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Öğe Aort darlığında plazma homosistein yüksekliği koroner arter hastalığı varlığını gösterebilir mi?(2003) Gündüz, Hüseyin; Akdemir, Ramazan; Tamer, Ali; Binak, Emrah; Ayarcan, YaseminAmaç: Kalsifik aort kapak hastalığı tespit edilen hastalardaki kardiyak risk faktörleri koroner arter hastalığı (KAH) ile benzer olup, koroner arter hastalığı prevalansı artmıştır. Son zamanlarda yapılan çalışmalarda; artmış plazma homosistein konsantrasyonunun koroner arter hastalığı için bağımsız bir risk faktörü olduğu, çeşitli mekanizmalarla ateroskleroza yol açarak aterosklerotik damar hastalıklarını ve venöz sistemde trombüs oluşumunu kolaylaştırıcı etki gösterdiği tespit edilmiştir. Fakat aort darlığı olan hastalarda plazma homosistein düzeyinin koroner arter hastalığı varlığı ile ilişkisi araştırılmamıştır. Bu çalışmanın amaçları; orta-ileri aort darlığı olan hastalarda plazma homosistein düzeyininin koroner arter hastalığı varlığını ne şekilde etkilediğini araştırmak ve aort darlığında homosistein düzeyi, koroner arter hastalığı varlığının noninvaziv bir belirleyicisi olabilir mi sorusuna cevap aramaktır. Gereç ve Yöntem: Çalışmaya transtorasik ekokardiyografi ile orta-ileri derecede aort darlığı tespit edilen ve sonrasında koroner anjiyografi yapılan toplam 58 hasta (koroner arter hastalığı olan 30, koroner arter hastalığı olmayan 28 hasta) alındı. Hastaların 12 saatlik açlık sonrası venöz kan örnekleri alınarak serum total kolesterol, LDL ve HDL kolesterol, trigliserid ve ELİSA yöntemiyle homosistein düzeyleri ölçüldü. Bulgular: Koroner arter hastalığı olan hastalarda (17 erkek,13 kadın, ortalama yaş 66±10 yıl) total kolesterol 266±45 mg/dL, trigliserid 194±93 mg/dL, LDL mg/dL 174±44, HDL 45±5 mg/dL, Homosistein düzeyi 13.2±3.1 µmol/l bulundu. Koroner arter hastalığı olmayan hastalarda ise (18 erkek,10 kadın, ortalama yaş 61±12 yıl) total kolesterol 204±38 mg/dL trigliserid 122±73 mg/dL, LDL 132±33 mg/dL, HDL 48±5 mg/dL, homosistein düzeyi 8.3±2.2 µmol/l bulundu. Koroner arter hastalığı olan hastalarda total kolesterol (p<0.01), LDL (p<0.05) ve homosistein düzeyi (p<0.01) anlamlı olarak yüksek bulundu. Sonuç: Bu sonuçlar orta-ileri aort darlığı olan hastalarda plazma homosistein düzeyindeki yüksekliğin koroner arter hastalığı varlığı ile korele olduğunu göstermektedir. Ayrıca aort darlığında koroner arter hastalığı varlığını gösteren bir noninvaziv test olarak araştırılması gerektiğini düşündürtmektedir.Öğe Can serum lipid and CRP levels predict the "severity" of aortic valve stenosis?(Taylor & Francis Ltd, 2003) Gündüz, Hüseyin; Akdemir, Ramazan; Binak, Emrah; Tamer, Ali; Keser, Nurgül; Uyan, CihangirBackground - Results of the studies performed have suggested that hypercholesterolaemia and inflammation are important aetiologic factors in aortic valve stenosis (AVS). However up to now no such data has been obtained to evaluate whether these predictors may still serve as valuable tools to estimate the progression and severity of AVS. If factors contributing to the "progression" of degenerative process can be understood and preventive measures can be taken, both clinical and economical beneficial effects can be achieved. The objective of this study is to investigate the correlation of serum cholesterol, triglyceride and CRP levels with the severity of aortic stenosis echocardiographically evaluated in patients with aortic valve stenosis. Material and methods -Aortic valvular areas of 60 patients (pts) hospitalized in our clinic with suspected AVS were calculated with Doppler echocardiography. Patients were grouped into mild, moderate and advanced AVS, each category containing 20 pts, and then were subclassified regarding those with and without coronary artery disease(CAD). Results -Total cholesterol and CRP levels were found to be 215 +/- 42 mg/dl and 2.0 +/- 1.4 mg/dl; 224 +/- 43 mg/dl and 2.4 +/- 2.1 mg/dl; 225 +/- 55 mg/dl and 2.7 +/- 2.1 mg/dl in pts with mild, moderate and advanced AVS, respectively. A statistically significant difference was not detected among the three groups (p>0.05). When subclasses were classified the levels were found to be much more increased in those patients having additional CAD. Conclusion - We have demonstrated that severity of AVS does not correlate significantly with hypercholesterolaemia and CRP and their levels do not rise in accordance with increasing severity of AVS. Elevations of lipid levels in AVS were found to correlate with the presence of CAD rather than the severity of AVS. So, not in patients with simply AVS but in patients under higher cardiovascular risks, investigation of CRP plus lipid levels might provide benefit with respect to preventive treatment and benefit from cholesterol-lowering drugs can be expected in such kind of patients.Öğe A case of coronary artery fistula with mitral stenosis(Kluwer Academic Publ, 2003) Gündüz, Hüseyin; Akdemir, Ramazan; Binak, Emrah; Ayarcan, Yasemin; Kurtoğlu, Nuri; Uyan, CihangirCoronary artery fistulae, being a rare form of congenital anomalies of the coronary arteries, are usually discovered by chance during coronary arteriography. However, these fistulae can cause an important coronary morbidity and mortality leading to angina, syncope, congestive heart failure, myocardial infarction and sudden death. The coincidence of mitral stenosis and congenital artery fistula is rare in the literature. In our case report, a patient with a coronary artery fistula originating from the circumflex, draining to the main pulmonary artery, discovered at cardiac catheterization and coronary angiography done with a prediagnosis of mitral stenosis is presented in the light of the literature.Öğe The relation between homocysteine and calcific aortic valve stenosis(Karger, 2005) Gündüz, Hüseyin; Arınç, Hüseyin; Tamer, Ali; Özhan, Hakan; Akdemir, Ramazan; Binak, Emrah; Uyan, CihangirBackground: In patients diagnosed with calcific aortic valve stenosis, cardiac risk factors are similar to those of coronary artery disease; homocysteine concentration is an independent risk factor for coronary artery disease. The aim of this study was to investigate the correlation between plasma homocysteine levels and aortic valve stenosis and the influence of homocysteine levels on the coexistence of coronary artery disease in patients with moderate to severe aortic valve stenosis. Methods: Fifty-eight patients who had been diagnosed with moderate to severe aortic stenosis formed the test group of this study, and 47 healthy subjects without coronary artery disease or aortic valve stenosis formed the control group. The patients with aortic stenosis were divided into two groups according to the presence or absence of coronary artery disease in their coronary angiograms. After 12 h fasting venous blood samples were collected and total cholesterol, low-density lipoprotein, high-density lipoprotein, triglycerides and homocysteine levels were measured and compared between the two groups. Measurements and Results: The mean blood homocysteine level was 10.8 +/- 3.3 mu mol/l in patients with aortic valve stenosis and 8.1 +/- 4.7 mu mol/l in the control group; the difference between these levels was statistically insignificant. The patients with aortic valve stenosis had significantly higher levels of total cholesterol and hypertension and were more likely to have a positive family history for coronary artery disease. When the two subgroups of patients with aortic valve stenosis were compared, mean blood homocysteine levels were 13.2 +/- 3.1 and 8.3 +/- 2.2 mu mol/l, respectively, showing significantly higher levels in the group with coronary artery disease. In this comparison patients with coronary artery disease were also found to have significantly higher levels of total cholesterol and LDL and they were more likely to be smokers. Conclusions: Although there was no relation between blood homocysteine levels and the existence of aortic valve stenosis, in cases with both coronary heart disease and aortic stenosis homocysteine levels were significantly higher than in the patients with pure aortic valve stenosis.Öğe The relation between impaired glucose tolerance and slow coronary flow(Elsevier Ireland Ltd, 2006) Binak, Emrah; Gündüz, Hüseyin; Şahin, Müslüm; Kurtoğlu, Nuri; Dindar, İsmetBackground: Impaired glucose tolerance is a preliminary stage in the development of type 2 diabetes mellitus and has been shown to increase the risk of cardiovascular morbidity and mortality in addition to causing endothelial dysfunction. In this study, we sought to determine if impaired glucose tolerance is related to slow coronary flow, an angiographic phenomenon caused by coronary micro and macrovascular endothelial dysfunction. Methods: The population of this prospective study consisted of 28 patients with documented slow coronary flow, defined according to TIMI frame count method, [20 (71.4%) males; 51 +/- 9 years] and 30 patients with normal coronary flow [17 (56.6%) males; 47 +/- 6 years]. All study patients underwent an oral glucose tolerance test after 12 h of fasting. Lipid profile, hemoglobin Ale and systemic blood pressure were measured in all patients. Results: There was no difference between two groups with respect to age, fasting plasma glucose, triglyceride, total cholesterol, high density lipoprotein, low density lipoprotein, hemoglobin Ale, systolic-diastolic blood pressure levels, history of smoking and alcohol consumption. Plasma glucose at 2 h of oral glucose tolerance test was significantly higher in slow coronary flow patients compared to control group (145 +/- 44 vs. 112 +/- 38 mg/dl, P=0.001, respectively). In addition, the number of patients who met the criteria of impaired glucose tolerance was significantly higher in slow coronary flow patient group [16 (57%) vs. 7 (23%), P=0.002, respectively). Conclusions: Our results suggest that impaired glucose tolerance may be an independent etiological factor for slow coronary flow phenomenon.Öğe Relation between stage of left ventricular diastolic dysfunction and QT dispersion(Taylor & Francis Ltd, 2003) Gündüz, Hüseyin; Akdemir, Ramazan; Binak, Emrah; Tamer, Ali; Uyan, CihangirObjective - In 30-40% of patients with clinical heart failure diastolic dysfunction is present although systolic function is normal. Evaluation of diastolic functions are important for the patient's early diagnosis, treatment and prognosis. QT dispersion is an important parameter that reflects heterogeneity of ventricular repolarization and predicts ventricular arrhythmia and sudden death. According to several studies, QT dispersion is significantly increased in patients with diastolic dysfunction due to ischemic heart disease and left ventricular hypertrophy compared to the patients without diastolic dysfunction. However, a study about the relation between the stage of left ventricular diastolic dysfunction and QT dispersion is not present. The aim of this study was to investigate the correlation between the stage of left ventricular diastolic function determined by transthoracic echocardiography and QT dispersion. Methods and Results - In our study the left ventricular diastolic functions of 80 patients were evaluated by transthoracic echocardiography. Eighty patients were divided to four stages each containing 20 patients. Stage 0 was defined as normal, stage I as prolonged relaxation pattern, stage 2 as pseudonormal pattern and stage 3 as restrictive pattern. We measured QT dispersion (QT D) and corrected QT dispersion (QTc D) values according to Bazzet's formula in their ECGs. QT D and QTc D were found 20 +/- 8 ms vs. 26 +/- 1 ms in normal patients, 25 +/- 8 ms vs. 37 +/- 9 ms in the patients with prolonged relaxation pattern, 28 +/- 10 ms vs. 38 +/- 11 ms in the patients with pseudonormal pattern and 38 13 ms vs. 41 +/- 14 ms in the patients with restrictive pattern. A significant direct relation was found between the stage of left ventricular diastolic function and QT, QTc dispersion (p<0.01). Furthermore, when classified according to the aetiology of the left ventricular diastolic dysfunction (stage 1, 2, 3) QT D and QTc D were 24 6 ms vs. 32 9 ms in the patients with left ventricular hypertrophy (LVH), and 32 +/- 9 ms vs. 41 +/- 12 ms in the patients with ischaemic heart disease (IHD). The differences between the two groups were statistically significant (p<0.01). Conclusions -These findings show that QT D and QTc dispersion values increase in relation to increasing left ventricular diastolic functional stage that is determined by echocardiography and that the patients with ischaemic heart disease have much more increased QT values than the patients with left ventricular hypertrophy.Öğe Relationship between P Wave Dispersion and Diastolic Dysfunction(Turkish Anaesthesiology and Intensive Care Society, 2003) Gündüz, Hüseyin; Binak, Emrah; Akdemir, Ramazan; Tamer, Ali; Ayarcan, Yasemin; Özkekelif, Mehmet; Uyan, CihangirDiastolic dysfunction of hypertrophic or ischemic left ventricle causes an increase in ventricular enddiastolic pressure and left atrial size. In this situation, continuity of sinus rhythm and atrial contractions are of great value for the maintenance of cardiac output. The aim of our study was to investigate the relationship between P wave dispersion, which is easily measured on the surface ECG and used in assessing the risk of atrial fibrillation, and left ventricular diastolic function. In our study, a total of 133 patients were included (73 patients with diastolic dysfunction assessed by transthorasic echocardiography and 60 patients without). P wave dispersions were calculated by measuring the P minimum and P maximum values on the surface ECG. The relation between P wave dispersion and presence of diastolic dysfunction, its etiology, severity and echocardiographic measurements were investigated. P dispersion was 53±9 ms in patients with diastolic dysfunction and 43±9 ms in the control group (p< 0.01). When the patients were grouped according to the stage of diastolic dysfunction, P dispersion was 48±7 ms in stage 1, 54±8 ms in stage 2 and 58±9 ms in stage 3. It was noted that as the severity of diastolic dysfunction increased, P dispersion also increased without reaching statistical significance (p> 0.05). When the etiology of diastolic dysfunction was considered, P dispersion was 53±8 ms in patients with ischemic heart disease, and 52±9 ms in patients with left ventricular hypertrophy and a significant difference was not present (p> 0.05). Hence, in patients with diastolic dysfunction, P dispersion increases but this increase is not related to the severity of diastolic dysfunction or its etiology. When clinical and echocardiographic parameters are taken into account, there was a weak but significant correlation only between P dispersion and left ventricular ejection fraction.Öğe The relationship between P wave dispersion and diastolic dysfunction(Texas Heart Inst, 2005) Gündüz, Hüseyin; Binak, Emrah; Arınç, Hüseyin; Akdemir, Ramazan; Özhan, Hakan; Tamer, Ali; Uyan, CihangirWe investigated the relationship between P wave dispersion, which is easily measured on the surface electrocardiogram and may be used in evaluating the risk of atrial fibrillation, and left ventricular diastolic function. There were 133 patients: 73 with diastolic dysfunction and 60 without. P wave dispersions were calculated by measuring minimum and maximum P wave duration values on the surface electrocardiogram. The relationships between P wave dispersion and the presence, cause, severity, and echocardiographic measurements of diastolic dysfunction were investigated. P wave dispersion was 53 +/- 9 ms in patients with diastolic dysfunction and 43 9 ms in the control group (P < 0.01). When patients were grouped according to stage of diastolic dysfunction. P wave dispersion was 48 +/- 7 ms in stage 1, 54 +/- 8 ms in stage 2 and 58 +/- 9 ms in stage 3. As the severity of diastolic dysfunction increased, P wave dispersion increased but the difference did not reach statistical significance (P < 0.05). When the cause of diastolic dysfunction was considered, P wave dispersion was 53 +/- 8 ms in patients with ischemic heart disease and 52 +/- 9 ms in patients with left ventricular hypertrophy (P > 0.05). We conclude that P wave dispersion increases in diastolic dysfunction, but that this increase is not related to the severity or cause of diastolic dysfunction. When clinical and echocardiographic variables are taken into account, there is a weak but significant correlation only between P wave dispersion and left ventricular ejection fraction.Öğe Sol ventrikül diyastolik fonksiyon bozukluğu ile P dalga dispersiyonu arasındaki ilişki(2003) Gündüz, Hüseyin; Binak, Emrah; Akdemir, Ramazan; Tamer, Ali; Ayarcan, Yasemin; Özkökeli, Mehmet; Uyan, CihangirHipertrofiye veya iskemik ventrikülde görülen diyastolik fonksiyon bozukluğu sol ventrikül diyastol sonu basıncında ve sol atriyum boyutunda artışa yol açmakta, sinüs ritminin idamesi ve atriyal kontraksiyonların varlığı kardiyak debinin devamı için büyük önem taşımaktadır. Çalışmamızın amacı yüzey elektrokardiyogramından kolayca elde edilen ve atriyal fibrilasyon gelişme riskini belirlemede kullanılan P dalga dispersiyonunun sol ventrikül diyastolik fonksiyonu ile olan ilişkini araştırmaktır. Çalışmaya kardiyoloji kliniğimizde trantorasik ekokardiyografi ile diyastolik fonksiyon bozukluğu belirlenen 73 olgu ( 39 erkek, 34 kadın, ortalama yaş 60±6 ) ve belirlenmeyen 60 olgu (27 erkek, 33 kadın, ortalama yaş 55±8 ) olmak üzere toplam 133 olgu alındı. Yüzey elektro kardiyogramlarından P maksimum ve P minimum değerleri ölçülerek P dalga dispersiyonları hesaplandı. P dispersiyonunun diyastolik fonksiyon bozukluğunun varlığı, etyolojisi, şiddeti ve ekokardiyografık ölçümlerle olan ilişkisi araşt ırıldı. Diyastolik fonksiyon bozukluğu olan hastalarda P dispersiyonu 53±9 ms, kontrol grubunda ise 43±9 ms idi ve iki grup arasında anlamlı fark mevcuttu (p<0.01). Diyastolik fonksiyon bozukluğu olan hastalar evrelendirildiğinde; P dispersiyonu evre 1'de 48±7 ms, evre 2'de 54±8 ms, evre 3'te 58±9 ms idi. Diyastolik disfonksiyonunun şiddeti arttıkça P dispersiyonunun arttığı görüldü ancak bu artış istatistiksel olarak anlamlı değildi (p>0.05). Diyastolik fonksiyon bozukluğu yapan etyoloji gözönüne alındığında P dispersiyonu iskemik kalp hastalığı olanlarda 53±8 ms, sol ventrikül hipertrofisi olanlarda 52±9 ms idi ve iki grup arasında anlamlı fark tespit edilmedi (p>0.05). Sonuç olarak diyastolik fonksiyon bozukluğu olan hastalarda P dıspersiyonun arttığı, bu artışın diyastolik fonksiyon bozukluğunun şiddeti ve etyolojisi ile ilişkili olmadığı, P dispersiyonu ile klinik ve ekokardiyografik parametrelerden sadece sol ventrikül ejeksiyon fraksiyonu arasında zayıf ancak anlamlı ilişki olduğu te spit edildi.Öğe Sol ventrikül diyastolik fonksiyon bozukluğunun evresi ile QT dispersiyonu arasındaki ilişki(2003) Gündüz, Hüseyin; Akdemir, Ramazan; Binak, Emrah; Tamer, Ali; Erikçi, Hakan; Keser, Nurgül; Uyan, CihangirAmaç: Klinik olarak kalp yetersizliği bulguları taşıyan hastaların %30-40'ında sistolik fonksiyonlar normal olduğu halde diyastolik fonksiyon bozukluğu vardır. Diyastolik fonksiyonlar genellikle sistolik fonksiyonlardan önce bozulur. Bu yüzden diyastolik fonksiyonlar, özellikle kalp hastalıklarının erken teşhisi, takip, tedavi ve prognozun belirlenmesi açısından büyük önem taşırlar. Ventriküler repolarizasyondaki heterojenitenin bir yansıması olan QT dispersiyonu ise ventriküler aritmi ve ani kardiyak ölüm gibi olayları önceden haber veren önemli bir parametredir. Araştırmalar ekokardiyografik olarak tespit edilebilen diyastolik fonksiyon bozukluğu yapan iskemik kalp hastalığı ve sol ventrikül hipertrofisi olan hastalardaki QT dispersiyonunun diyastolik fonksiyon bozukluğu olmayan hastalara oranla anlamlı olarak arttığını göstermektedir. Ancak literatürde sol ventrikül diyastolik fonksiyon bozukluğunun evresi ile QT dispersiyonu arasındaki ilişkiyi inceleyen çalışma bulunmamaktadır. Çalışmamızın amacı transtorasik ekokardiyografi ile değerlendirilen sol ventrikül diyastolik fonksiyonlarının evresi ile QT dispersiyonu arasındaki ilişkiyi incelemektir. Gereç ve Yöntem: Çalışmamızda hipertansif olduğu bilinen 80 hastanın transtorasik ekokardiyografi ile sol ventrikül diyastolik fonksiyonları incelendi. Hastalar evre 0 normal patern, evre 1 uzamış gevşeme paterni, evre 2 yalancı normal patern, evre 3 restriktif paterni olanlar şeklinde yirmişer hastalık dört evreye ayrıldı. Bu hastaların standart EKG'lerinden, QT dispersiyonu (QT D) ve Bazett's formülüne göre düzeltilen QTc (QTc D) dispersiyon değerleri ölçüldü. Bulgular: Normal paterni olan hastalarda QT dispersiyonu 20±8 ms, QTc dispersiyonu 26±11ms, uzamış gevşeme paternine sahip hastalarda QT dispersiyonu 25±8 ms, QTc dispersiyonu 37±9 ms, yalancı normal paterne sahip hastalarda QT dispersiyonu 28±10 ms, QTc dispersiyonu 38±11 ms, restriktif paterni olan hastalarda ise QT dispersiyonu 38±13 ms, QTc dispersiyonu 41±14 ms bulundu. Sol ventrikül diyastolik fonksiyonun evresi ile QT ve QTc dispersiyonu arasında anlamlı ilişki tespit edildi(p<0.01). Ayrıca sol ventrikül diyastolik fonksiyon bozukluğu olan hastalar (evre 1,2,3) etyoloji gözönüne alınarak değerlendirildiğinde sol ventrikül hipertrofisi olan hastaların QT dispersiyonu 24±6 ms QTc dispersiyonu 32±9 ms, iskemik kalp hastalığı olanlarda ise QT dispersiyonu 32±9 ms, QTc dispersiyonu 41±12 ms olarak bulundu. İki grup arasındaki fark istatistiksel olarak anlamlı idi (p<0.01). Sonuç: Sonuç olarak QT ve QTc dispersiyonu değerinin ekokardiyografik olarak değerlendirilen sol ventrikül diyastolik fonksiyonunun evresi ile ilişkili olarak değiştiğini, ayrıca iskemik kalp hastalığı olanlarda bu değerlerin sol ventrikül hipertrofisi olanlara oranla daha belirgin arttığı saptandı.Öğe Spontaneous rupture of a coronary artery aneurysm - a case report and review of the literature(Int Heart Journal Assoc, 2004) Gündüz, Hüseyin; Akdemir, Ramazan; Binak, Emrah; Tamer, Ali; Uyan, CihangirCoronary artery aneurysm (CAA) is. a rare disorder, characterized by abnormal dilatation of a localized portion or diffuse segments of the coronary artery. CAA may cause angina, myocardial infarction, sudden death due to thrombosis, embolisation, or rupture. In this report, a 63 year old Turkish male patient is presented who had an acute non-Q wave myocardial infarction due to spontaneous rupture of the left circumflex artery aneurysm. An extremely rare clinical presentation of rupture of a left circumflex CAA is discussed.
