OBJECTIVE:The aim of the present study was to investigate the relationship between pericoronary fat and the severity and extent of atherosclerosis, quantified using 64-multidetector computed tomography, in patients with suspected coronary artery disease.METHODS:The study population consisted of 131 patients who were clinically referred for noninvasive multislice computed tomography coronary angiography for the evaluation of coronary artery disease. Patients were classified as follows: no atherosclerosis, Group 1; nonobstructive atherosclerosis (luminal narrowing <50% in diameter), Group 2; and obstructive atherosclerosis (luminal narrowing ≥50%) in a single vessel or obstructive atherosclerosis in the left main coronary artery and/or multiple vessels, Group 3. Epicardial adipose tissue was defined as the adipose tissue between the surface of the heart and the visceral layer of the pericardium (visceral epicardium). Epicardial adipose tissue thickness (mm) was determined in the right ventricular anterior free wall. The mean thickness of the pericoronary fat surrounding the three coronary arteries was used for the analyses.RESULTS:The average thickness over all three regions was 13.2 ± 2.1 mm. The pericoronary fat thickness was significantly increased in Group 3 compared with Groups 2 and 1. The epicardial adipose tissue thickness was significantly increased in Group 3 compared with Groups 2 and 1. A receiver operating characteristic curve for obstructive coronary artery disease was assessed to verify the optimum cut-off point for pericoronary fat thickness, which was 13.8 mm. A receiver operating characteristic curve for obstructive coronary artery disease was also assessed to verify the optimum cut-off point for epicardial adipose tissue, which was 6.8 cm.CONCLUSION:We showed that the epicardial adipose tissue and pericoronary fat thickness scores were higher in patients with obstructive coronary artery diseases.

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P wave duration and PWD are found prolonged in hyperthyroid patients and propylthiouracil treatment decreased them effectively. This mechanism may establish how the anti-thyroid treatment may prevent the development of atrial fibrillation in hyperthyroid patients.

ÖZETAmaç: Biz bu çalışmada, tokluk trigliserid (TTG) düzeyi ve koroner arter hastalığı (KAH) arasındaki ilişkiyi araştırmayı amaçladık. Yöntemler: Bu prospektif kohort çalışmasına toplam 80 hasta dahil edildi ve TTG düzeyini ölçmek için ağızdan lipit yüklemesi yapıldı. Aç olarak ve lipitten zengin bir kahvaltı sonrası 2., 4., 6. ve 8. saatte tok olarak trigliserid düzeyi enzimatik yöntemle ölçüldü. Açlık trigliserid yüksekliği olan ve olmayan bireylerde lipit yüklemesinin trigliserid düzeyi üzerine etkisinin değerlendirilmesi için alt grup analizi uygulandı. Lipid yüklemesi sonrası trigliserid düzeyleri ve trigliserid düzeyindeki yüzde değişim oranları "tekrarlayan değerler için genel lineer model" analizi ile değerlen-dirildi. Örneklem büyüklüğü hesaplandı. Bulgular: Başlangıçtaki klinik, demografik ve biyokimyasal ölçümlerin sonuçları gruplar arasında benzerdi. Her iki grupta da zirve trigliserid seviyesi lipit yüklemesi sonrası 4. saatteydi. Lipit yüklemesi sonrası her iki grupta da trigliserid düzeyleri başlangıca göre anlamlı olarak arttı (p<0.001) ancak bu değişimler iki grup arasında farklı değildi (p=0.279). Alt grup analizlerinde; açlık trigliserid yüksekliği olan alt grupta, trigliserid düzeyi eğrisi altında kalan alanda KAH grubunda kontrol grubuna göre anlamlı yükseklik vardı (334±103 vs. 233±58 mg/dl, p=0.02). Sonuç: Bizim sonuçlarımız, açlık trigliserid düzeyi yüksek olan hastalarda TTG yüksekliğinin KAH ile ilişkili olabileceğini, ancak açlık trigliserid düzeyi yüksek olmayan hastalarda TTG düzeyi ile KAH arasında bir ilişki olmadığını göstermektedir. ABSTRACTObjective: We aimed to evaluate the relationship between postprandial triglyceride (PPTG) levels and coronary artery disease (CAD). Methods: A total of 80 patients were included in this prospective cohort study. Oral lipid loading was used in order to measure PPTG levels. In the fasting state and after the high fat breakfast, triglyceride levels were measured by enzymatic methods at 2 nd , 4 th , 6 th and 8 th hours. We made subgroup analysis to show the effects of lipid loading on triglyceride levels in patients with and without fasting hypertriglyceridemia. We evaluated triglyceride levels and changes of triglyceride levels in percentages after lipid loading using a general linear model for repeated measures. Sample size analysis was performed. Results: Baseline clinical, demographic and laboratory characteristics of both groups were similar. The peak triglyceride levels were seen at the 4 th hour in both groups. Triglyceride levels were significantly increased after lipid-rich-breakfast loading compared to baseline levels in both groups (p<0.001) but these changes were not significant (p=0.279). In patients with elevated fasting triglyceride levels, the area under the plasma triglyceride concentration curve was significantly larger in CAD group than control group (334±103 vs. 233±58 mg/dl, p=0.02). Conclusion: Our data show that in patients who have a high fasting triglyceride level, high levels of PPTG may be related to CAD, however high...

Metoprolol succinate therapy seems to have no cardioprotective effect in limiting troponin-I rise after PCI.