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OBJECTIVE In daily clinical practice, we encounter ST segment elevation myocardial infarction (STEMI) patients loaded with clopidogrel upon admission to primary angioplasty. These patients are loaded with ticagrelor, if there is no contraindication. This study aimed to compare the level of injury between STEMI patients who were first loaded with clopidogrel and the ones first loaded with ticagrelor. Although patients were switched from clopidogrel to ticagrelor at the first hour of angioplasty, antiplatelet action may still be lower than the others. METHODS This study included STEMI patients with angina onset of ≤3 h and who had primary angioplasty to proximal segment of one coronary artery. All patients had total thrombotic occlusion at the proximal segment. Δtroponin level (6th-hour troponin-admission troponin) was calculated to compare the level of myocardial injury. RESULTS A total of 105 patients were included; 52 were loaded with ticagrelor and 53 with clopidogrel first and switched to ticagrelor. Baseline characteristics were similar in the two groups, except from type B2 lesions being more common in the ticagrelor-loaded group. Δtroponin levels were significantly higher in the clopidogrel-loaded group compared with the ticagrelor-loaded group (p=0.013). Major bleeding and in-hospital MACE rates were similar in both groups. CONCLUSION In STEMI patients, the degree of troponin rise was more prominent in clopidogrel-loaded patients, despite the switch to ticagrelor in the first hour of intervention. Clopidogrel is slow and modest, and variable platelet inhibition may continue to be a negative factor for protection from myocardial injury, even after switching to ticagrelor.

Coronary artery aneurysm/ectasia (CAE) is defined as a dilatation of a coronary artery segment to more than 1.5-fold normal size in diameter. The leading etiologic factor of CAE is atherosclerotic coronary artery disease, but it can be seen rarely secondary to inflammatory diseases in romatological diseases (e.g. Kawasaki disease, Takayasu’s arteritis, Systemic Lupus Erythematosus (SLE), rheumatoid arthritis). We present here in a giant coronary aneurysm, possible etiologic causes and treatment in a patient with SLE who had a previous coronary intervention. Treatment was performed successfully with a covered stent. We thought that the aneurysm was developed secondary to the drug eluting stent that was previously implanted while SLE was in remission. This case report emphasizes that coronary artery disease should be considered in SLE patients who do not have traditional risk factors for coronary artery disease.

Textiloma (gossypiboma), a retained surgical sponge or gauze, is a rare though important complication of cardiac surgery. It may cause heart failure, chronic chest pain, abscess formation or fistulas. As a result of non-specific clinical and radiological presentations, and medicolegal issues, this diagnosis is usually overlooked. A 60-year-old male patient was admitted with complaints of exertional dyspnea, chest pain, and cough, ongoing for nearly 4 months. His medical history included atrial fibrillation, an ischemic cerebrovascular accident and a coronary artery by-pass operation for three-vessel disease 15 years previously. Physical examination revealed jugular venous distention, irregular heart rate with Levine grade 4 pansystolic murmur at the apex, and inspiratory crackles at the middle and basal fields of the right lung, hepatomegaly and +1 pitting pretibial edema. His electrocardiogram was consistent with atrial fibrillation with rapid ventricular response. A chest X-ray revealed a rightsided pleural effusion (Figure A). A transthoracic echocardiography showed severe tricuspid and mitral regurgitation, bi-atrial dilatation and leftventricular hypertrophy. After intravenous diuretic therapy, a control chest X-ray was obtained to show regression of the effusion, and revealed a suspicious mass at the right heart border (Figure B). A transesophageal echocardiography was performed, and a left atrial thrombus, and a mass lesion with diameters of 46 mm × 43 mm compressing the right atrium were seen (Figure C, Video 1*). Multi-sliced computed tomography showed a mass consistent with textiloma, measuring 6.4cm × 4.7cm, compressing the right atrium and a right-sided pleural effusion (Figure D). After the diagnosis of textiloma had been made, the patient underwent re-do cardiac surgery for mass removal. Median Sternotomy revealed a textiloma behind the right atrium, which was non-capsulated and hard. Following an uneventful postoperative period, he was discharged. A clinic visit 1 month later showed him to be in good condition. 686

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

Lutembacher syndrome is a rare combination of congenital atrial septal defect (ASD) and acquired mitral stenosis (MS). Although it is traditionally corrected by surgical treatment, both conditions are amenable to transcatheter treatment without the need for surgery. We present a 49-year-old woman with Lutembacher syndrome. On pretreatment transthoracic echocardiography, planimetric mitral valve area was 1.5 cm(2), maximum diastolic gradient was 17 mmHg, and mean diastolic gradient was 9 mmHg. Combined percutaneous treatment was performed including balloon valvuloplasty for MS and closure of the ASD with the Amplatzer septal occluder. The patient was discharged uneventfully. Transthoracic echocardiography performed a week later showed planimetric mitral valve area as 2.1 cm(2), maximum diastolic gradient as 9 mmHg, and mean diastolic gradient as 4 mmHg. Complete closure of the ASD was achieved. Transcatheter treatment may be an effective alternative to surgery in selected patients with Lutembacher syndrome.

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.

Background: Angiotensin II induces various growth factors such as vascular endothelial growth factor, platelet-derived growth factor, and fibroblast growth factor, and recent studies suggest that the expression of these growth factors promotes collateral growth. We hypothesized that the blockage of angiotensin II production by ACE inhibitors might interfere with collateral development in patients with coronary occlusion. Methods: The study group consisted of 187 patients (114 males, mean ages, 62 ± 11 years) who had chronic (> 1 month) coronary occlusion (TIMI flow grade ≤ 1) in one of 3 epicardial coronary arteries. Collaterals were graded using the Rentrop classification, and the patients were divided into 2 groups according to having good (grade 2 and 3) or poor (grade 0 and 1) collaterals (n = 127 and 60, respectively). Clinical and angiographic characteristics were compared in the 2 groups. Results: ACE inhibitor use (52% versus 35%, P = 0.04) and the prevalence of diabetes mellitus (DM) (43% versus 27%, P = 0.02) was higher in patients with poor collaterals. Patients with poor collaterals had a higher frequency of circumflex artery (Cx) occlusion, worse wall motion, and lower ejection fraction. In multivariate analysis, ACE inhibitor use (OR: 2.4; 95% CI = 1.23-4.68, P = 0.01) and the occlusion of Cx (OR: 3.3, 95% CI; 1.33-8.12, P = 0.01) were found to be independent predictors for poor collateral development, whereas there was a trend for DM as a predictor for poor collaterals (OR: 1.9, 95% CI = 0.97-3.8, P = 0.06). Conclusion: The findings suggest that ACE inhibitor therapy may contribute to poor collateral development in patients with coronary occlusion.

To investigate the role of angiotensin-converting enzyme (ACE) gene polymorphism in patients with degenerative aortic valve calcification (AVC).Our study consisted of 305 Turkish patients of European descent (139 male, 166 female; mean plus or minus age, 68 plus or minus 9 years) referred to our echocardiography laboratory for aortic valve evaluation between June 2, 2003, and April 29, 2005. The severity of AVC was graded from 1 to 6 by echocardiography. We used polymerase chain reaction to determine ACE gene polymorphism.The ACE insertion/deletion genotype distributions for the study population were in Hardy-Weinberg equilibrium (chi square equals 3.5, P equals .18). The study population was divided into 3 groups based on the severity of AVC: those with grade 1 calcification were in group 1, those with grades 2 to 4 in group 2, and those with grades 5 to 6 in group 3. Group 1 patients were significantly younger, less likely to have hypertension and diabetes, and had higher high-density lipoprotein cholesterol levels. The genotype frequencies were significantly different among groups, with the insertion/insertion genotype being less prevalent in group 3 patients. In multivariate analysis, independent predictors of severe AVC were hypertension (odds ratio [OR], 5.6; 95% confidence interval [CI], 2.8 to 11.0; P less than .001), low high-density lipoprotein cholesterol (OR, 2.7; 95 percent CI, 1.5 to 4.9; P equals .001), and the deletion/deletion and insertion/deletion vs insertion/insertion genotype (OR, 3.2; 95 percent CI, 1.5 to 7.2; P equals .004).These results suggest that ACE gene polymorphism may be associated with severe AVC.

A recent ex vivo study suggests that the metabolic activation of clopidogrel is catalyzed by cytochrom P450 (CYP) 3A4 and is competitively inhibited by atorvastatin, but not pravastatin.To determine whether the incidence of procedure-related myocardial injury, assessed by cardiac troponin T (cTnT) release, is altered when clopidogrel is coadministered with a statin that is predominantly CYP3A4-metabolized.Of the 211 consecutive patients who underwent coronary stenting after pretreatment with clopidogrel, 114 were receiving a CYP3A4-metabolized statin (59 simvastatin and 55 atorvastatin, Group 1), and 37 were receiving a non-CYP3A4-metabolized statin (30 pravastatin and 7 fluvastatin, Group 2) whereas 60 patients were not taking any statins (Control). All were troponin-negative before the procedure. The overall incidence of postprocedural cTnT positivity (0.10 ng/ml) was 30.8%. Group 2 patients were less likely to exhibit cTnT rise relative to Group 1 patients (8% versus 41.6%; p = 0.004) and relative to controls (8% versus 32.5%; p0.001). Multivariate analysis identified the use of a non-CYP3A4-metabolized statin before coronary stenting as the sole independent predictor for lower incidence of procedure-related cTnT elevation with estimated Odds ratios of 0.16 relative to no statin therapy (95% CI: 0.04-0.59; p = 0.006) and 0.18 relative to CYP3A4-metabolized statin therapy (95 CI: 0.053-0.637; p = 0.008)Benefit derived from the preprocedural use of pravastatin and fluvastatin but not atorvastatin and simvastatin suggest that the ex vivo finding of a negative interaction when coadministering a CYP3A4-metabolized statin with clopidogrel may be of clinical significance.

A single coronary artery (SCA) constitutes a rare congenital anomaly. The reported incidence of SCA ranges from 0.2 1.6% of the population undergoing coronary angiography. The congenital absence of the ostium of the right coronary artery (RCA) with the origin of the RCA as a continuation of the distal circumflex artery is an extremely rare variant of the SCA. Its real incidence is unknown. We report a case of a 38-year-old white female with non-obstructive hypertrophic cardiomyopathy associated with SCA, in which the RCA arises as an extension of the circumflex artery.

This nonrandomized study evaluated the incidence of minor myocardial injury (MMI) in prospectively selected patients with simple lesion morphology and class II stable angina undergoing stenting with or without predilatation.A total of 154 patients were divided into two arms based on the stenting technique used: direct stenting without predilatation (Group I; n = 78) and stenting with predilatation (Group II; n = 76). Cardiac troponin T (cTnT) was measured immediately before, at 12 hours and 24 hours postprocedure. The primary endpoint was the MMI in-hospital. The secondary endpoint of the study was the major clinical event (MCE) rate in-hospital and up to 6 months.The frequency increase in Group I was found to be significantly lower compared with Group II (5.1% vs. 21%, respectively; p0.007), as was the amount of cTnT release (0.28 0.04 vs. 0.51 0.12 ngr/ml at 12 hours, p0.001; 0.28 0.06 vs. 0.51 0.10 ngr/ml at 24 hours, p0.0004). No MCE was seen during the in-hospital period in both groups. Furthermore, no significant differences were found between the 2 groups with respect to MCE (12.8% vs. 18.4%, respectively; p0.05) at 6 months. The balloon inflation time (BIT) was significantly longer in patients with abnormal cTnT level than in those with normal cTnT level in Group II (120.3 4.7 seconds vs. 118.2 1.3 seconds; p0.002) but there wasn t any statistical difference in Group I (32.4 2.1 seconds vs. 30.6 2.4 seconds; p0.05). Furthermore, there was not any statistical difference with respect to the number of balloon inflations in patients with normal and abnormal cTnT levels in either group (1.2 0.2 inflations vs. 1.3 0.4 inflations in Group I, p0.05; 3.2 0.9 inflations vs. 3.0 1.4 inflations in Group II, p0.05).This study showed that MMI probably occurs less frequently after direct stenting.

To evaluate the feasibility and safety of direct stenting and to compare it with conventional implantation techniques in patients with acute coronary syndrome (ACS).A total of 145 patients were divided into two arms based on the stenting technique used: group I (n = 71) = direct stenting without predilatation group that included only single-vessel procedures and group II (n = 74) = stenting with predilatation group that included only single-vessel conventional stent implantations. The primary endpoint of the study was the major adverse clinical event (MACE) rate in-hospital, at 1 month, and at 6 months and the secondary endpoint was the balloon inflation time (BIT), the number of balloon inflations (NBI), the radiation exposure time (RET), the amount of contrast dye used (ACD) and the no-reflow phenomenon.Primary success rate was 89% in group I and 95% in group II; overall procedural success rate was 94% in group I and 100% in group II. The rate of MACE was not different during the follow-up period between the two groups. The RET, BIT and NBI were significantly lower in group I than in group II (p0.001 for all). The ACD used was also significantly lower in group I than in group II (125 60 ml versus 155 71 ml; p = 0.006). Furthermore, the rate of no-reflow was significantly lower in group I than in group II (2.8% versus 13.5%; p = 0.03).Direct stenting is a feasible and safe technique. It is equivalent to single-vessel conventional stent implantation techniques with respect to MACE rate in-hospital, at 1 month, and at 6 month follow-up in selected patients with ACS.

Carotid sinus massage (CSM) is commonly performed as a bedside test for determining the type and sometimes also the mechanism of different rhythm disturbances, or for routine investigation of older patients who experience syncope, dizziness, or unexplained falls.1 Recently, it has been reported that the response to CSM is affected by the patient's position, and in patients with unexplained syncope or drop attacks, upright CSM is recommended if initial supine CSM is not diagnostic.2 3 On the other hand, time of day at which massage is performed is usually not taken into consideration. Circadian rhythm, which is the variability of physiology and biochemistry of humans in a predictable fashion during a 24 hour period, may also have an effect on response to CSM as well as the patient's position. There has been no study, to our knowledge, that has prospectively evaluated the relation between circadian rhythm and response to CSM. For this reason, we conducted such a study. A total of 120 consecutive patients (mean (SD) age 56.9 (12.4) years, 76 men and 44 women) who were in sinus rhythm were included in the study. Patients with a history or clinical findings consistent with cerebrovascular disease and who had murmurs on carotid arteries were excluded. …

Amaç: 12 derivasyonlu EKG nin farklı derivasyonları arasında QT interval süresinde değişkenlik birçok klinik durumda ventriküler aritmiler için bir risk göstergesi olarak öngörülürken, QTd-V nin değeri henüz açık değildir. Çalışmanın amacı reentran ventriküler takiaritmilere (VT) duyarlılığı olan hastaları belirlemede ventriküler premature atımlarda QT dispersiyonu’nun (QTd-V) değerini araştırmaktır. Gereç ve Yöntem: Elektrofizyolojik çalışma yapılmış 34 hastada indüklenebilir VT nin tahmini için prekordiyal QTd-V, sinyal ortalamalı EKG de geç potansiyeller ve azalmış sol ventrikül ejeksiyon fraksiyonu karşılaştırıldı. Bulgular: İndüklenebilir VT li 12 hastadaki QTd-V (110±50 msec) VT nin indüklenemediği 22 hastadaki QTd-V den (65±38 msec, p=0.006) daha büyük bulundu. Ejeksiyon fraksiyonu ve geç potansiyel varlığının dahil edildiği çok değişkenli analiz QTd-V nin ventriküler takiaritmilere duyarlı hastaları belirlemede bağımsız bir faktör olmadığını gösterdi. Sonuç: Artmış QTd-V tek başına reentran ventriküler takiaritmilere duyarlılıkla ilintili olsa da, geç potansiyeller ve sol ventrikül ejeksiyon fraksiyonu hesaba katıldığında ilave tanısal bilgi sağlamadığı gözükmektedir.

Coronary artery ectasia (CAE) is characterised by irregular, diffuse, saccular, or fusiform dilatation of the coronary arteries. Although the underlying mechanisms are not fully understood, CAE is considered an original form of vascular remodelling in response to atherosclerosis. However, it is not clear why some patients develop CAE while most do not. Experimental data suggest that activation of the renin angiotensin system may lead to an increased inflammatory response in the vessel wall or to an activation of matrix metalloproteinases.1,2 In addition, an insertion/deletion (ID) polymorphism of angiotensin converting enzyme (ACE) has been associated with coronary vascular tone3 and the development of aneurysms.4 Accordingly, we hypothesised that the gene polymorphism of ACE may be a potential factor influencing the genesis of CAE. We prospectively evaluated 3427 consecutive patients undergoing coronary angiography for the evidence of CAE. Coronary diameters and percent stenosis were measured by using computerised quantitative angiography in a biplane mode (Philips DCI, Eindhoven, Netherlands). CAE was defined as an arterial segment with a diameter of at least 1.5 times the diameter of the adjacent normal coronary artery. If no adjacent normal segment could be identified, the mean diameters of coronary segments in a control group without coronary disease (n = 81) served as normal values. ACE ID genotype was determined in two groups of patients. Group 1 consisted of 152 patients who were …