The aim of this study was to determine the endothelial function in patients with primary Sjögren's syndrome (SS). We also aimed to determine whether endothelial (dys)function correlates with extraglandular manifestations, specific autoantibodies and the severity of salivary gland involvement of SS. Endothelium-dependent vasodilation and endothelium-independent vasodilation of the brachial artery were assessed by a high-resolution ultrasound on 25 patients with primary SS and on 29 healthy controls. Patients with primary SS had significantly less mean endothelium-dependent vasodilation than did controls (3.0 +/- 0.4% vs 4.2 +/- 0.3%; p = 0.012). Endothelium-independent vasodilation induced by sublingual glycerol trinitrate was not different between the two groups (12.9 +/- 1.4% vs 14.1 +/- 1.2%; p = 0.86). We concluded that endothelium-dependent vasodilation was impaired in primary SS patients, in particular those presenting with Raynaud's phenomenon, when compared with the healthy controls and this impairment was not associated with the presence of RF, ANA, anti-Ro/SS-A, anti-La/SS-B and with the other extraglandular manifestations of the disease.

The aim of this study was to assess the effect of secondary Sjögren's syndrome (SjS) on QT dispersion and corrected QT dispersion in patients with rheumatoid arthritis (RA). We performed electrocardiography and Doppler echocardiography on 58 patients with RA whom we divided into two groups according to the presence of secondary SjS, and on 29 healthy controls. All patients revealed significantly longer QT dispersion and corrected QT dispersion values ( P< 0.05). Diastolic function variables were significantly different in all patients compared to controls. QT dispersion and corrected QT dispersion values were significantly longer in RA patients with secondary SjS than in those without. We concluded that secondary SjS could be a cardiovascular risk factor contributing to the well documented cardiovascular disease in RA patients.

Single point mutations in the genes coding for hemostatic factors were shown to be major inherited predisposing factors for venous thromboembolism. However, their contribution in the development of non-diabetic coronary artery disease [nDCAD] remains controversial. Angiographically demonstrated nDCAD patients (n = 86) and healthy controls (n = 90) were included in the study. Genotype analysis of hemostatic gene polymorphisms were assessed by using CVD strip assay, based on allele specific oligonucleotide probes. The carrier frequency of factor V (FV) H1299R, prothrombin G20210A, glycoprotein (Gp) IIIa L33P, plasminogen activator inhibitor-I (PAI-1) 4G/5G, 4G/4G, 5G/5G, methylenetetrahydrofolate reductase (MTHFR) A1298C and beta-fibrinogen -455 G > A were similar between patients and controls. In contrast, frequency of FV Leiden was significantly higher among patients (12.5%) than controls (5%, OR: 7.94; 95%CI: 1.9-49.6) and FXIII V34L was significantly lower among patients (23.7%) than controls (40%, OR: 0.24; 95%CI: 0.1-0.89). In addition, the frequency of the MTHFR C677T polymorphism was 32.5% among patients compared with 42.5% in controls, of which the T/T genotype was significantly lower among patients (5%) than controls (17.5%, OR: 0.06; 95%CI: 0.01-0.58). No difference was observed in prevalence of prothrombin G20210A, FV H1299R, Gp IIIa L33P, PAI-1 4G5G, MTHFR A1298C, beta fibrinogen 455 G > A mutations between patients and controls. However, lower frequency of FXIII Val34Leu and MTHFR C677T polymorphisms may decrease, while FV Leiden polymorphism may increase development of nDCAD.

Paper AbstractObjectives. The aim of this study was to assess the effects of losartan treatment on exercise tolerance and echocardiographic parameters in patients with mitral regurgitation (MR) secondary to mitral valve prolapse or rheumatic heart disease. Methods. Twenty-seven patients (14 males, 13 females, mean age 51±11, range 21-76) with moderate MR due to mitral valve prolapse or rheumatic heart disease were examined by means of Doppler echocardiography.The subjects were submitted to treadmill exercise tests using the modified Bruce protocol at baseline, after six hours and after the six-week treatment period to be evaluated based on their exercise tolerance. Mitral Regurgitant Volume (MRV), effective regurgitant orifice diameter, left atrial volume, left ventricle (LV) end-diastolic volume index, LV end-systolic volume index, LV ejection fraction (LVEF), left ventricle mass index were calculated at baseline and after six weeks of treatment with single dose of losartan (50 mg/day).

ÖZETÇok sayıda randomize kontrollü çalışmadan gelen veriler kardiyovasküler olayların önlenmesinde düşük-dansiteli lipoprotein (LDL) kolesterolün düşürülmesinin önemini ortaya koymuştur. Bu olumlu sonuçlara karşın LDL kolesterolü düşürülen hastaların tamamında benzer risk düşmesi sağlanamadığı ve bir grup hastanın statin tedavisine rağmen olay geçirmeye devam ettiği gözlenmiştir. Düşük LDL sağlanmasına karşın damarsal olaylara neden olabilen bu arta kalan risk faktörlerinin tespit edilmesi kritik önem taşımaktadır. Yeni veriler plak biyolojisinde etkili olan yangı aracıları, yüksek non-HDL (yüksek-dansiteli lipoprotein) kolesterol ya da apolipoprotein B, küçük-yoğun LDL, tip-2 diyabetes mellitus ve yaşam tarzı özelliklerinin arta kalan damarsal risk üzerine etkili olabileceğini düşündürmektedir. Bu derlemede, söz konusu arta kalan risk faktörlerinin belirlenmesinin önemi ve bunlara karşı geliştirilebilecek yeni tedavi stratejilerini gözden geçirdik. Ayrıca, yeni ilaç tedavilerinin etkilerini ölçme-de kullanılan arter duvarının görüntülenmesinin önemi de göz önünde bulunduruldu. (Anadolu Kardiyol Derg 2011; 2: 163-7) Anahtar kelimeler: Arta kalan risk, LDL, aterojenik dislipidemi, apolipoprotein B ABSTRACTCompelling evidence from randomized controlled studies demonstrated the crucial role of lowering low-density lipoprotein cholesterol (LDL-C) in the prevention of vascular events. However, not all patients with low LDL-C levels show similar reduction in event rates. The residual risk factors associated with ongoing vascular events despite achieving low LDL-C levels remain to be elucidated. New data suggest that beyond statin therapy, inflammatory mediators, high non-HDL (high-density lipoprotein) cholesterol or apolipoprotein B, small dense LDL-C, type 2 diabetes mellitus, and lifestyle features may have impact on residual vascular risk. In this review, we discussed the significance of identifying these residual risk factors and developing new treatment strategies to further decrease vascular events. The importance of imaging arterial wall to evaluate the effect of various medical therapies has also stated. (Anadolu Kardiyol Derg 2011; 2: 163-7) Key words: Residual risk, LDL, atherogenic dyslipidemia, apolipoprotein B Randomize kontrollü çalışmalardan gelen çok sayıda güçlü kanıt düşük-dansiteli lipoprotein kolesterolün (LDL-K) aterosklerotik kardiyovasküler (KVS) hastalık patogenezindeki temel ve kritik rolünü ortaya koymuştur. Birincil ve ikincil koruma çalışma-larında statin tedavisi ile LDL-K düşürülmesinin KVS morbidite ve mortalitede düşme sağladığı gösterilmiştir (1-3). Dahası KVS olaylardaki bu azalmanın LDL-K düşme düzeyi ile de ilişkili olduğu bulunmuştur. Doksan bin hastayı kapsayan bir meta-analizin sonuçları her 40 mg/dl LDL-K düşüşünün majör KVS olaylarda %23'lük bir azalma sağladığını göstermiştir (4). Bu kanıtlar ışığın-da on yılı aşkın bir süredir statinler ile LDL-K düşürülmesi koroner arter hastalığı (KAH) tedavisinin temel taşlarından biri haline gelmiştir. Statinler lehine giderek artmakta ol...