Necati Dagli

Is inflammatory bowel disease a risk factor for early atherosclerosis

Objectives: Chronic inflammatory diseases are associated with an accelerated atherosclerotic process. Recent studies have discussed whether inflammatory bowel diseases (IBDs) can predict early atherosclerosis. We investigated this possibility. Methods: The study consisted of IBD cases (group 1, n = 40) and healthy persons (group 2, n = 40). The IBD group was selected so as not to have vascular disease or the presence of established major cardiovascular risk factors. Results: Group 1 cases showed a significant increase in carotid intima media thickness (cIMT; P = .01). Carotid artery stiffness was impaired in group 1 (P = .03) and high-sensitivity C-reactive protein (hsCRP), homeostasis model assessment of insulin resistance (HOMA-IR), and homocysteine (Hyc) were higher in group 1 patients (P = .02, P = .03, P = .05). Conclusions: Inflammatory bowel disease patients have an increased risk of early atherosclerosis as shown by greater values of cIMT, carotid artery stiffness, Hyc, hsCRP, and insulin resistance.

Are maximum P wave duration and P wave dispersion a marker of target organ damage in the hypertensive population

BackgroundHigh blood pressure, left ventricular hypertrophy and diastolic dysfunction may cause hemodynamic and morphological changes in the left atrium, consequently instability and heterogeneity in atrial conduction. This is seen as an increase in maximum P wave duration (Pmax) and P wave dispersion (PD) on the electrocardiogram (ECG). P wave dispersion on ECG has been encountered as a risk factor for atrial fibrillation (AF). The aim of this study is to examine whether PD and Pmax can be used as a non-invasive marker of target organ damage (LVH and diastolic dysfunction) in a hypertensive population.Material and methodsThe study registered a total of 120 cases (mean age 46.9 ± 10.6 years; 58 [48.3%] males and 62 [51.7%] females), of whom 60 were patients diagnosed as essential hypertension (group 1), and 60 were healthy individuals, who constituted the control group (group 2). Systolic and diastolic functions of all cases were evaluated by echocardiography, and maximum P wave duration (Pmax), and PD was calculated.ResultsMaximum P wave duration was 91.6 ± 10.2 ms in group 1, and 64 ± 10.2 ms in group 2 (p < 0.01), while PD was 56.1 ± 5.8 ms in group 1, and 30.3 ± 6.6 ms in group 2 (p < 0.01). Blood pressure, left atrium diameter, DT, IVRT, and E/A ratio, as well as left ventricular mass index increased markedly in group 1.ConclusionHigh blood pressure, LVH, diastolic dysfunction and increased left atrium diameter and volume shows parallelism in hypertensive cases. These physiopathological changes may cause different and heterogeneous atrial electrical conduction. This led to a marked increase in Pmax and PD in our cases. Thus, the results support the hypothesis that PD can be used as a non-invasive marker of target organ damage (LVH and LV diastolic dysfunction) in the hypertension population.

Serum Adiponectin and Vaspin Levels in Rheumatoid Arthritis

BACKGROUND AND AIMS The risks of insulin resistance and accelerated atherosclerosis are increased in chronic inflammatory diseases including rheumatoid arthritis (RA). Adipo-(cyto)kines are associated with insulin resistance, atherosclerosis and inflammation. This study aimed to determine serum adiponectin and vaspin levels and their associations with the predictors of atherosclerosis in RA and Behcets disease (BD). METHODS The study involved 56 patients with RA, 37 patients with BD, and 29 healthy controls (HC). Serum adiponectin and vaspin levels, homeostasis model assessment for insulin resistance (HOMA-IR) index, and common carotid intima-media thickness (IMT) were determined. RESULTS Serum adiponectin levels in both patient groups and serum vaspin level in only the RA group were higher, whereas serum vaspin level was lower in the active BD subgroup, compared to the HC group. However, adiponectin and vaspin levels were correlated with neither HOMA-IR index nor IMT in the RA group. Adiponectin level was correlated with DAS-28 and IL-6 level in the RA group, and it was higher in the active BD subgroup than in the inactive BD subgroup and the HC group. CONCLUSIONS Adiponectin and vaspin levels are higher in RA but associated with neither HOMA-IR index nor IMT. Adiponectin is related with disease activity remarks in RA and BD. Therefore, it may be suggested that adiponectin may be involved in the regulation of inflammatory responses in inflammatory diseases. Moreover, in contrast to in RA, vaspin level declines in active BD, and these results suggest that different chronic inflammatory diseases exert different influences on either adipokines.

Visfatin levels and intima-media thicknesses in rheumatic diseases.

Chronic inflammatory rheumatic diseases lead to increased prevalence of atherosclerosis. However, this early and accelerated atherosclerosis cannot be explained by traditional cardiovascular risk factors alone. The permanent overexpression of cellular adhesion molecules and pro-inflammatory cytokines in chronic inflammatory conditions may participate in accelerated atherosclerosis. Visfatin, a novel adipocytokine, has a potential insulin-like action and pro-inflammatory effects. Therefore, the aim of the study was to determine serum visfatin level and its association with common carotid intima-media thickness (IMT), which is a predictor of atherosclerosis, in patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), systemic sclerosis (SSc), and Behçet’s disease (BD). The study involved 29 RA, 26 SLE, 25 SSc, 30 BD patients, and 29 healthy controls (HC). Serum levels of TNF-α, IL-6, and visfatin were analyzed using enzyme-linked immunosorbent assay method and homeostasis model assessment for insulin resistance (HOMA-IR) indexes, and IMTs were determined. Serum visfatin level was higher in the RA group than all the other groups. In addition, visfatin level was higher in the active BD subgroup than the inactive BD subgroup. In the study groups, visfatin levels were not correlated with HOMA-IR indexes and IMTs. Whereas visfatin serum concentration was not associated with insulin resistance and carotid atherosclerosis in selected rheumatic diseases, it was higher in the RA and active BD groups, but not in the SLE and SSc groups. Visfatin levels may be associated with Th1/Th2 balance. Further studies are needed for more precise elucidation of the pro-inflammatory activities of visfatin.

Effect of Ongoing Inflammation in Rheumatoid Arthritis on P-Wave Dispersion:

It has been emphasized recently that there is a strong association between atrial fibrillation and inflammation. Rheumatoid arthritis (RA), characterized by ongoing inflammatory activity, can increase the risk of atrial arrhythmia. P-wave dispersion has been encountered as a risk factor for atrial fibrillation and the effect of inflammation on P-wave dispersion has not been studied thoroughly. The aim of this study was to examine the effect of ongoing inflammatory activity in RA on P-wave dispersion. The study comprised 82 patients diagnosed with RA and 41 healthy volunteers as controls. Systolic functions of all participants were evaluated by echocardiography. Maximum P-wave duration and dispersion were calculated and found to be significantly increased in the RA group compared with the healthy controls. These parameters were also significantly correlated with C-reactive protein levels. The findings of this study suggest that RA may be associated with increases in P-wave dispersion and maximum P-wave duration, and that this association may result from ongoing inflammation.

P-Wave Dispersion in Panic Disorder

Background: P-wave dispersion (PWD) is defined as the difference between the maximum and the minimum P-wave (Pmax and Pmin, respectively) duration. Significant variation in cardiac atrial PWD has been correlated with changes in systemic autonomic tone such as during periods of anxiety. It is also known that the degree of PWD seen on 12-lead electrocardiogram (ECG) may be a predictor of susceptibility of the atrial myocardium to future atrial fibrillation (AF). Therefore, we firstly aimed to show an association between PWD and panic disorder, a state of high sympathetic tone. Methods: PWD was measured in 40 outpatients with panic disorder and in 40 physically and mentally healthy age- and gender-matched controls. In addition, the Panic Agoraphobia Scale (PAS) and the Hamilton Depression Rating Scale (HDRS) were scored concomitantly. Results: Both Pmax and Pmin were significantly higher than those of healthy controls. PWD was significantly greater in the panic disorder group than in the controls. As expected, the mean score on PAS was significantly higher for the panic disorder group than for the controls and correlated significantly with PWD. Heart rate (measured as RR intervals in milliseconds on electrocardiogram) did not differ significantly between the groups. Conclusions: The findings of the present study suggest that the disorder may be associated with an increase in PWD. This association may result from prolonged anxiety and increase in sympathetic modulation, which are main characteristics of panic disorder. PWD = P-wave dispersion; Pmax = maximum P-wave duration; Pmin = minimum P-wave duration; HRV = heart rate variability; AF = atrial fibrillation; ECG = electrocardiogram; PAS = The Panic Agoraphobia Scale; HDRS = Hamilton Depression Rating Scale; ANS = autonomic nervous system; DSM-IV = Diagnostic and Statistical Manual of Mental Disorders IV.

The Investigation of Serum Vaspin Level in Atherosclerotic Coronary Artery Disease

Background It was speculated that fatty tissue originated adipocytokines may play role in pathogenesis of atherosclerosis. These adipocytokines may alter vascular homeostasis by effecting endothelial cells, arterial smooth muscle cells and macrophages. Vaspin is a newly described member of adipocytokines family. We aimed to investigate whether plasma vaspin level has any predictive value in coronary artery disease (CAD). Methods Forty patients who have at least single vessel ≥ 70 % stenosis demostrated angiographically and 40 subjects with normal coronary anatomy were included to the study. The vaspin levels were measured from serum that is obtained by centrifigation of blood and stored at -20 oC by ELISA method. The length, weight and body mass index of patients were measured. Biochemical parameters including total cholesterol, low density lipoprotein, high density lipoprotein, creatinine, sodium, potassium, hemoglobine, uric acid and fasting glucose were also measured. Results Biochemical markers levels were similar in both groups. Serum vaspin levels were significantly lower in CAD patients than control group (respectively; 256 ± 219 pg/ml vs. 472 ( 564 pg/ml, P < 0.02). Beside this serum vaspin level was lower in control group with high systolic blood pressure. Conclusion Serum vaspin levels were found significantly lower in patients with CAD than age-matched subjects with normal coronary anatomy. Vaspin may be used as a predictor of CAD. Keywords Coronary artery disease; Vaspin; Adipokine

Serum salusin-alpha level in rheumatoid arthritis

Rheumatoid arthritis (RA), a chronic inflammatory disease, leads to early and accelerated atherosclerosis; however, its pathogenesis is not yet fully documented. Salusin-α and β are novel bioactive peptides. Salusin-α suppresses macrophage foam cell formation, while salusin-β stimulates. Moreover, decreased serum salusin-α level has been reported previously in patients with coronary artery disease. The aims of the study were to assess serum salusin-α level and its association with predictors of atherosclerosis in a cohort of patients with RA. The study included 56 RA patients, 37 Behcets disease (BD) patients, and 29 healthy controls (HC). TNF-α, IL-6 and salusin-α levels, homeostasis model assessment (HOMA-IR) index and common carotid intima-media thickness (IMT) were determined. In the RA and BD groups, salusin-α levels (p<0.001 and p<0.01, respectively) and IMTs (p<0.001 for both) were higher compared to the HC group. However, the level of salusin-α was not directly associated with the IMT in all the groups. Serum salusin-α levels are increased in RA and BD, although they have increased IMT. Salusin-α has been reported to have anti-atherogenic effects in previous studies. However, it seems that salusin-α does not directly affect the atherogenesis in RA and BD. Further studies are needed to understand the regulation of salusin-α and determination of its relations with the predictors of atherosclerosis in RA and BD.

Adiponectin levels in coronary artery ectasia

Etiopathogenesis of coronary artery ectasia (CAE), which is defi ned as abnormal dilatation of a segment of the coronary artery to 1.5 times of an adjacent normal coronary artery segment, is unclear. However, it is speculated that CAE develops in the atherosclerosis process through degeneration of coronary artery media layer. Our objective in this study is to compare levels of adiponectin between cases with CAE and normal coronary anatomy, and to examine whether adiponectin plays a role in CAE etiopathogenesis. The study registered a total of 66 cases, consisting of CAE cases (group 1, n = 36) and cases with normal coronary anatomy (group 2, n = 30). Taking coronary artery diameters of the control group cases as the reference, patients with abnormal segments 1.5 times larger than the adjacent segments were accepted as CAE. Serum adiponectin levels were 4.31 ± 2.02 µg/ml in group 1 and 6.73 ± 4.0 µg/ml in group 2 (P = 0.02). High-sensitivity Creactive protein was 4.8 ± 3.8 mg/l in group 1 and 3.6 ± 3.4 mg/l in group 2 (P > 0.05). There was a negative correlation between ectatic coronary artery diameter and plasma adiponectin level (P = 0.03; r = −0.339). It was known that adiponectin levels dropped in atherosclerotic heart disease. In this study we found low plasma adiponectin levels in acquired CAE, attributed to atherosclerosis. Therefore, we think that adiponectin might be playing a role in etiopathogenesis and progression of CAE. This in turn may indicate that hypo-adiponectinemia may be useful in revealing a realized risk in CAE. However, larger, randomized, multicenter studies are required to examine the role of adiponectin in the development of CAE.

Effects of tirofiban on acute systemic inflammatory response in elective percutaneous coronary interventions

SUMMARY Objective: In this study the effect of a specific glycoprotein IIb/IIIa inhibitor, tirofiban [which also has antiplatelet activity on acute systemic inflammatory responses (IR) during elective percutaneous coronary intervention (PCI)] was evaluated. Patients and methods: Patients with stable angina pectoris and similar baseline characteristics who angiographically had a single lesion in their coronary arteries with a PCI performed on that lesion were enrolled in the study. One group of patients (control group, n = 52) received 0.9% NaCl (15 mL/h for 24h) and the other group (tirofiban group, n = 55) had tirofiban (10|ig/kg bolus infusion in 3min and 0.15jj,g/kg/mir for 24h) in addition to stenting without pre-dilatation. The effect of interventional procedure on levels of cardiac troponin T (cTnT) and several parameters of acute IR (leukocytes, fibrinogen, C-reactive protein, interleukin-1, interleukin-6, interleukin-8 and tumor necrotizing factor-α) was assessed on blood samples obtained from all patients before PCI and at pre-specified time points after PCI. Results: During the follow-up after PCI, the number of patients becoming cTnT-positive (> 0.1 ng/mL) was greater in the control group [12 (23%) patients vs. 3 (5%) patients, p = 0.01]. However, both groups had changes (generally observed as elevations) in their levels of all inflammatory parameters during the study and C-reactive protein, interleukin-6 and tumor necrotizing factor-α levels were elevated significantly. Yet, no significant difference occurred between groups due to these changes in any phase of the study (p > 0.05). Conclusions: Based on the findings of this study, it was concluded that although tirofiban limits development of myocardial necrosis during elective PCI, it does not directly affect the acute systemic inflammatory responses.