Men seem to have a higher activity relative to women for the drug efflux transporter P-gp. Our results suggest that carvedilol will cause drug interaction with digoxin following the inhibition of P-gp-mediated transcellular transport of digoxin in males.

Amaç: Atriyal fibrilasyonda sol atriyal trombüs oluşması açısından koagülasyon parametrelerinin rolü yeterince araştırılmamıştır. Atriyal fibrilasyonlu hastalarda sol atriyal trombüs ile veya onun öncüsü olduğu düşünülen spontan eko-kontrast varlığı (SEK) ile beta fibrinojen gen polimorfizmi ile trombosit glikoprotein IIIa gen polimorfizmi arasındaki ilişkiyi araştırmayı amaçladık. Yöntemler: Transözofageal ekokardiyografi yapılan atriyal fibrilasyonlu 47 hasta enine kesitsel gözlemsel çalışmamıza dahil edildi. Hastalar 2 gruba ayrıldı. Sol atriyal trombüsü olanlar Grup 1'i (n=24) ve trombüsü olmayanlar grup 2'yi (n=23) oluşturdu. Beta fibrinojen gene polimorfizm veya glikoprotein IIIa gen polimorfizmlerini saptamak için genetik analizler yapıldı. İstatistiksel analizde Mann Whitney U ve Ki-kare testleri kullanıldı. Bulgular: Demografik ve klinik özellikler bakımından gruplar arasında fark saptanmadı. Beta fibrinojen 455 G/A gen polimorfizm sıklığı grup 1'de (%37.5) grup 2'ye göre (%15) istatistiksel anlamlılığa ulaşmayacak şekilde (p=0.23) daha yüksek saptandı. Çalışma grubuna ciddi SEK'i olan hastalar da eklendiğinde (trombüs ve ciddi SEK n=27) 2 grup arasındaki fark (%44.4-%10) istatistiksel anlamlılığa ulaşmaktaydı (p=0.01). Glikoprotein IIIa Pl A1/A2 polimorfizmi ise gruplar arasında (p=0.73) SEK eklense de (p=0.82) farklı bulunmadı. Grup I'de grup II'ye göre mitral yetmezliği skoru daha düşük olma eğiliminde (p=0.08), SEK skoru ise anlamı olarak daha yüksek idi (p=0.03). ÖZETOb jec ti ve: The role of coagulation parameters left atrial thrombus formation in atrial fibrillation has not been investigated before. We aimed to investigate the association between the beta-fibrinogen gene polymorphism or glycoprotein IIIa gene polymorphism and presence of left atrial (LA) thrombus or spontaneous echo contrast (SEC) in patients with atrial fibrillation (AF). Methods: Forty-seven patients with AF, in whom transesophageal echocardiography was performed, were included to this cross-sectional observational study. Patients were divided in two groups; those with LA thrombus (n=24) were assigned to group 1 and those without thrombusin group 2 (n=23). DNA analysis was conducted to determine gene polymorphism in all patients. Mann-Whitney U test or Chi-square tests were used for statistical analysis Results: There were no significant differences between groups regarding to demographic and clinical characteristics. The frequency of betafibrinogen 455 G/A polymorphism was higher (37.5%) in group 1 as compared to group 2 (15.1%) but it did not reach statistical difference (p=0.23). When we added patients with severe SEC in the study group (patients with severe SEC and/or thrombus n=27) the difference (44.40%-10%) reached the statistical difference (p=0.01). Glycoprotein IIIa Pl A1/A2 polymorphism was not different between groups with (p=0.82) or without SEC (p=0.73). Conclusion: In patients with atrial fibrillation, beta-fibrinogen 455 G/A gene polymorphism is associated with the presence of left atrial thrombus and severe SEC...

SUMMARYPatients with diabetes mellitus (DM) have advanced atherosclerosis compared with nondiabetics. Restenosis after intracoronary stent implantation occurs frequently in diabetic patients. Angiotensin II is an important growth factor for the development of neointimal hyperplasia after vascular injury. The aim of our study was to evaluate the relationships between angiotensin converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and coronary artery disease (CAD) and stent restonosis in diabetic patients.One hundred and thirty consecutive patients with CAD and 47 consecutive patients (14 males, mean age, 58.0 ± 10.0) without CAD were enrolled in the study. All patients had type 2 (noninsulin dependent) DM. The patients with CAD underwent percutaneous transluminal coronary angioplasty (PTCA) and stenting. Ninety-four (59 males, mean age, 60.3 ± 9.8) underwent control coronary angiography at the end of the follow-up period (mean duration, 9.1 ± 2.9 months). ACE gene I/D genotyping was identified in all patients.No significant difference was found among patients with and without CAD with respect to ACE gene I/D polymorphism (P = 0.460). In the control coronary angiography, stent restenosis and new lesion development were comparable in each genotyping subgroup. However, a significant relationship was observed between restenosis and the use of ACE inhibitors (ACEI) in patients with D allele (ACEI ratio, 43.5% in the restenosis group and 56.5% in non-restenotic group, P < 0.05).We did not find any relationship between ACE gene I/D polymorphism and CAD and stent restenosis and new lesion development in diabetic patients. On the other hand, ACEI treatment may reduce stent restenosis in type 2 diabetic patients with D allele (DD or ID). (Int Heart J 2005; 46: 889-897)