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Percutaneous septal ablation for left mid-ventricular obstructive hypertrophic cardiomyopathy: a case report
Istemihan Tengiz, Ertugrul Ercan, Emin Alioglu, Ugur O Turk
BMC Cardiovascular Disorders , 2006, DOI: 10.1186/1471-2261-6-15
Abstract: The present case represents successful percutaneous treatment with septal ablation to patient with MVOHC associated with systolic anterior motion of the mitral valve and obstruction at both the mid-ventricular and outflow levels.Alcohol septal ablation has been proposed as less invasive alternatives to surgery in patients with MVOHC.Hypertrophic cardiomyopathy (HC) is a hereditary myocardial disorder, caused by mutations of sarcomeric proteins [1]. In roughly 25% of cases of HC there is associated obstruction to left ventricular (LV) outflow [1]. Obstruction can occur at several locations within the ventricle, depending on the distribution of hypertrophy, including a) the mitral valve level in association with systolic anterior motion (SAM) of the mitral valve; b) the mid-ventricle; or c) within the cardiac apex [1].In about 5% of patients a mid-ventricular obstruction (MVO) can be observed [2]. These patients are often symptomatic from hemodynamic causes and are also prone to symptomatic and even lethal ventricular arrhythmias. MVO may be associated with hypertrophy of the papillary muscle(s) and apical LV aneurysm. MVO usually presents as local obstruction but can be associated with SAM and obstruction at both the mid-cavitary and outflow levels [1].During the past 10 years, atrio-ventricular sequential pacing and alcohol septal ablation have been proposed as less invasive alternatives to surgery for patients who fail to respond to pharmacologic therapy [3,4]. However, atrio-ventricular sequential pacing is not currently thought to be dramatically beneficial [5,6]. We report on percutaneous septal ablation in a patient with left mid-ventricular obstructive hypertrophic cardiomyopathy (MVOHC) associated with SAM of the mitral valve and obstruction at both the mid-ventricular and outflow levels, which seems to be an alternative therapy in these patients.A 34-year-old man with HC (primarily diagnosed 6 years ago) was referred to our clinic with the complaints of palp
G protein b3 subunit gene polymorphism in Turkish hypertensives
Emin Alioglu,Ertugrul Ercan,Istemihan Tengiz,Ahmet Yildiz
Anadolu Kardiyoloji Dergisi , 2008,
Abstract: Objective: G protein is one of the most important regulators of intracellular signaling pathways. C825T polymorphism of G protein b3 subunit is associated with increased intracellular signal transduction. The 825T allele has been found associated with a variety of cardiovascular risk factors, including hypertension. The aim of the present study was to investigate the association between the C825T polymorphism of the G protein b3 subunit and essential hypertension in Turkish population.Methods: This cross-sectional, case-controlled study included 209 patients with essential hypertension (Patient group) and 82 subjects with normal blood pressure (Control group). The G protein b3 subunit C825T gene polymorphism was determined by polymerase chain reaction. Hypertension was defined according to JNC VII criteria. Statistical analysis was performed using Chi square and unpaired t tests. Logistic regression analysis was used to study association between hypertension and genotypes. Results: We found that the frequencies of the G protein b3 subunit C825T polymorphism in hypertensive and control groups were 17.7%, 59.3%, 23.0% and 32.9%, 48.8%, 18.3%, (CC, CT, TT) respectively (c2=7.963, p=0.019). In the multivariate logistic regression analysis CT genotype had 2.2 (OR=2.262, 95% CI 1.228-4.167, p=0.009), and TT genotype had 2.3 times (OR=2.335, 95% CI 1.089-5.008, p=0.029) greater risk of hypertension compared to CC genotype.Conclusion: It seems that the G protein b3 subunit C825T gene polymorphism is associated with systolic and diastolic blood pressure. Furthermore, the study indicates that the G protein b3 subunit may be a susceptible gene to essential hypertension.
Metin Ergün,Istemihan Tengiz,Ugur Türk,Seckin Senisik
Journal of Sports Science and Medicine , 2006,
Abstract: As studying with population carrying no classical cardiovascular risk factors seems to be an advantage in isolating effects of regular exercise on endothelial functions, inflammatory and thrombotic activity; the present study was designed to evaluate the clear effects of long-term regular exercise in middle-aged, healthy men. A total of 32 regularly exercising (three times per week, 12.8 ± 6.8 years) men (Group I, mean age = 53.2 ± 6. 1 yrs) and 32 sex- and age-matched sedentary subjects (Group II, mean age = 51.0 ± 7.7 yrs) were involved in the study. All participants were non-smokers and with no history of hypertension and diabetes. During one day preceding tests, the subjects refrained from training and maintained their normal diet. In all subjects, body mass index (BMI), percentage of body fat (% BF) and maximal oxygen uptake (VO2max) were calculated. Serum uric acid, glucose, HbA1c, lipids, high-sensitive C-reactive protein (hs-CRP), fibrinogen levels, white blood cell (WBC) and platelet count were measured. Resting heart rates and blood pressures were recorded and standard exercise stress test was applied using the modified Bruce protocol. Flow-mediated and nitrate-induced dilatation (FMD and NID) of the brachial artery and carotid intima-media thickness (cIMT) were evaluated as markers of endothelial functions and early atherosclerosis. Mean BMI, % BF, systolic and diastolic blood pressures, WBC and platelet count, HbA1c, total and LDL cholesterol, hs-CRP and fibrinogen levels were similar between the groups. Group I had significantly lower serum glucose, uric acid and triglyceride (p < 0.05, p < 0.005 and p < 0.05, respectively) and higher HDL cholesterol levels (p < 0.0001) than in Group II. FMD values were significantly higher in Group I than in Group II (p < 0.005) while there were no significant differences in NID and cIMT measures between the groups. VO2max and cIMT showed a negative correlation in Group I (r = -0.463, p < 0.0001). Negative correlations also existed between VO2max and fibrinogen levels in both Group I and II (r = -0.355, p < 0.05 and r = -0.436, p < 0.05, respectively). These results are concordant with the concept of favorable effects of regular physical exercise on cardiovascular health based on enhancement of endothelial functions even in subjects who have low cardiovascular risk profile.
Presence of factors that activate platelet aggregation in mitral stenotic patients' plasma
Istemihan Tengiz, Ertugrul Ercan, Fahri Sahin, Emin Alioglu, Can Duman, Guray Saydam, Filiz Buyukkececi
Trials , 2005, DOI: 10.1186/1468-6708-6-2
Abstract: Sixteen newly diagnosed patients with rheumatic MS (Group P) and 16 healthy subjects (Group N) were enrolled in the study. Platelet-equalized plasma samples were evaluated to determine in vitro platelet function, using adenosine diphosphate (ADP), collagen and epinephrine in an automated aggregometer. In vitro platelet function tests in group N were performed twice, with and without plasma obtained from group P.There were no significant differences between the groups with respect to demographic variables. Peripheral venous fibrinogen levels in Group P were not significantly different from those in Group N. Adenosine diphosphate, epinephrine and collagen-induced platelet aggregation ratios were significantly higher in Group P than in Group N. When plasma obtained from Group P was added to Group N subjects' platelets, ADP and collagen-induced, but not epinephrine-induced, aggregation ratios were significantly increased compared to baseline levels in Group N.Platelet aggregation is increased in patients with MS, while fibrinogen levels remain similar to controls. We conclude that mitral stenotic patients exhibit increased systemic coagulation activity and that plasma extracted from these patients may contain some transferable factors that activate platelet aggregation.Systemic thromboembolism represents a major complication in patients with mitral stenosis (MS), especially in those who have atrial fibrillation [1,2]. A hypercoagulable state has been reported in patients with MS and sinus rhythm [3,4]. The association between MS and higher levels of coagulation is well-known; however, the source of increased coagulation remains unclear. Increased regional left atrial coagulation activity may be involved, even when systemic coagulation assessed by peripheral blood sampling is normal [5,6]. Others have reported no significant variation in thrombogenesis, platelet activation, and endothelial dysfunction between the left atrium, right atrium and peripheral arteries or veins
Elevated levels of matrix metalloprotein-3 in patients with coronary aneurysm: A case control study
Istemihan Tengiz, Ertugrul Ercan, Emil Aliyev, Cevad Sekuri, Can Duman, Imre Altuglu
Trials , 2004, DOI: 10.1186/1468-6708-5-10
Abstract: Thirty patients with aneurysmal coronary artery disease and stable angina were enrolled into study (Group 1). Fourteen coronary artery disease patients with stable angina were selected as control group (Group 2). MMP-1, MMP-3 and C-reactive protein (CRP) were measured in peripheral venous blood and matched between the groups.Serum MMP-3 level was higher in patients with aneurismal coronary artery disease compared to the control group (20.23 ± 14.68 vs 11.45 ± 6.55 ng/ml, p = 0.039). Serum MMP-1 (13.63 ± 7.73 vs 12.15 ± 6.27 ng/ml, p = 0.52) and CRP levels (4.78 ± 1.47 vs 4.05 ± 1.53 mg/l, p = 0.13) were not significantly different between the groups.MMPs can cause arterial wall destruction. MMP-3 may play role in the pathogenesis of coronary aneurysm development through increased proteolysis of extracellular matrix proteins.Coronary artery aneurysms are defined as dilated coronary artery segments that are greater than 1.5 times the diameter of adjacent normal segments [1,2]. The gold standard for diagnosing this type of aneurysm is coronary angiography, which provides information about the size, shape, location and number of aneurysms.Coronary aneurysms may occur during the development of coronary atherosclerosis. Previous studies have shown that coronary aneurysms are observed in 1% to 5% of patients with angiographic evidence of coronary artery disease [3-6]. In some studies, coronary aneurysms have been associated with an increased risk of myocardial infarction [3,4]. Although the mechanisms responsible for coronary aneurysm formation during the atherosclerotic process are unclear, atherosclerosis-induced aneurysms derive primarily from thinning and/or destruction of the media [6-8].Possible factors contributing to aneurysms are matrix-degrading enzymes such as collagenases, gelatinases, and stromelysins [9,10]. More specifically, matrix metalloproteinases (MMPs) are enzymes that can degrade the structural proteins of connective tissue. Degradation of extracellul
Decreased soluble cell adhesion molecules after tirofiban infusion in patients with unstable angina pectoris
Ertugrul Ercan, Huseyin Bozdemir, Istemihan Tengiz, Cevad Sekuri, Emil Aliyev, Azem Akilli, Mustafa Akin
Thrombosis Journal , 2004, DOI: 10.1186/1477-9560-2-4
Abstract: Thirty-five patients with unstable AP (Group I), ten patients with stable AP (Group II) and ten subjects who had angiographycally normal coronary arteries (Group III) were included the study. Group I was divided into two subgroups for the specific treatment regimens: Group IA (n = 15) received tirofiban and Group IB (n = 20) did not. Blood samples for investigating the cell adhesion molecules were drawn at zero time (baseline; 0 h) in all patients and at 72 h in Group I.The baseline levels of sICAM-1 and sVCAM-1 were higher in Group I than in Groups II and III. They were higher in Group IA than in Group IB. However, the sICAM-1 and sVCAM-1 levels decreased significantly in Group IA after tirofiban infusion. In contrast, these levels remained unchanged or were increased above the baseline value in Group IB at 72 h.The levels of cell adhesion molecules in patients with unstable AP decreased significantly after tirofiban infusion. Inhibition of platelet function by specific glycoprotein IIb/IIIa antagonists may decrease platelet-mediated inflammation and the ischemic end-point.The inflammatory response, initiated by neutrophil and monocyte adhesion to endothelial cells, is important in the pathogenesis of acute coronary syndromes, especially unstable angina pectoris (AP) [1-3]. Soluble intercellular adhesion molecule-1 (sICAM-1) and vascular cell adhesion molecule-1 (sVCAM-1) are expressed on endothelial cell membranes and are responsible for the attachment of neutrophils, monocytes and lymphocytes [4-6]. sICAM-1 and sVCAM-1 are cell surface proteins inducible by tumor necrosis factor-α, interferon-γ and interleukin-1β [7,8].Tirofiban blocks glycoprotein (GP) IIb/IIIa receptors and thus prevents fibrinogen binding to platelets. The main effect of GP IIb/IIIa inhibitors is their strong anti-platelet effect, which has been clinically proven in large-scale randomized trials [9-13]. Platelets play an important role in inflammatory process by interacting with monocytes and
Cardiac thrombi in a patient with protein-C and S deficiencies: a case report
Ertugrul Ercan, Istemihan Tengiz, Cevad Sekuri, Fahri Sahin, Emil Aliyev, Mustafa Akin, Unal Ac?kel
Thrombosis Journal , 2004, DOI: 10.1186/1477-9560-2-2
Abstract: Surgical removal of emboli has been validated but cannot be proposed to all patients since it is a high-risk intervention. Fibrinolysis is generally efficient but exposes the patient to risk of migration of the intra-cavity thrombus, with occasionally deleterious evolution. Systemic thrombolytic therapy is usually recommended if (a) it is not contraindicated and (b) the thrombi are demonstrated in more than one cardiac chamber, entailing a higher risk of surgical intervention. However, the infusion rate and duration of thrombolytic therapy are important determinants of successful and uncomplicated lysis. Low dose and long infusion time should be chosen to avoid fragmentation of the thrombus and related complications.A 56-year-old man was admitted to our hospital with chest pain and severe dyspnea at rest. Expiratory ronchus and S4 gallop were apparent on physical examination. The patient's systolic/diastolic blood pressures and heart rate were 160/100 mmHg and 110 beats/min respectively. Precordial T wave inversion and sinus tachycardia were seen on electrocardiography. Transthoracic echocardiography (TTE) showed multiple floating thrombi in the right ventricle (3 × 1 × 1 cm) and right atrium (5.5 × 1 × 1 cm). The patient was diagnosed as recurrent pulmonary embolism on the basis of his history. Initial treatment comprised nasal oxygen 6 L/min, heparin 5000 U IV bolus followed by 1000 U/h infusions, diltiazem 25 mg IV (10 min intervals, three times) and aspirin 300 mg/day. The arterial blood gas analysis was; PO2: 113 mmHg and PCO2: 37 mmHg. Clinical complaints were relieved after 4 h of the initial treatment. The patient was consulted by cardiovascular surgeons for surgical removal of the thrombus. However, it was thought that TTE might not screen adequately for additional cardiac thrombi. Urgent transesophageal echocardiography (TEE) was planned to evaluate the other cardiac chambers for intracardiac thrombi before surgery; at that time the patient's hemodynamic s
Non ST-segment elevation myocardial infarction in patient with essential thrombocythemia
Emin Alioglu, Nurullah Tuzun, Fahri Sahin, Buket Kosova, Serkan Saygi, Istemihan Tengiz, Ugur Turk, Nazan Ozsan, Ertugrul Ercan
Thrombosis Journal , 2009, DOI: 10.1186/1477-9560-7-1
Abstract: Essential thrombocythemia (ET) is a clonal disorder of unknown etiology involving a multipotent hematopoietic progenitor cell and is manifested clinically by the overproduction of platelets in the absence of a definable cause [1]. In 2008, the World Health Organization accepted the presence of the JAK2V617F mutation as a new diagnostic criterion for myeloproliferative neoplasms (MPNs) like polycythemia vera (PV), essential thrombocythemia (ET) and primary myelofibrosis (PMF) [2]. Platelets in this disorder also tend to be dysfunctional, in addition to being elevated in number [3]. The disease is associated with an elevated risk of thrombosis, hemorrhage, and vasomotor symptoms. Thrombotic events are not common but are usually deep venous thrombosis and pulmonary emboli [4,5]. Coronary artery involvement is uncommon. We present a case of coronary thrombus involving the right coronary artery in a patient with ET.A 68-year-old woman was admitted to our institution because of severe and sudden-onset chest pain. She underwent coronary angiography a year before which revealed a normal right coronary artery (RCA) with nonsignificant atherosclerotic lesions involving the other remaining coronary arteries. Her past medical history was significant for high platelet counts with a nonrevealing workup for myeloproliferative disease, and diabetes which was controlled medically. The patient's blood pressure on presentation was 135/70 mmHg with a heart rate of 70 beats/minute. Physical examination revealed splenomegaly without any other significant pathological findings. Electrocardiography showed regular sinus rhythm with ST segment depression in the inferior derivations. The patient was diagnosed as having acute coronary syndrome (ACS). She was transported immediately to the catheterization laboratory. Coronary angiography, performed via the right femoral artery, showed subtotal occlusion and thrombus-like filling defect in the mid portion of the RCA (Figure 1). The left circumfl
Digoxin intoxication: An old enemy in modern era

Bahadir Kirilmaz,Serkan Saygi,Hasan Gungor,Ugur Onse Turk,Emin Alioglu,Serdar Akyuz,Fatih Asgun,Istemihan Tengiz,Ertugrul Ercan,

老年心脏病学杂志(英文版) , 2012,
Abstract: Objectives Although development of new treatment modalities limited digoxin usage, digoxin intoxication is still an important issue which could be easily overlooked. In this report we analyzed a case series definitively diagnosed as digoxin intoxication in the modern era. Methods We analyzed 71 patients hospitalized with digoxin intoxication confirmed by history, complaints, clinical and electrocardiograph (ECG) findings, and serum digoxin levels > 2.0 ng/mL, during a five year period. The demographic and clinical data, indications for digoxin use, digoxin dosage, concurrent medications, laboratory data, hospital monitoring, and ECG findings were obtained from all patients. Results Thirty-eight of 71 patients (53.5%) had symptoms of heart failure during admission or later. Sixty-four percent of patients were older than 75 years. The percentage of females was 67%. Atrial fibrillation, hypertension and gastrointestinal complaints were more frequent in the females (64% in females, 30% in males, P = 0.007; 81% in female, 52% in males, P = 0.01; 50% in female, 17.3% in males, P = 0.008, respectively). The mortality rate during the hospital course was 7%. Conclusion This report demonstrated the reduced mortality rates in patients with digoxin intoxication over the study period. Gastrointestinal complaints are the most common symptoms in this population.
World Hypertension Congress 2013
?stemihan Tengiz
Anadolu Kardiyoloji Dergisi , 2013,
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