Julide Yagmur

Aortic valve calcification: association with bone mineral density and cardiovascular risk factors

BackgroundCardiovascular risk factors are reported to increase the incidence of aortic valve calcification. Among older women, low bone mineral density appears to be associated with increased prevalence of aortic calcification. We aimed to assess and compare cardiovascular risk factors and bone mineral density of patients with and without aortic valve calcification. Materials and methodsCardiovascular risk factors and bone mineral density measurements have been assessed in 49 patients with aortic valve calcification and in 65 patients without aortic valve calcification. All patients were subsequently referred to the nuclear medicine department to measure bone mineral density after echocardiographic evaluation. ResultsNo statistically significant differences were observed between the two groups with respect to sex, body mass index, history of coronary artery disease, diabetes mellitus, hypercholesterolemia, and smoking status. Although height and weight of the patients with aortic valve calcification were significantly lower than those of patients without aortic valve calcification, they were not independent risk factors. Age and hypertension were found to be independent positive risk factors for aortic valve calcification, whereas T score was found to be negatively associated with aortic valve calcification. ConclusionWe have shown that aortic valve calcification is positively associated with age and hypertension, whereas bone mineral density is negatively associated with aortic valve calcification. The mechanism underlying the association between decreased bone mineral density and aortic valve calcification remains to be clarified in further studies.

Evaluation of cardiovascular risk factors and bone mineral density in post menopausal women undergoing coronary angiography

BACKGROUND The underlying mechanism by which osteoporosis and cardiovascular disease may be linked is not fully understood. However studies mainly focused on the association between bone mineral density (BMD) and cardiovascular risk factors or atherosclerosis itself by only assessing the presence of vascular calcification. In this study we aimed to evaluate both cardiovascular risk factors, and presence of coronary artery disease (CAD) in post-menopausal women patients with and without low BMD. MATERIALS AND METHODS Study population consisted of post menopausal women who were scheduled to coronary angiography. Two hundred and twenty seven consecutive female patients were included in the study and evaluated for the presence of cardiovascular risk factors and CAD. Bone mineral density was measured in all patients either the day before or the day after coronary angiography. Low BMD was defined as T score<-1 and normal BMD was defined as T score > or = -1. For statistical analysis patients were divided into two groups: patients with low BMD and patients with normal BMD. RESULTS There were not statistically significant differences between two groups in respect to body mass index, presence of diabetes mellitus, hypercholesterolemia, and smoking status. Age and presence of CAD was found to be statistically different between two groups being higher in patients with low BMD. Logistic regression analysis revealed that age was positively and independently associated with low BMD in post menopausal female patients (Odds ratio=1.072 CI: 1.036-1.11, p=0.001). CONCLUSION Age is found to be an independent predictor of decreased BMD in our study population recruited from the coronary angiography laboratory. However, neither cardiovascular risk factors, nor coronary artery disease itself has been found to be associated with low BMD.

Subclinical left ventricular dysfunction in Behcet's disease assessed by two-dimensional speckle tracking echocardiography

AIMS The aim of this study was to evaluate the left ventricular (LV) systolic strain by speckle tracking echocardiography (STE) in order to provide the early detection of myocardial dysfunction in patients with Behcets disease (BD). We also aimed to examine the relationship between LV systolic strain and N-terminal pro-B type natriuretic peptide (NT-proBNP), which is a cardiac biomarker of ventricular dysfunction. METHODS AND RESULTS Longitudinal and circumferential systolic strain assessed by STE was obtained in 32 BD patients and 27 age-matched controls. NT-proBNP levels were also measured in all subjects. Regional and mean longitudinal strain (-17.8 ± 2.7 vs. -20.5 ± 1.8%; P < 0.0001) was significantly lower in BD patients when compared with the healthy controls. Whereas regional and mean circumferential strain values (-22.0 ± 1.6 vs. -22.2 ± 2.3%; P = 0.62) did not reveal a significant difference between the patients and the controls. NT-proBNP was significantly higher in the patients than in the controls (65.18 ± 84.51 vs. 30.84 ± 14.75 pg/mL; P = 0.003). Linear regression analyses revealed only NT-proBNP as the independent correlate of mean LV longitudinal strain (R = 0.603, P = 0.001). CONCLUSION Longitudinal myocardial systolic function assessed by STE, which is a sensitive marker of subclinical ventricular dysfunction is impaired in BD. Increased NT-proBNP levels may be a sign of subclinical ventricular dysfunction in these patients.

The impact of metabolic syndrome on left ventricular function: Evaluated by using the index of myocardial performance

AIM To evaluate the impact of metabolic syndrome on global left ventricular function by using the index of myocardial performance. METHODS The study population included 106 patients with metabolic syndrome (66 male, 40 female, mean age =54+/-11 years) and 106 control subjects without metabolic syndrome (71 male, 35 female, mean age=53+/-10). The diagnosis of metabolic syndrome was based on The National Cholesterol Education Program Adult Treatment Panel III criteria. All patients underwent two-dimensional and Doppler echocardiographic examination. The index of myocardial performance was determined as the sum of isovolumic relaxation time and isovolumic contraction time divided by left ventricular ejection time. RESULTS The index of myocardial performance was found to be significantly higher in patients with metabolic syndrome compared with control subjects without metabolic syndrome (0.55+/-0.06 vs 0.38+/-0.04 respectively, p<0.001). CONCLUSION In the present study, we have shown the presence of impaired global left ventricular function in patients with metabolic syndrome compared with control subjects without metabolic syndrome. This finding emphasizes the importance of early diagnosis and management of metabolic syndrome to prevent the progression of ventricular dysfunction to overt structural and symptomatic cardiac disease.

Assessment of atrial conduction time by tissue Doppler echocardiography and P-wave dispersion in patients with mitral annulus calcification.

The aim of our study was to investigate atrial conduction time in patients with mitral annulus calcification (MAC) using P-wave dispersion (PWD) and electromechanical coupling measured with the surface electrocardiogram and the tissue Doppler echocardiography. Fifty-nine patients with MAC and 43 control subjects underwent resting the surface electrocardiogram and tissue Doppler echocardiography. The difference between the maximum (Pmax) and minimum P-wave durations was calculated and defined as PWD. Interatrial and intraatrial electromechanical delays were measured with tissue Doppler echocardiography. Both Pmax and PWD were higher in patients with MAC compared with controls (111.4 +/- 15.8 vs 97.3 +/- 18.8 milliseconds; P < .0001 and 46.4 +/- 14.6 vs 31.4 +/- 13.1 milliseconds; P < .0001, respectively). Both interatrial and intraatrial conduction time were also delayed in patients with MAC compared with controls (29.8 +/- 13.3 vs 17.6 +/- 12.5 milliseconds; P < .0001; 9.4 +/- 5.1 vs 6.8 +/- 4.0 milliseconds; P < .008, respectively). Left atrial (LA) diameter was significantly higher in patients with MAC compared with controls (35.4 +/- 5.0 mm vs 32.3 +/- 4.2 mm; P < .001). The LA diameter correlated significantly with both interatrial conduction times and PWD (r = 0.56; P < .0001 and r = 0.47; P < .0001, respectively). There is a delay in both intraatrial and interatrial electromechanical coupling intervals in patients with MAC.

Assessment of atrial electromechanical delay by tissue Doppler echocardiography in obese subjects.

Our aim was to evaluate whether atrial electromechanical delay measured by tissue Doppler imaging (TDI), which is an early predictor of atrial fibrillation (AF) development, is prolonged in obese subjects. A total of 40 obese and 40 normal‐weight subjects with normal coronary angiograms were included in this study. P‐wave dispersion (PWD) was calculated on the 12‐lead electrocardiogram (ECG). Systolic and diastolic left ventricular (LV) functions, inter‐ and intra‐atrial electromechanical delay were measured by TDI and conventional echocardiography. Inter‐ and intra‐atrial electromechanical delay were significantly longer in the obese subjects compared with the controls (44.08 ± 10.06 vs. 19.35 ± 5.94 ms and 23.63 ± 6.41 vs. 5.13 ± 2.67 ms, P < 0.0001 for both, respectively). PWD was higher in obese subjects (53.40 ± 5.49 vs. 35.95 ± 5.93 ms, P < 0.0001). Left atrial (LA) diameter, LA volume index and LV diastolic parameters were significantly different between the groups. Interatrial electromechanical delay was correlated with PWD (r = 0.409, P = 0.009), high‐sensitivity C‐reactive protein (hsCRP) levels (r = 0.588, P < 0.0001). Interatrial electromechanical delay was positively correlated with LA diameter, LA volume index, and LV diastolic function parameters consisting of mitral early wave (E) deceleration time (DT) and isovolumetric relaxation time (IVRT; r = 0.323, P = 0.042; r = 0.387, P = 0.014; r = 0.339, P = 0.033; r = 0.325, P = 0.041; respectively) and, negatively correlated with mitral early (E) to late (A) wave ratio (E/A) (r = −0.380, P = 0.016) and myocardial early‐to‐late diastolic wave ratio (Em/Am) (r = −0.326, P = 0.040). This study showed that atrial electromechanical delay is prolonged in obese subjects. Prolonged atrial electromechanical delay is due to provoked low‐grade inflammation as well as LA enlargement and early LV diastolic dysfunction in obese subjects.

Elevated Oxidative Stress Markers and its Relationship With Endothelial Dysfunction in Behçet Disease

Behçet’s disease (BD) is a multisystemic disorder characterized by endothelial dysfunction. However, the relationship between oxidative stress and endothelial function has not been clearly shown. We investigated the relationship between oxidative stress markers and endothelial function in patients with BD. Patients with BD (n = 40) having active disease and sex- and age-matched 40 controls were included. Endothelial function was assessed by flow-mediated dilatation (FMD) technique. Serum gamma-glutamyltransferase (GGT) and high-sensitive C-reactive protein levels (hsCRP) were measured in all participants. Brachial artery FMD was significantly lower in patients with BD than in controls. Gamma-glutamyltransferase and hsCRP levels were higher in patients with BD than in controls. Also, GGT and hsCRP levels were inversely correlated with endothelial function. Oxidative stress markers are elevated in patients with BD having active disease. This may be one of the reasons behind the vasculitis in active BD.

Serum Gamma-Glutamyl Transferase (GGT) Levels and Inflammatory Activity in Patients With Non-dipper Hypertension

Non-dipper hypertension is associated with increased cardiovascular morbidity and mortality. We aimed to evaluate serum gamma-glutamyl transferase (GGT) level, which is accepted as a marker for oxidative stress and its relationship with inflammatory activity in patients with non-dipper hypertension. Age and sex matched 43 dipper hypertensive patients, 40 non-dipper patients, and 46 healthy subjects were included into the study. Serum GGT and C-reactive protein (CRP) levels were measured and compared between each of the groups. Serum GGT activity was higher in the non-dipper and the dipper hypertensive groups than in the control group (33.5 ± 11.8 and 28.1 ± 10.1 U/l, respectively, vs. 21.2 ± 6.5U/l; p < 0.001). There was a statistically significant difference in serum GGT activity between the non-dippers and the dippers (p = 0.021). When compared with the control group, serum CRP levels were significantly increased in both the non-dipper and the dipper hypertensive groups (6.1 ± 2.6 and 5.4 ± 2.1 mg/l, respectively, vs. 2.8 ± 1.7mg/L; p < 0.001). Increased CRP levels were higher in non-dippers than dippers (p = 0.046). A significant correlation was found between GGT and CRP measurements (r = 0.37, p = 0.002). Serum GGT levels, which are markers of the oxidative stress and CRP levels, are both increased in non-dipper hypertension. Increased GGT activity, found to be correlated with CRP levels, may be one of the reasons behind the non-dipper hypertension related cardiovascular complications.

Relationship of urocortin-2 with systolic and diastolic functions and coronary artery disease: an observational study.

OBJECTIVE The urocortin (Ucn) hormones have many important roles in the cardiovascular system. Apart from systolic dysfunction (SD), there is no sufficient data on the relationship between serum Ucn-2 and diastolic dysfunction (DD), or coronary artery disease (CAD). We investigated serum Ucn-2 levels in SD, DD, and CAD. METHODS In this observational cross-sectional study, study population was enrolled among outpatients who underwent coronary angiography with the pre-diagnosis of CAD. By examining the echocardiography 86 subjects were selected to study after coronary angiography. The subjects distributed over three groups to investigate the relationship between serum Ucn-2 and SD according to their ejection fraction (EF): subjects with moderate to severe SD (Group A, EF=33.6%), subjects with mild to moderate SD (Group B, EF=46.1%), and those without SD (Group C, EF=64.5%). Apart from these groups, the serum Ucn-2 levels were compared between subjects with and without DD (EF≥45%), and also compared between subjects with and without CAD (EF≥55%). Statistical analyses were performed using one-way ANOVA, Kruskal-Wallis, Chi-square, Mann-Whitney U, Spearman correlation and multiple regression analyses tests. RESULTS Serum Ucn-2 levels were decreased in Group A and were increased in Group B compared to Group C (9.4±3.4, 12.8±3.6 vs. 10.4±3.9 pg/mL, respectively, p=0.003). Unlike SD; there was no significant difference in serum Ucn-2 levels between subjects with and without DD (11.4±4.1 vs 11.7±3.9 pg/mL, p=0.8) or CAD (10.7±4.7 vs 10.2±3.2 pg/mL, p=0.7). CONCLUSION Ucn-2 is elevated in mild to moderate SD. But, DD (impaired relaxation pattern), or CAD (without myocardial infarction) seems to have no effect on Ucn-2 hormone levels.

Increased plasma levels of cystatin C and transforming growth factor-??1 in patients with coronary artery ectasia: can there be a potential interaction between cystatin C and transforming growth factor-??1

Cystatin C, known as an inhibitor of the cathepsin family of cysteine proteases, has been evaluated in several cardiovascular disorders such as atherosclerosis and acute myocardial infarction. The potential interaction between transforming growth factor-&bgr;1 and cystatin C has also been demonstrated in some cell types. Accordingly, we aimed to compare the plasma levels of cystatin C and transforming growth factor-&bgr;1 in patients with coronary artery ectasia coexisting with coronary artery disease and those with coronary artery disease alone. Thirty-nine patients with coronary artery ectasia and coronary artery disease and 35 age and sex-matched patients with coronary artery disease alone were prospectively enrolled in the study. Blood samples of all patients and control participants for measuring plasma cystatin C and transforming growth factor-&bgr;1 levels were drawn ≥24 h after the coronary angiography. Cystatin C concentrations in plasma were measured by latex-enhanced reagent on a Behring Nephelometer II. Plasma levels of transforming growth factor-&bgr;1 were measured by using transforming growth factor-&bgr;1 enzyme-linked immunosorbent assay kit (BioSource International, Inc., Camarillo, California, USA). Plasma level of cystatin C was significantly higher in patients with coronary artery ectasia+coronary artery disease than in patients with coronary artery disease alone (1.05±0.30 mg/dl vs. 0.92±0.18 mg/mdl, P=0.025, respectively). Transforming growth factor-&bgr;1 was also found to be significantly higher in patients with coronary artery ectasia+coronary artery disease compared with those with coronary artery disease (2.47±0.43 vs. 2.22±0.43 pg/ml, P=0.02, respectively). The plasma level of cystatin C was significantly but weakly correlated with that of transforming growth factor-&bgr;1 (r=0.217 P=0.02). We conclude that plasma levels of cystatin C and transforming growth factor-&bgr;1 are significantly higher in patients with combined coronary artery ectasia and coronary artery disease than in those with coronary artery disease. Correlation between transforming growth factor-&bgr;1 and cystatin C may also suggest that pathogenesis of coronary artery ectasia might have some different pathways from atherosclerosis with respect to the regulation of extracellular matrix remodeling. Therefore, the role of cystatin in the pathogenesis of coronary artery ectasia and its potential interaction with transforming growth factor-&bgr;1 should be evaluated in further studies.