Behçet's disease and risk of vascular events.

PURPOSE OF REVIEW: We discuss the relationship between several factors and the risk of vascular events in patients with Behçet's disease. RECENT FINDINGS: Behçet's disease, a systemic, chronic relapsing vasculitis, is mainly seen in the Mediterranean area and is typically characterized by recurrent oro-genital ulcers, ocular inflammation, and skin manifestations, including articular, vascular, gastroenteric, and neurological involvement. It is a chronic inflammatory disease with relapses and remissions. The prognosis varies. Behçet's disease can cause venous or arterial lesions. Vascular involvement contributes to the mortality and morbidity associated with Behçet's disease. SUMMARY: The cause of thrombosis or vascular events in Behçet's disease remains incompletely understood; several factors have been studied with conflicting results. Vasculitis is considered to underlie several clinical manifestations of Behçet's disease.

The relation between monocyte to HDL ratio and no-reflow phenomenon in the patients with acute ST-segment elevation myocardial infarction.

BACKGROUND: No-reflow phenomenon is a prognostic value in ST-segment elevation myocardial infarction (STEMI). Monocyte to high density lipoprotein ratio (MHR) has recently emerged as a marker of inflammation and oxidative stress in the cardiovascular disease. PURPOSE: In this study, we aimed to investigate the relation between MHR and no-reflow phenomenon in patients with STEMI undergoing primary percutaneous coronary intervention (pPCI). MATERIAL AND METHODS: A total of 600 patients with STEMI (470 men; mean age, 62 ± 12 years) admitted within 12 hours from symptom onset were included into this study. Patients were classified into 2 groups based on postintervention Thrombolysis in Myocardial Infarction (TIMI) flow grade: no-reflow-TIMI flow grade 0, 1, or 2 (group 1); angiographic success-TIMI flow grade 3 (group 2). RESULTS: According to admission whole-blood cell count results, the patients in the no-reflow group had significantly higher monocyte count and MHR values when compared with those of the reflow patients. After multivariate backward logistic regression, MHR remained independent predictors of no reflow after pPCI. Adjusted odds ratios were calculated as 1.09 for MHR (P< .001; confidence interval [CI], 1.07-1.12). Receiver operating characteristic curve analysis suggested that the optimum MHR level cutoff point for patients with no-reflow was 22.5, with a sensitivity and specificity of 70.2% and 73.3%, respectively (area under curve, 0.768; 95% CI, 0.725-0.811). CONCLUSION: In conclusion, MHR levels are one of the independent predictors of no reflow in patients with STEMI after pPCI.

Endocan, a novel marker of endothelial dysfunction in patients with essential hypertension: comparative effects of amlodipine and valsartan.

Vascular inflammation plays an important role in the pathophysiology of hypertension and high levels of endocan may reflect ongoing vascular inflammation in hypertensive patients. In the present hypothesis-generating study, we aimed at investigating the comparative effects of amlodipine and valsartan on endocan levels in newly diagnosed hypertensive patients. The study population consisted of 37 untreated hypertensive patients who were randomized to the two treatment arms. After baseline assessment, each patient was randomly allocated to either 10 mg daily of amlodipine (n = 18, 7 males) or 160 mg daily of valsartan (n = 19, 3 males) and treated for a 3-month period. Sphygmomanometric blood pressure (BP) and serum endocan were measured before and every 2 weeks during drug treatment. There was no statistically significant difference between the two treatment arms as far as baseline socio-demographic and clinical characteristics are concerned. After a 3-month treatment period, systolic and diastolic BP values significantly reduced by antihypertensive treatment (p < 0.001). Furthermore, endocan levels were significantly decreased in both treatment arms (p < 0.05). However, amlodipine caused a greater percent decrease in circulating endocan levels compared with valsartan at the end of the treatment period. Both drugs reduced high sensitivity C-reactive protein values. However, the statistical significant difference vs baseline was achieved only in the group treated with amlodipine. No correlation was found between endocan plasma levels and BP reduction. The results of this hypothesis-generating study suggest that amlodipine and valsartan decrease endocan levels in newly diagnosed hypertensive patients. The effects, which are more evident with amlodipine, may contribute to the anti-inflammatory effects exerted by the two drugs on the vascular target.

Increased frequency of mitral valve prolapse in patients with deviated nasal septum.

Any abnormality of collagen may affect the tissues with higher collagen content, e.g., joints, heart valves, and great arteries. Mitral valve prolapse (MVP) is a characteristic of generalized collagen abnormality. Nasal septum (NS) is constituted by osseous and cartilaginous septums that are highly rich in collagen. We evaluated the co-existence of deviation of NS (DNS) in patients with MVP. We retrospectively evaluated the recordings of echocardiographic and nasal examinations of subjects with MVP and DNS. We analyzed the features of MVP and anatomical classification of DNS among subjects. Totally, 74 patients with DNS and 38 subjects with normal nasal passage were enrolled to the study. Presence of MVP was significantly higher in patients with DNS compared to normal subjects (63 vs 26%, p < 0.001). Prolapse of anterior, posterior and both leaflets was higher in patients with DNS. Thickness of anterior mitral leaflet was significantly increased in patients with DNS (3.57 ± 0.68 vs 4.59 ± 1.1 mm, p < 0.001) compared to normal subjects. Type I, II, and III, IV DNS were higher in frequency in patients with MVP while type V and VI were higher in normal subjects. DNS is highly co-existent with MVP and increased thickness of mitral anterior leaflet. Generalized abnormality of collagen which is the main component of mitral valves and nasal septum may be accounted for co-existence of MVP and DNS. Also co-existence of them may exaggerate the symptoms of patients with MVP due to limited airflow through the nasal passage.

Why aortic elasticity differs among classical and non-classical mitral valve prolapsed?

BACKGROUND: Mitral valve prolapse (MVP) is the most common valvular heart disease and characterized by the displacement of an abnormally thickened mitral valve leaflet into the left atrium during systole. There are two types of MVP, broadly classified as classic (thickness ≥5 mm) and non-classic (thickness <5 mm) according to the morphology of the leaflets. We aimed to investigate elastic properties of the aorta in young male patients with classical and non-classical MVP. MATERIAL/METHODS: In the present study, 63 young adult males (mean age: 22.7 ± 4.2) were included. Patients were divided into classic MVP (n = 27) and non-classic MVP (n = 36) groups. Aortic strain, aortic distensibility and aortic stiffness index were calculated by using aortic diameters obtained by echocardiography and blood pressures measured by sphygmomanometer. RESULTS: There was no significant difference between the groups in terms of age, body mass index, left ventricular mass and ejection fraction. When comparing the MVP group it was found that aortic strain and aortic distensibility were increased (p = 0.0027, p = 0.016, respectively) whereas the aortic stiffness index was decreased (p = 0.06) in the classical MVP group. CONCLUSION: We concluded that the elastic properties of the aorta is increased in patients with classic MVP. Further large scale studies should be performed to understand of morphological and physiological properties of the aorta in patients with MVP.

QT dispersion increases with low glomerular filtration rate in patients with coronary artery disease.

OBJECTIVE: We aimed to evaluate the relationship between estimated glomerular filtration rate (eGFR) and QT dispersion (QTd) in patients with coronary artery disease (CAD). METHODS: Sixty patients(mean age 62.72 ± 12.48 years) included 46 male, (mean age 60.89 ± 12.70 years)and 14 female (mean age 68.71± 9.86 years) were enrolled in this study. Patients were divided into 2 groups according to their eGFR using the 6 variable MDRD equation. Group 1 consisted of patients with estimated eGFR<60 ml/min/1.73m(2) and Group 2 consisted of patients witheGFR ≥ 60 ml/min/1.73m(2). RESULTS: Baseline patient characteristics were homogeneous in both groups except for age, gender and smoking.Also, the extent of CAD was similar in both groups (p > 0.05) QTd values were found higher in group 1 than those of group 2 (57.23 ± 40.65 ms vs. 31.23 ± 14.47 ms, p = 0.002). After adjustment for age, gender and smoking using one-way ANCOVA test, statistically significant difference in QTd still existedbetween the groups (p=0.038). CONCLUSION: QTd tends to be higher in patients with poor renal function independent of severity of angiographical CAD. QTd may be a potentially useful non-invasive test in the management of patients with poor renal function, especially those with CAD.

Comparative effects of nebivolol and metoprolol on red cell distribution width and neutrophil/lymphocyte ratio in patients with newly diagnosed essential hypertension.

High level of circulating red cell distribution width (RDW) and neutrophil/lymphocyte (N/L) ratio may reflect ongoing vascular inflammation and play an important role in pathophysiology of hypertension. We evaluate the effects of nebivolol and metoprolol on the RDW and N/L in new essential hypertensive patients. After baseline assessment, 72 patients were randomly allocated to 5 mg/d of nebivolol (n = 37, 20 men) or 100 mg/d of metoprolol (n = 35, 18 men) and treated for 6 months. Blood pressure (BP), heart rate (HR), RDW, and N/L were measured before and after treatment. BP significantly decreased with both drugs (P < 0.001). Analog reduction was observed for resting HRs (P < 0.001), but metoprolol caused greater HR fall as compared with nebivolol (P < 0.001). After 6 months of treatment, nebivolol significantly lowered not only RDW but also the total white blood cell and N/L (P < 0.001, P = 0.023, P = 0.017, respectively). No changes were observed in metoprolol group. Percent decrease in RDW was found to be significantly higher in nebivolol than in the metoprolol group (P = 0.001) and remained also after correction for confounders (P = 0.012). Nebivolol improved RDW and N/L to a greater extent than metoprolol in patients with hypertension. These favorable effects may participate, together with the BP reduction, at the favorable properties of the drug in hypertension.

Vascular inflammation and aortic stiffness relate to early left ventricular diastolic dysfunction in prehypertension.

Prehypertension is characterized by an increased cardiovascular risk and by an increased prevalence of target organ damage compared with the pure normotensive state. The present study was designed to assess in prehypertensive subjects the possible relationships between early left ventricular dysfunction, vascular inflammation and aortic stiffness. The study population consisted of 31 untreated prehypertensive subjects (age: 34 ± 6 years, mean ± SD) and 31 age-matched pure normotensive controls. Left ventricular function was assessed by echocardiography, aortic distensibility parameters were derived from aortic diameters measured by ultrasonography, and high-sensitivity C-reactive protein was assessed by latex-enhanced reagent. Prehypertensive subjects displayed a significantly lower E/A ratio and a significantly greater deceleration time and isovolumetric relaxation time compared with normotensive controls. They also displayed aortic systolic diameter, diastolic diameter and mean aortic stiffness index beta significantly increased while systo-diastolic diameter change, mean aortic distensibility and aortic strain were significantly reduced compared with controls. Values of inflammatory markers were increased. At multiple regression analysis, E/A ratio was significantly related to high-sensitivity C-reactive protein and aortic stiffness index beta, after correction for age, left ventricular mass index and mean blood pressure (ß coefficient = -0.49, overall r(2) = 0.24, p = 0.01 and ß coefficient =-0.46, overall r(2) = 0.21, p = 0.02, respectively). Thus, in prehypertension, left ventricular dysfunction is significantly related to vascular inflammation and aortic stiffness, suggesting that early cardiac and vascular alterations may have an increased inflammatory process as a common pathophysiological link.

Circadian variation of acute st segment elevation myocardial infarction by anatomic location in a Turkish cohort.

BACKGROUND: To evaluate the relationship between site of infarction (anterior vs. inferior) and circadian variation in patients with ST segment elevation myocardial infarction (STEMI) in a Turkish cohort. MATERIAL/METHODS: This restrospective study enrolled 465 patients (407 male, mean age 65±7 years) with STEMI. Patients were then categorised into 4 6-hour increments according to the time of day during which the symptoms began (12:00 AM-06:00 AM, 06:00 AM-12:00 PM; 12:00 PM-06:00 PM and 06:00 PM-12:00 AM hours). Characteristics of patients by site of infarction (anterior vs. inferior) were compared. RESULTS: The frequency of onset of acute anterior MI as determined by onset of pain demonstrated significant circadian variation among the 4 time periods, demonstrating bimodal peaks (afternoon and morning) and a trough between 06:00 PM to 06:00 AM. The incidence of occurrence of MI between 06:00 AM to 06:00 PM was 4.50 times that of the average frequency of the remaining 12 hours of the day. The frequency of onset of acute inferior MI as determined by onset of pain exhibited significant circadian variation among the 4 time periods, demonstrating bimodal peaks (midnight to 06:00 AM and 06:00 AM to noon) and a trough between noon to midnight. The incidence of occurrence of MI between midnight to noon was 4.25 times that of the average frequency of the remaining 12 hours of the day. CONCLUSIONS: Different circadian periodicity in the time of onset of STEMI was found regarding infarction site in a Turkish cohort. This may be related to genetic and/or demographic characteristics of the Turkish population.

Increased platelet activation in young patients with prehypertension.

Mean platelet volume (MPV) and sP-selectin levels are considered as indicators of platelet activation. In this study, we assessed platelet activation in prehypertensive patients by comparing MPV and sP-selectin levels of these patients with healthy conrols. The study population consisted of 25 newly diagnosed prehypertensive individuals (18 men, mean age = 34 ± 6 y) and 25 healthy control subjects (16 men, mean age = 33 ± 6 y) eligible for the current study. Blood pressure (BP) , lipid profile, plasma glucose, HOMA-IR values, sP-selectin levels, platelet counts, and MPV were measured in both groups. Other than systolic blood pressure (SBP) and diastolic blood pressure (DBP), baseline demographic characteristics of both groups were similar. No significant difference was found between the platelet counts of the two groups. Despite comparable platelet counts, platelet activation parameters were found significantly higher in the prehypertensives. Prehypertensives had larger a MPV value compared to that of the control group (8.24 ± 0.46 fl vs. 7.70 ± 0.64 fl; P = 0.001) and plasma sP-selectin levels were also significantly higher in the prehypertensive patients (163.60 ± 41.21 ng/ml vs. 132.80 ± 36.46; P = 0.007). Spearman correlation analysis revealed moderate positive correlation between SBP and platelet activation parameters (for SBP and MPV, r = 0.60, p = 0.001; for SBP and sP-selectin r = 0.51, p = 0.009). Prehypertension causes platelet activation as evidenced by increased MPV and plasma sP-selectin levels. Increased platelet activation might be related to increased vascular thrombotic risk in those patients.

Increased platelet activation in patients with slow coronary flow.

We tested the hypothesis that increased platelet activation may be present in patients with slow coronary flow (SCF) and may contribute to the pathogenesis of slow coronary flow phenomenon (SCFP). Fifty patients angiographically proven normal coronary flow (control group; mean age = 61.3 +/- 7.0 years, 43 male) and 50 patients with angiographically proven SCF in all coronary arteries (patient group; man age = 62.7 +/- 6.7 years, 38 male) were included in the present study. Coronary flow rates of all subjects were documented by Thrombolysis In Myocardial Infarction frame count (TIMI frame count). Patients with a corrected TIMI frame count greater than two standard deviations from normal published range for the particular vessel were considered as having SCF. Complete blood count and mean platelet volume (MPV) was measured from whole blood sample with Abbott Cell-Dyne 4000 cell counter. Plasma sP-selectin concentrations were analyzed with sP-Selectin ELISA kit. There were no statistically significant differences between the two groups with respect to baseline demographic, clinical and lipid parameters. Not only MPV values but also plasma sP-selectin levels were significantly higher in patients with the patients with SCF compared to those of controls (for MPV; 8.2 +/- 0.7 vs. 7.2 +/- 0.6 fl, P < 0.001, for sP-Selectin; 1.5 +/- 0.3 vs. 1.0 +/- 0.2 ng/ml, P < 0.001). Interestingly, significant positive correlations were detected between mean TIMI frame counts and MPV and sP-selectin levels (for MPV; r = 0.56, P < 0.001, for sP-selectin r = 0.67, P < 0.001). The current study demonstrates that platelet activity is increased in the patients with SCF compared to that of the patients with normal coronary flow.

The relationship of gamma-glutamyltransferase to aortic elastic properties in young patients with prehypertension.

Some cross-sectional studies have demonstrated a positive association between serum gamma-glutamyltransferase (GGT) levels and blood pressure. Accordingly, we aimed to analyze serum GGT levels in patients with prehypertension and examine the relationship with aortic elasticity parameters. The study population consisted of 25 newly diagnosed prehypertensive individuals and 25 healthy control subjects. Aortic strain, distensibility index, and stiffness index beta were calculated from aortic diameters measured by echocardiography and blood pressures simultaneously measured by sphygmomanometry. Prehypertensive patients were detected to have significantly lower aortic distensibility and strain indexes compared to control subjects aortic distensibility. However, aortic stiffness index beta of the prehypertensive group was significantly higher compared to that of the control group (3.73 ± 1.41 vs. 2.97 ± 0.82, p = 0.02). The mean GGT levels were found to be higher in patients with prehypertension compared to those of controls (47.9 ± 15.9 U/L vs. 36.1 ± 9.4 U/L, p = 0.003). When multiple linear regression analysis was done to clarify the contributions of GGT to aortic elasticity adjusting for age, body mass index, uric acid, serum glucose, heart rate, low-density lipoprotein (LDL)-cholesterol, high-density lipoprotein (HDL)-cholesterol, and triglyceride, we observed that only serum GGT levels were significantly associated with aortic elasticity parameters (for aortic strain beta = -0.247, p < 0.001; for aortic distensibility beta = -0.108, p < 0.001; for stiffness index beta = 0.063, p < 0.001). Whatever the mechanism is, young patients with prehypertension have higher serum GGT levels compared to healthy control subjects. More importantly, increased GGT levels are independently associated with impaired aortic elasticity in patients with prehypertension.