Hcy concentrations on development of collateral circulation in single-vessel chronic total occlusion., Methods and Results: Collateral status was determined by Rentrop's classification. Of 817 patients, 56 cases of pure single-vessel chronic total occlusion were studied. Plasma Hcy concentrations in patients with single-vessel total coronary occlusion were higher compared with controls (17.3 +/-12.6 micromol/L vs 10.9+/-4.9 micromol/L, p=0.015). There was no significant difference in plasma Hcy concentrations of the good and poor collateral groups (17.2+/-13.7 micromol/L vs 15.3+/-9.3 micromol/L, p=0.834). Plasma Hcy concentrations in individual Rentrop subclasses 0, 1, 2 and 3 were as follows: 15.9 +/-9.1, 16.3+/-12.4, 17.1+/-14.1 and 20.1+/-13.5 micromol/L (p=0.893). There was a positive linear correlation between Rentrop subclass and angina pectoris duration (r=0.41, p=0.003). Angina pectoris duration was the only independent variable affecting the development of coronary collaterals in the present study (odds ratio [confidence interval]: 1.85 [1.12-2.91], p=0.014)., Conclusion: Patients with single-vessel chronic total occlusion had higher plasma Hcy concentrations than controls, but similar Hcy concentrations when compared according to the presence of poor or good coronary collaterals. There is a lack of association between plasma Hcy concentration and coronary collateral status in the current study.

Background: Little is known about the relationship between exercise intolerance and lipid peroxidation in chronic heart failure (CHF) patients. This study was designed to investigate the relationship between exercise-induced plasma malondialdehyde (MDA) changes in CHF patients and to determine whether there is any association between plasma MDA levels and exercise capacity assessed by cardiopulmonary exercise testing., Methods: Cardiopulmonary exercise testing was applied to 31 CHF patients (16 ischemic, 15 idiopathic) and controls. Rest and peak exercise blood samples were analyzed for MDA., Results: Patients with CHF had elevation of plasma MDA levels during exercise compared with controls (p < 0.001 vs. p = 0.588). MDA change remained significant both in ischemic and idiopathic cardiomyopathy groups (p < 0.05 and p < 0.01, respectively). Delta MDA (peak exercise MDA - rest MDA) showed significant inverse correlation with peak oxygen consumption in patients with CHF., Conclusion: Lipid peroxidation is increased in patients with CHF during exercise regardless of etiology, and this increase is inversely related to oxygen consumption., ((c) 2007 S. Karger AG, Basel.)

Brucella endocarditis is a zoonosis transmitted by contaminated dairy products. Endocarditis is a rare complication of brucellosis and mainly the aortic valve is infected. We present the case of a female patient with prosthetic mitral valve endocarditis associated with QT prolongation and torsades de pointes. Transesophageal echocardiography revealed vegetation on both anterior and posterior mitral annulus. She was seropositive with Brucella agglutination titers of up to 1/320. The QT interval was markedly prolonged upon admission (QTc 530 ms). She experienced torsades de pointes several times. She underwent reoperation under an appropriate antibiotic regimen. She continued on triple antibiotic therapy for 12 months. She is now well and free of symptoms.

An attenuated heart rate recovery (HRR) immediately after exercise has been shown to be predictive of mortality. It is not known whether HRR predicts mortality when measured in patients with heart failure. The present study was undertaken to evaluate the ability of HRR to predict mortality in patients with heart failure. We studied 84 NYHA class II or III chronic congestive heart failure patients who had a left ventricular ejection fraction < or = 40%. All patients underwent symptom limited cardiopulmonary exercise testing. The value for the HRR was defined as the difference in heart rate between peak exercise and one-minute later; a value < or = 18 beats per minute was considered abnormal. The patients were divided into 2 groups according to the value of HRR. Those with abnormal HRR were assigned to group I and those with normal HRR were assigned to group II. The 2 groups were compared with each other regarding baseline characteristics and exercise capacity assessed by peak VO2. There were 26 patients (31%) in group I and 58 patients (69%) in group II. Group II patients had better performance on treadmill exercise testing than group I patients. They had greater exercise duration (7.5 +/- 3.8 minutes versus 5 +/- 3.5 minutes, P = 0.006), better heart-rate reserve (79 +/- 25% versus 63 +/- 27%, P = 0.01), and higher values of maximal heart-rate (141 +/- 18 beats/min versus 132 +/- 17 beats/min, P = 0.04). Group II patients also had higher peak VO2 values (16.8 +/- 4.4 mL/kg/min versus 14.4 +/- 3.6 mL/kg/min, P = 0.01). When we separated the groups according to beta-blocker usage, beta-blockers had no prominent effect on HRR. In the follow-up period (mean 14.1 +/- 6.1 months), the presence of abnormal HRR and lower peak VO2 (< or = 14 mL/kg/min) were the only significant predictors of mortality in our patient population (adjusted hazard ratio [HR] 5.2, 95% CI, 1.3 to 24, P = 0.03 and adjusted HR 13, 95% CI, 2.1 to 25.6, P = 0.005, respectively). It seems that the attenuated HRR value one minute after peak exercise appears to be a reliable index of the severity of exercise intolerance in heart failure patients and this study supports the value of HRR as a prognostic marker among heart failure patients referred for cardiopulmonary exercise testing for prediction of prognosis.

Glycoprotein IIb/IIIa inhibitor therapy during primary percutaneous coronary intervention (PCI) decreases the incidence of major adverse cardiac events. These effects directly result from the level of platelet inhibition. It was shown that standard dosing of tirofiban is insufficient for optimal platelet inhibition. We sought to determine the efficacy and safety of single high-dose bolus (HDB) tirofiban with high-dose clopidogrel loading in primary PCI in acute ST elevation myocardial infarction. A total of 100 patients (mean age 55.2 +/- 9.9 years, male/female = 86/14) undergoing primary PCI, pretreated with clopidogrel (450 mg) and aspirin (325 mg), were consecutively randomized into two groups. Group I (n = 50) received a standard dose bolus of tirofiban (10 microg/kg/3 min) with 24-h infusion at a rate of 0.15 microg/kg/min. Group II received single HDB tirofiban (25 microg/kg/3 min). The assessed angiographic, clinical, and echocardiographic endpoints were: initial and final Thrombolysis in Myocardial Infarction (TIMI) grade flow (TGF), corrected TIMI frame count (CTFC), ST-segment resolution (STR) at 90 min, in-hospital bleeding complications, echocardiographic left ventricular ejection fraction (LVEF), death, reinfarction, and repeat target vessel revascularization at 1 month. Platelet function inhibition was measured using PFA-100 (Behring-Dade, Liederbach, Germany) with a test cartridge unit containing a membrane coated with 2 microg of equine Type I collagen and 50 microg adenosine diphosphate before, and 10 min, 2, 4, 6, 12, and 24 h after the bolus of the tirofiban in the first 10 cases of each group. There were no significant differences in baseline characteristics between groups. Initial TGF III was more frequent (24% vs 8%, P = 0.029) and the value of CTFC was lower (75 +/- 34 vs 89 +/- 25, P = 0.03) in group II. Postprocedural TGF, CTFC, STR, bleeding complications, and LVEF at 1 month were not different between the two groups. There was a higher rate of reinfarction in group II (8%) compared with group I (2%), but this difference was not statistically significant (P > 0.05). The results of platelet function analyses showed that group II patients had significantly prolonged platelet function assay closure times (299 +/- 6 s) compared with group patients (236 +/- 97 s) at 10 min after the bolus dose (P = 0.04). However, after the first dose between 2 and 24 h, PFA closure times were significantly prolonged in patients with tirofiban infusion. High-dose bolus of tirofiban seems to be safe and more effective than conventional dose at the periprocedural time, whereas continuous infusion of tirofiban may be necessary in the first 24 h before stable and safe antiplatelet status is reached with clopidogrel. However, safety and efficacy of HDB tirofiban and high-loading-dose clopidogrel together with tirofiban infusion requires further studies with a larger population.

Background/aims: The timing of GpIIb/IIIa inhibitor administration may be important in achieving early epicardial and myocardial reperfusion. We evaluated the effect of early tirofiban on myocardial salvage and cardiovascular outcome in patients with acute myocardial infarction (AMI) undergoing infarct-related artery stenting., Methods: Patients (n = 66) with a first AMI presenting <6 h from onset of symptoms were randomized to either early administration of tirofiban in the emergency room (n = 32) or later administration in the catheterization laboratory (n = 34) (tirofiban bolus dose of 10 microg/kg, followed by 0.15 microg/kg for 24 h). The primary end-point was the degree of myocardial salvage, determined by means of serial scintigraphic studies with technetium-99m sestamibi. Thirty-day major adverse cardiac events were also assessed., Results: There were no significant differences in patient characteristics or in their presentation. The mean door-to-balloon time was similar in both groups (43 +/- 12 and 53 +/- 9 min, p = 0.08). The early and late treatment groups received tirofiban 18 +/- 4 and 52 +/- 10 min after admission, respectively. Angiographic analysis revealed a higher initial frequency of TIMI grade 3 flow in the early group (31% vs. 12%, p = 0.04). Procedural success was achieved in all patients. Myocardial risk area were comparable between early and late treatment groups (35.6 +/- 12.2% vs. 39.3 +/- 14.0%, p = 0.6). Scintigraphic outcomes demonstrated a significant reduction in the final infarction size (11.8 +/- 5.2% vs. 22.4 +/- 6.2%, p = 0.01), and improvement in salvage index (0.68 +/- 0.22 vs. 0.44 +/- 0.18, p = 0.003) in favor of the early tirofiban group. The thirty-day composite end-point of death, recurrent MI or rehospitalization also favored the early group (6% early, 15% late, p = 0.06)., Conclusion: Early tirofiban administration enhanced the degree of myocardial salvage and clinical outcome in patients with AMI undergoing infarct-related artery stenting., (2006 S. Karger AG, Basel)

Unlabelled: Effect of hormone replacement (HRT) therapy on plasma lipoproteins and apolipoproteins, endothelial function and myocardial perfusion in postmenopausal women with estrogen receptor-alpha (ER-alpha) IVS1-397 C/C genotype and established coronary artery disease., Background/aims: Associations between various ER-alpha polymorphisms and clinical phenotypes have been studied, including lipid levels and coronary atherosclerosis. We studied 48 postmenopausal women to determine the effect of ER-alpha IVS1-397 polymorphism on the response to treatment with HRT., Methods: The study had a randomized, double-blind, placebo-controlled and crossover design. Patients were divided into two groups according to ER-alpha IVS1-397 polymorphism: CC genotype (n = 9); CT or TT genotype (n = 39). HRT was given continuously for 4 weeks, with 4-week washout periods between the treatment periods. Brachial artery Doppler and Tl-201 scintigraphy were performed at the end of each treatment period., Results: HRT lowered total cholesterol, LDL-c and Apo-B levels from baseline values (all p < 0.05) and to a similar degree in CC and CT/TT genotype patients. HRT increased estradiol, HDL-c and Apo A-1 levels relative to baseline values, but to a greater degree in CC patients (p = 0.04, 0.05 and 0.04 by ANOVA, respectively). HRT increased peak forearm blood flow, brachial artery diameter during reactive hyperemia and endothelium-dependent dilation in both groups, but to a greater degree in CC patients (p = 0.03, 0.03 and 0.04 by ANOVA, respectively). Summed stress and rest scores were also more markedly reduced in CC patients (p = 0.04 and 0.05, respectively). The increase in estradiol levels was strongly correlated with the improvement in endothelium-dependent dilation (r = 0.66, p < 0.01), which in turn showed negative correlation with summed stress (r = -0.62, p < 0.01) and rest scores (r = -0.52, p < 0.05) in the CC genotype group., Conclusion: These data suggest that the improvement in endothelium-dependent dilation and the reduction in perfusion abnormalities by increasing estradiol levels with HRT in postmenopausal women with coronary artery disease may differ with respect to different genotypes, the effect being more prominent in those patients with ER-alpha IVS1-397 CC genotype., (Copyright 2006 S. Karger AG, Basel)

Neurofibromatosis is a rare cause of coronary aneurysm. We present a case of multiple coronary artery aneurysms in a patient with neurofibromatosis. Coronary angiography was performed because of postmyocardial infarction angina. Coronary angiography revealed multiple coronary aneurysms in the left anterior descending and circumflex arteries, and diffuse irregularities in the right coronary artery. None of the coronary arteries showed critical stenosis. The patient was successfully managed with aspirin, clopidogrel, and beta-blocker therapy.

A single coronary artery with an anomalous origin between the pulmonary artery and aorta is an unusual congenital anomaly. We present a 60 year old female patient with stable angina pectoris. Her coronary angiogram revealed that the right coronary artery originated from the left main stem and coursed between the great vessels. There was 90% stenosis in the left anterior descending coronary artery. We performed a fractional flow reserve study of both the anomalous origin artery and stenosed vessel. Fractional flow reserve study of the anomalous RCA did not reveal functional ischemia. We did not refer the patient to coronary artery bypass grafting but instead performed percutaneous coronary revascularization of the LAD. The patient is alive and has been free of symptoms during the 1 year follow-up.

Left atrial (LA) function is associated with left ventricular (LV) diastolic filling and cardiac output response to exercise. But the relation between LA function and exercise performance has not been adequately evaluated. The aim of this study was to investigate the relation between LA function and exercise capacity in dilated cardiomyopathy (DCM) with cardiopulmonary exercise testing. Forty-four patients with a left ventricular end-diastolic dimension (LVDd) > or = 60 mm and an ejection fraction (EF) < or = 40%, and in normal sinus rhythm were included in this study. Patients were divided into group 1 and group 2 according to their exercise peak oxygen uptake (VO2) (group 1: peak VO2 >14 mL/kg/min, group 2: peak VO2 < or = 14 mL/ kg/min). LA function indices were defined as follows: LA end-systolic diameter (LASd), end-diastolic diameter (LADd), LA systolic volume (LASV), LA diastolic volume (LADV), LA ejection volume (LAEV), and LA ejection fraction (LAEF). LASd, LADd, LASV, and LADV were significantly increased in group 2 (P < 0.001, P < 0.001, P < 0.05, P < 0.005). Group 1 had significantly higher LAEF (P < 0.001 ) and LVEF (P < 0.05). Group 2 had significantly shorter exercise duration, and decreased anaerobic threshold levels and minute ventilation volumes (P < 0.001, P < 0.001, P < 0.005 ). There was a positive correlation between peak VO2 and LVEF (r = 0.46, P = 0.002), and LAEF (r = 0.61, P < 0.001), peak A wave velocity (r = 0.39, P = 0.009), E wave deceleration time (r = 0.56, P < 0.001), and isovolumic relaxation time (IVRT) (r = 0.35, P = 0.04). There was a negative correlation between peak VO2 and LASd (r = -0.53, P < 0.001) LADd (r = -0.59, P < 0.001), LASVI (r = -0.34, P = 0.027), LADVI (r = -0.37, P = 0.001), and the E/A ratio (r = -0.41, P = 0.006), Decreased LAEF and increased LA sizes were associated with decreased peak VO2. The results clearly demonstrate that LA functions at rest are related to exercise performance in patients with heart failure.

Background: Angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism has been associated with the development of left ventricular hypertrophy, myocardial infarction, and remodeling. However, little is known about its role in ischemic chronic heart failure (CHF). We investigated the relationship between ACE gene I/D polymorphism and ischemic CHF and its influence on exercise capacity., Methods: ACE gene I/D polymorphism was analyzed in 209 Turkish patients with coronary artery disease (CAD) undergoing coronary angiography. ACE genotype distributions were examined in 84 consecutive patients with ischemic CHF, functional capacity class II-IV to New York Heart Association and left ventricular ejection fraction (LVEF) < 40% and 125 consecutive patients with stable angina pectoris and LVEF > or = 40%. Furthermore the results of the cardiopulmonary exercise testing (CPX) in each ACE genotype were compared in medically treated ischemic CHF patients (n = 84)., Results: ACE genotype distributions were similar between the patients with and without symptomatic CHF in CAD. The odds ratios were 0.95 for D homozygotes (p > 0.05) and 0.98 for the D allele (p > 0.05). In patients with ischemic CHF the differences in CPX findings were statistically not significant in ACE D/D, I/D and I/I genotypes (peak oxygen consumptions 13.7 +/- 4.6; 14.6 +/- 5.1 and 14.5 +/- 5.0 ml/kg/min, respectively (p >0.05)., Conclusions: In this study population, there was no evidence that ACE gene I/D polymorphism plays a role in the development of CHF in CAD or any influence on exercise capacity in treated patients with ischemic CHF.