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Cerebral infarction in patients with atrial fibrillation (AF) may clinically vary from being silent to catastrophic. Silent cerebral infarction (SCI) is the neuronal injury in the absence of clinically appearent stroke or transient ischaemic attack. Serum neuron specific enolase (NSE) is suggested to be a valid surrogate biomarker that allows to detect recent neuronal injury. We aimed to evaluate the incidence of recent SCI by positive NSE levels in patients with non-valvular AF (NVAF) on oral anticoagulants. Blood samples for NSE were collected from 197 consecutive NVAF patients. NSE levels of greater than 12 ng/ml was considered as positive and suggestive of SCI. Patients were mainly female with a mean age of 69 years. Ninety-eight of them (49.7%) were taking warfarin. Mean INR level was 2.3 ± 0.9. Mean CHA2DS2-VASc score of the study population was 3.5 ± 1.5. Seventy-two patients (36.5%) were found to have NSE elevation. They were more likely to have history of chronic heart failure and previous stroke/TIA. Increased left atrial diameter and higher CHA2DS2-VASc were other factors associated with SCI. Patients on DOACs and patients taking aspirin on top of oral anticoagulant treatment were less likely to have SCI. Multivariate analysis demonstrated that increased left atrial diameter (OR: 2.5; 95% CI: 1.52–4; p < 0.001) and use of warfarin (OR: 2.8; 95% CI: 1.37–5.61; p = 0.005) were detected as independent predictors of SCI. Our study revealed that DOACs were associated with significantly reduced SCIs compared with warfarin, probably due to more effective and consistent therapeutic level of anticoagulation.

Case Presentation A 24-year-old woman, a baby-sitter with no known comorbidities, presented to the outpatient department with complaints of modified Medical Research Council grade IV breathlessness for 3 months, chest pain, and dry cough for 2 weeks. There was no known disease history, including respiratory, flu-like illness, or connective tissue disorder. There was no use of chemotherapeutic, oral contraceptive drugs, exposure to toxic substances, or smoking. A review of systems was negative for fever, arthralgia, myalgia, Raynaud phenomenon, skin thickening, rash, or leg swelling. The patient had no family history suggestive of a genetic syndrome.

Aim To investigate the relationship between malnutrition and follow-up cardiovascular (CV) events in non-ST-segment elevation myocardial infarction (NSTEMI).Material and methods A retrospective study was performed on 298 patients with NSTEMI. The baseline geriatric nutritionalrisk index (GNRI) was calculated at the first visit. The patients were divided into three groups accordingto the GNRI: >98, no-risk; 92 to ≤98, low risk; 82 to Results Follow-up data showed that MTH risk group had significantly higher incidence of repeat PCI and all-cause mortality compared to other groups (p0.05). The mean GNRI was 84.6 in patients needing repeat PCI and99.8 in patients who did not require repeat PCI (pConclusion GNRI value may have a potential role for the prediction of repeat PCI in patients with NSTEMI.

PURPOSE: The geriatric nutritional risk index (GNRI) is a simple and objective nutritional assessment tool for elderly patients. Lower GNRI values are associated with a worse prognosis in heart failure with reduced ejection fraction (HFrEF). Our aim is to investigate the relationship between malnutrition and follow-up cardiovascular (CV) events in HFrEF. METHODS: A retrospective study was performed on 362 patients with HFrEF. The baseline GNRI was calculated at the first visit. The patients were divided into three groups according to the GNRI: >98, no-risk group; 92 to 0.05). Mean GNRI value was 83.3 in NVAF patients and 101.1 in patients without NVAF (p

New-generation oral anticoagulants (NOACs) are now preferred as a first-line treatment in the management of atrial fibrillation for prevention of thromboembolic complications. Mean platelet volume (MPV), one of the indicators of increased platelet activity, is also associated with an increased stroke risk in atrial fibrillation patients. The aim of this study was to evaluate changes in MPV, platelet distribution width (PDW) and plateletcrit following use of NOACs. The study included 116 patients with non-valvular atrial fibrillation without previous NOAC use. Complete blood counts, biochemical analyses and echocardiography were performed for all patients. No significant differences were observed in MPV or other platelet indices at 6 months compared to baseline. Our results indicate that MPV and other platelet indices are not affected by NOAC use in non-valvular atrial fibrillation patients.Neue orale Antikoagulanzien (NOAC) werden mittlerweile für die Erstlinientherapie bei Vorhofflimmern zur Prävention thromboembolischer Komplikationen bevorzugt eingesetzt. Das mittlere Thrombozytenvolumen („mean platelet volume“ [MPV]), ein Indikator der erhöhten Thrombozytenaktivität, ist auch mit einem erhöhten Schlaganfallrisiko bei Patienten mit Vorhofflimmern assoziiert. Ziel der vorliegenden Studie war es, Veränderungen im MPV, der Thrombozytenverteilungsbreite und dem Thrombokrit nach Einsatz von NOAC zu untersuchen. Eingeschlossen wurden 116 Patienten mit nichtvalvulärem Vorhofflimmern ohne vorherige NOAC-Einnahme. Bei allen Patienten wurden große Blutbilder erstellt, zudem wurden biochemische Analysen und eine Echokardiographie durchgeführt. Im Vergleich zur Ausgangsmessung fanden sich nach 6 Monaten keine signifikanten Unterschiede im MPV oder in anderen Thrombozytenparametern. Unsere Ergebnisse zeigen, dass das MPV und andere Thrombozytenparameter bei Patienten mit nichtvalvulärem Vorhofflimmern nicht durch eine NOAC-Einnahme beeinträchtigt sind.

BACKGROUND: Lipoprotein-associated phospholipase A2 (Lp-PLA2) activity has been associated with the risk of clinical cardiovascular events. OBJECTIVES: In this study, we aimed to investigate whether the activity of Lp-PLA2 presents a risk for subclinical atherosclerosis in young patients with premature ovarian failure (POF). METHODS: Consecutive patients with clinical and biochemical evidence of naïve POF (n = 66) in January and February 2018 and age-matched healthy controls (n = 73) were enrolled. Lp-PLA2 activity, fibrinogen concentrations, high- sensitivity C-reactive protein (Hs-CRP) levels, and carotid intima-media thickness (CIMT) were measured in all participants. RESULTS: Plasma Lp-PLA2 activity (24.6 ± 3.2 nmol/mL vs. 18.6 ± 1.6 nmol/mL; p < 0.001), mean Hs-CRP (0.620 ± 0.26 mg/dL vs. 0.450 ± 0.28 mg/dL; p < 0.001) and fibrinogen (0.310 ± 0.12 g/dL vs. 0.24 ± 0.11 g/dL; p < 0.001) levels were significantly higher in the patients with POF than control subjects. Mean CIMT was significantly higher in the POF patients than in controls (0.499 ± 0.122 mm vs. 0.323 ± 0.079 mm; p < 0.001). There was a possitive and strong correlation between CIMT and Lp-PLA2 activity (r = 0.548; 95% CI 0.445-0.644; p < 0.001) and a weak correlation Hs-CRP (r = 0.228, 95% CI 0.060-0.398; p = 0.007). In multivariate analysis, Lp-PLA2 activity (B = 1.456, 95% CI 0.908-2.003; p < 0.001) and 17β-E2 (B = -0.077, 95% CI -0.131 - -0.023; p = 0.006) were found to be independently associated with CIMT (R(2) = 0.46). CONCLUSIONS: The present study showed that mean CIMT and Lp-PLA2 activity were significantly higher in POF subjects than control subjects. Moreover, Lp-PLA2 activity and 17β-E2 levels were independently associated with CIMT in young POF patients.

Background Graves' disease has a multitude of effects on the cardiovascular system. In the detection of subclinical left ventricular dysfunction, speckle-tracking echocardiography is more useful than conventional echocardiography. The aim of the present study was to compare the longitudinal global strain values and venous blood concentration of (tissue inhibitor of metalloproteinase-1) TIMP-1, a regulator of the extracellular matrix, among hyperthyroid patients with Graves' disease, euthyroid patients with Graves' disease and healthy control subjects. Materials and methods The study enrolled 40 hyperthyroid patients with newly diagnosed Graves' disease, 40 patients with Graves' disease who were euthyroid for at least 6 months and 40 control subjects with normal thyroid function. Participants underwent conventional echocardiography and speckle-tracking echocardiography to obtain segmental and global longitudinal strain values. In addition, the serum TIMP-1 value was assessed in the venous blood samples of the participants. Results The hyperthyroid Graves' patients showed greater serum TIMP-1 levels versus the control group and the euthyroid Graves' group. Compared to the control group, the TIMP-1 level was also significantly higher in the euthyroid Graves' group. Lower GLS (global longitudinal strain) average and GLS2C, GLS3C, GLS4C values were observed in both the hyperthyroid and euthyroid Graves' patients compared to the control group. The euthyroid Graves' patients and hyperthyroid Graves' patients had similar GLS values. The serum TIMP-1 level was negatively correlated with global strain values. Conclusion Graves' disease coexists with impaired segmental and global longitudinal strain and increased TIMP-1 levels. This coexistence seems to be independent of serum thyroid hormone levels.

BACKGROUND AND AIMS Few studies have shown the direct effect of familial hypercholesterolemia (FH) on myocardial systolic function. Studies focused on heterozygote FH patients but not homozygote ones, and they did not perform genetic analyses. We aimed to evaluate all types of patients with FH using the potentially more sensitive speckle tracking echocardiography (STE) technique to identify early left ventricular (LV) dysfunction. METHODS Genetic analyses of patients with FH were conducted for LDL-receptor, PCSK9, and ApoB100. Nine homozygote, two compound heterozygote, and 82 heterozygote FH patients and 85 healthy subjects were prospectively studied. Longitudinal and circumferential strain measurements and conventional echocardiography findings were obtained. RESULTS LV ejection fractions were similar for all (homozygote, heterozygote, and control) groups. The LV average longitudinal strain (aLS) and average circumferential strain (aCS) levels were significantly reduced in the homozygote and heterozygote groups when compared with the controls (for aLS, P = .008 (

Key Clinical Message This report illustrates a feasible and anatomical solution aiming to improve the success and decrease the possible hazards such as atrioventricular block during ablation of parahisian PVCs. We tried to illustrate the specific anatomy pertaining parahisian region and to explain a retrograde subvalvular catheter technique to overcome these procedural obstacles.

Atrial fibrillation (AF) is the most common arrhythmia in clinical practice and is a major cause of morbidity and mortality. The upregulation of TRP channels is believed to mediate the progression of electrical remodelling and the arrhythmogenesis of the diseased heart. However, there is limited data about the contribution of the TRP channels to development of AF. The aim of this study was to investigate leukocyte TRP channels gene expressions in non-valvular atrial fibrillation (NVAF) patients. The study included 47 NVAF patients and 47 sex and age matched controls. mRNA was extracted from blood samples, and real-time polymerase chain reaction was performed for gene expressions by using a dynamic array system. Low levels of TRP channel expressions in the controls were markedly potentiated in NVAF group. We observed marked increases in MCOLN1 (TRPML1), MCOLN2 (TRPML2), MCOLN3 (TRPML3), TRPA1, TRPM1, TRPM2, TRPM3, TRPM4, TRPM5, TRPM6, TRPM7, TRPM8, TRPC1, TRPC2, TRPC3, TRPC4, TRPC5, TRPC6, TRPC7, TRPV1, TRPV2, TRPV3, TRPV4, TRPV5, TRPV6, and PKD2 (TRPP2) gene expressions in NVAF patients (P PKD1 (TRPP1) gene expression. This is the first study to provide evidence that elevated gene expressions of TRP channels are associated with the pathogenesis of NVAF.

Abstract. Background: The aim of this study was to compare the simultaneous double-protection method (proximal balloon plus distal filter) with distal-filter protection or proximal-balloon protection alone in asymptomatic patients during carotid artery stenting. Patients and methods: 119 consecutive patients were investigated for carotid artery stentings in the extracranial internal carotid artery with the use of distal filters (n = 41, 34.4 %), proximal balloon (MoMa) protection (n = 40, 33.6 %) or double protection (n = 38, 31.9 %). Magnetic resonance imaging (MRI) was performed on all patients before the procedure, and control diffusion-weighted MRI (DW-MRI) was obtained within 24–48 h after the procedure. Procedural data, complications, success rate, major adverse cardiovascular events, and MRI findings were collected. Results: New cerebral high-intensity (HI) lesions were observed in 47 (39.4 %) patients. HI lesions were observed in 22 (53.6 %), 15 (37.5 %), and 10 (26.3 %) of the patients with distal filters, proximal protection, and double protection, respectively (p = 0.004). The average number of HI lesions on DW-MRI was 1.80 in the distal-filter group, 0.90 in the proximal-balloon group, and 0.55 in the double-protection group (p < 0.001). Procedure and fluoroscopy times were slightly longer in the double-protection group compared to the distal- or proximal-protection groups (p = 0.001). Conclusions: The double (proximal plus distal) cerebral embolic protection technique is safe and effective for minimizing the risk of cerebral embolization, even in patients with asymptomatic carotid artery stenosis, despite slightly longer procedure and fluoroscopy times.

Atrial fibrillation (AF) is an arrhythmia caused by disorganized electrical activity in the atria, and it is an important cause of mortality and morbidity. There is a limited data about Rho/Rho-kinase (ROCK) pathway contribute to AF development. The aim of the present study was to elucidate leukocyte RHO/ROCK gene expressions in patients with non-valvular AF (NVAF). A total of 37 NVAF patients and 47 age and sex-matched controls were included in this study. mRNA was extracted from leukocytes, and real-time polymerase chain reaction was used for gene expression analysis. A marked increase in ROCK1 and ROCK2 gene expressions in patients with NVAF was observed (P

A 37-year-old male patient was referred to our clinic due to refractory right-sided heart failure. Physical examination showed generalised oedema in lower extremities bilaterally, ascites and hepat...

Ablation of premature ventricular complexes (PVCs) originating from left ventricular outflow tract (LVOT)/left ventricular summit (LVS) is challenging with considerable rate of failure. Recently, in a novel approach to ablation of these arrythmias, application of radiofrequency energy to anatomically opposite sites of presumed origin of arrythmia, has been associated with moderate procedure success. Although late elimination of PVCs that are persistent following an ablation procedure has been previously reported, this observation has not been studied sufficiently. In this report, firstly, we present three cases of lately eliminated LVS PVCs, then, we discuss possible mechanism of this observation and conclude that after an initial failed attempt of anatomic ablation, operators may choose a period of watchful waiting before attempting a redo procedure. Keywords: Idiopathic ventricular arrhythmias, Radiofrequency, Coronary sinus, Left ventricular summit, Anatomical approach

BACKGROUND Radiofrequency (RF) ablation of idiopathic ventricular arrhythmias (IVA) from the coronary venous system (CVS) has been increasingly performed, but real effect of ablation lesions from CVS on epicardial myocardium has not been studied. OBJECTIVE To compare effects of RF delivered inside the distal CVS during ablation of IVAs originating from left ventricular summit (LVS) with IVAs ablated from right ventricular outflow tract (RVOT) using cardiac magnetic resonance imaging (CMRI). METHODS Twenty consecutive patients with IVAs who underwent acutely successful RF ablation at initial appropriate sites, i.e., distal CVS (Group 1, n = 10) or RVOT (Group 2; n = 10) were enrolled. Detailed contrast-enhanced CMRI of each patient was performed 3 months later. Presence and location of scars, distance of CVS to epicardial ventricular myocardium were measured and analyzed. RESULTS Group 1 consisted of 10 and Group 2 consisted of 10 patients. Three months after the ablation, only three patients in Group 1 had detectable late gadolinium enhancement (LGE) on CMRI while nine out of 10 patients in Group 2 had evident LGE on CMRI (P: 0.02). The mean distance of distal CVS to epicardial anterobasal myocardium was measured to be 8.8 ± 1.6 mm in Group 1. In three cases that had detectable scar on superior anterobasal LV epicardium, the mean distance was 7.4 ± 1.1 mm. CONCLUSIONS RF delivery inside the CVS is less likely to produce detectable LGE on CMRI compared to RVOT. This may partially explain less than ideal long-term results after ablation of LVS IVAs from within the great cardiac vein/anterior interventricular vein.

Objective: Endothelial dysfunction (ED) is a condition that involves increased oxidative stress and decreased total antioxidant status (TAS) levels. Systemic lupus erythematosus (SLE) is also associated with ED. We aimed to determine the association between serum TAS and ED as assessed by flow-mediated dilation (FMD) in patients with SLE. Methods: Thirty-four patients with stable SLE who were not undergoing any treatment and 39 healthy volunteers without any overt cardiovascular disease were included in this cross-sectional study. Doppler ultrasound was used to measure FMD to assess ED in the study groups. Serum TAS levels were measured using a TAS kit. High-sensitivity C-reactive protein (hs-CRP) and anticardiolipin antibody (aCLA) levels were also measured to assess the inflammatory state. The SLE group further was divided into 2 groups according to presence or absence of aCLA. SLE disease activity was assessed using the SLE disease activity index (SLEDAI). Regression analysis was used to define independent predictors. Results: The mean TAS levels were significantly lower in patients with SLE than in controls (1.60±0.11 versus 1.73±0.15 mmol/L, p

Aim: The angiographic features of myocardial infarction in young patients and the factors affecting these features differ from those in elderly patients and have not been fully established. The aim of this study was to investigate the factors involved in the development of multivessel disease in patients aged 40 years or younger with ST-segment elevation myocardial infarction (STEMI).Material and Methods: A total of 148 patients aged 40 years or younger who underwent primary percutaneoustransluminal coronary angioplasty for STEMI were included in the study. The demographic features, angiographic features, biochemical data and risk factors of the patients were reviewed retrospectively. Results: Assessment of the risk factors showed that 91.2% of the patients were male, 73% were smokers, 56.8% were hyperlipidemic, 36.1% were hypertensive and 23.1% had diabetes mellitus. A positive family history was present in 31.1% of the patients. Hyperlipidemia was significantly more common (p=0.008) and the hemoglobin values were significantly lower (p0.001) in the patients with multivessel disease than those with single-vessel disease. Anemia was also significantly more prevalent in the patients with multivessel disease (p0.001).A multivariate regression analysis showed that anemia was associated with a 21.740-fold increase(95% CI: 2.921-161.817; p=0.003)in the likelihood of developing multivessel disease, irrespective of other risk factors, while hyperlipidemia was associated with a 3.742-fold increase (95% CI: 1.104-12.679; p=0.034) and male sex was associated with a 9.390-fold increase (95% CI: 1.019-86.570) (p=0.048).Conclusion: Anemia, hyperlipidemia and male sex are associated with multivessel disease in STEMI patients aged 40 years or younger.Keywords: Anemia;hyperlipidemia; multivessel; young myocardial infarction.

Aim: Ventricular repolarization were evaluated in patients who had POF by using novel electrocardiographic parameters including Tpe-interval and Tpe/QT and Tpe/QTc ratios. A few studies have investigated the association between premature ovarian failure (POF) and cardiovascular diseases. However, none have examined ventricular repolarization in this respect.Materials and Methods: This cross-sectional study included 60 female patients with POF (mean 32.6±4.7 years) and 54 control healthy female subjects (mean 30.9±4.6 years).All electrocardiogram (ECG) measurements were performed by a cardiologist using a computer, and the Tpe-interval, Tpe/QT, and Tpe/QTc were compared between groups.Results: There were no significant differences between groups in terms of baseline characteristics and laboratory parameters. The Tpe-interval, Tpe/QT, and Tpe/QTc were significantly prolonged in POF group than control subjects (p0.001 for all). There was a strong and positive correlation between the serum follicle-stimulating hormone (FSH) level and Tpe-interval (r=0.681; p0.001) and Tpe/QTc (r= 0.636; p0.001). Furthermore, high and negative correlation was found between serum estradiol and Tpe-interval (r=-0.531; p0.001) and Tpe/QTc (r=-0.510). Multivariate linear regression analysis showed that that the FSH and estradiol level were independent predictors of both the Tpe-interval (B=0.541 and p0.001, B=-0.202 and p0.001, respectively) and Tpe/QTc (B=0.442 and p0.001, B= -0.239 and p0.001, respectively).Conclusion: It was concluded in the study that ECG parameters of ventricular repolarization, namely, Tpe-interval, Tpe/QT, and Tpe/QTc were significantly prolonged in patients that had POF.

The relationship between bilirubin levels and peripheral artery disease has been documented. Our aim was to demonstrate the possible relationship between serum bilirubin levels and abdominal aortic aneurysms (AAAs). The study included 219 patients, 110 had a previous diagnosis of AAA and 109 patients were normal controls. Only patients with AAAs which had a size of 40 to 54 mm were included in the study. Baseline laboratory values and 2 computerized tomographic measurements 12 months apart were recorded. Patients with AAA had significantly higher white blood cell (WBC) counts and neutrophil–lymphocyte ratio (NLR) but lower total and direct bilirubin levels compared with the control patients ( P < .05). Multivariate logistic regression analysis showed that WBC, NLR, and total and direct bilirubin levels were independent predictors of the presence of an AAA ( P = .03, P = .001, P = .001, and P = .001, respectively). White blood cells and total bilirubin level were independent predictors of a rapidly enlarging AAA (>10 mm/y, P = .002 and P < .001, respectively). This study demonstrated that increased WBC and decreased total bilirubin levels were independent predictors of an AAA, especially the subgroup in which the AAA was rapidly expanding.

Lower extremity arterial disease (LEAD) is a well-established risk factor for concomitant coronary artery disease (CAD). There are no published data combining all three lower limb arterial segments (aortoiliac, femoropopliteal and below the knee vessels) in order to estimate CAD severity in LEAD patients. Herein has been derived a new scoring system for this purpose, which uses the wellknown TASC II classification, Syntax score and, for the first time in medical literature, a Syntax II score.The study population consisted of 178 patients who underwent lower limb and coronary diagnostic angiography for assessment of LEAD and CAD at the same session. Syntax and Syntax II scores were calculated. TASC II classifications of the lower limb arteries were done. A new scoring system, called "Total Peripheral Score" (TPS), for lower limbs was also calculated.A positive correlation was found between TPS and Syntax score and a less prominent positive correlation between TPS and Syntax II score (p0.001). A cut-off value of '6' for the new score was found for estimating high risk subgorup of CAD (Syntax score32; p0.001). Critical femoropopliteal arterial segment stenosis was the most predictive lower limb arterial zone for presence of severe CAD (Syntax score32; p = 0.011).Taking into account all lower limb arterial segments for predicting CAD during lower limb arterial angiography was recommended. A TPS of more than '6' is the practical cut-off value for estimating severe CAD. Femoropopliteal arterial critical stenosis is the most predictive arterial zone for estimating severe CAD.

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.

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 75–325mg daily doses of aspirin for at least 2 weeks were randomized for addition or no addition of 500mg 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 >1× 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 >3×ULN) 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 500mg 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.

Carcinogenic and toxic molecules produce DNA adducts that contribute to the development of atherosclerosis. Genetic polymorphisms of xenobiotic-detoxified enzymes, which control the level of DNA adducts, may affect both enzymatic activity and individual susceptibility to coronary artery disease (CAD). In this study we investigated the effects of genetic polymorphisms of the CYP1A1*2C, GSTT1, and GSTM1 enzymes on CAD risk in a Turkish population. Genotypes were determined for 132 CAD patients and 151 healthy controls by the polymerase chain reaction/restriction fragment length polymorphism method. There were no significant differences between patients and controls in terms of CYP1A1, GSTT1, and GSTM1 genotypes. Analysis of the possible interactions between the genotypes, after adjustment for the risk factors, demonstrated that individuals carrying CYP1A1 variant GSTT1 null genotypes had an 8.907-fold increased CAD risk compared to their wild status (p0.05). We suggest that genetic polymorphisms of xenobiotic-metabolizing enzymes could play an important role in CAD. Therefore, CYP1A1 and GSTM1 polymorphisms should be considered as important parameters for the prediction of CAD.

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