Ismet Durmus

Plasma fibronectin level and its association with coronary artery disease and carotid intima-media thickness.

Background The exact relation of fibronectin with coronary atherosclerosis is unknown. The aim of the present study was to examine the association of fibronectin level with presence and extent of coronary artery disease (CAD) and intima‐media thickness (IMT) of common carotid artery (CCA). Design The IMTs of CCA of 86 patients who underwent coronary angiography were measured; traditional vascular risk factors were also evaluated in these patients. Fibronectin, lipids, C‐reactive protein (CRP) and fibrinogen levels were determined. Results Plasma fibronectin levels of the patients with CAD were found to be significantly elevated compared to patients with normal vessels (0.46 ±0.11 and 0.36± 0.12 mg/dl respectively, P = 0.001). Fibronectin levels were not associated with extent of CAD. No significant association was observed between fibronectin level and traditional risk factors. IMTs of right and left CCA in patients with CAD were found to be elevated compared to patients with normal vessels (0.89 ± 0.1mm compared with 0.76 ± 0.1 mm, P = 0.001 and 0.93 ± 0.2 mm compared with 0.71 ± 0.1 mm, respectively P < 0.001). Fibronectin levels were positively correlated with CRP (r = 0.45, P < 0.001), low‐density lipoprotein‐cholesterol (r = 0.23, P = 0.03) and total cholesterol (r = 0.21, P = 0.04) levels and negatively correlated with high‐density lipoprotein‐cholesterol (HDLC) levels (r = ‐ 0.24, P = 0.02). IMT of left CCA was positively correlated with CRP levels (r = 0.23, P = 0.04) and negatively correlated with HDL‐C levels (r = 0.2, P = 0.04). Logistic regression analysis showed that age (P < 0.01) and fibronectin levels (P = 0.01) were independent predictors for the existence of CAD. Conclusions The results suggest that fibronectin levels may be a significant predictor of CAD. However, it was shown that fibronectin levels were not associated with extent of CAD and IMT of CCA. Coron Artery Dis 14:219‐224

Effects of P‐wave Dispersion on Atrial Fibrillation in Patients with Acute Anterior Wall Myocardial Infarction

Backround: P‐wave dispersion (P dispersion), defined as the difference between the maximum and the minimum P‐wave duration (P minimum), and maximum P‐wave duration (P maximum) have been used to evaluate the discontinuous propagation of sinus impulse and the prolongation of atrial conduction time respectively. The aim of this study was to investigate whether early assessment of P dispersion predicts paroxysmal atrial fibrillation (AF) in patients with acute anterior wall myocardial infarction (MI).

Assessment of Left Ventricular Function and Tei Index by Tissue Doppler Imaging in Patients with Slow Coronary Flow

Background: The aim of this study was to assess left ventricular (LV) function and the Tei index by tissue Doppler imaging (TDI), and also to evaluate the relationship of thrombolysis in myocardial infarction (TIMI) frame count (TFC) with the Tei index and LV function in patients with slow coronary flow (SCF). Methods: We prospectively evaluated 50 patients with SCF and 27 control subjects. Diagnosis of SCF was made by TFC. LV systolic and diastolic function was assessed by conventional echocardiography and TDI. Results: Early diastolic mitral annular velocity (Em), Em/Am, and peak systolic mitral annular velocity (Sm) were lower in patients with SCF than those in controls (13±2.8 cm/sec vs 15.2±2.8 cm/sec, P = 0.002; 0.88±0.22 vs 1±0.23, P = 0.03; and 14.1±3.51 vs 16.5±3.31, P = 0.005, respectively). In patients with SCF, the Tei index was significantly higher than that in controls (0.34±9.6 vs 0.29±9.5, P = 0.02, respectively). Mean TFC and RCA TFC were positively correlated with the Tei index (r = 0.3, P = 0.02 and r = 0.329, P = 0.02). Left circumflex (LCX) TFC was negatively correlated with Em/Am (r =–0.310, P = 0.03) only in patients with SCF. Conclusion: LV systolic and diastolic function is impaired in patients with SCF. TDI analysis of mitral annular velocities such as the Tei index, Em, Em/Am, and Sm is useful to assess LV systolic and diastolic dysfunction in patients with SCF. Mean TFC and RCA TFC were positively correlated with the Tei index and LCX TFC was negatively correlated with Em/Am. TDI may be better than conventional echocardiography in assessing LV function in patients with SCF. (ECHOCARDIOGRAPHY, Volume 26, November 2009)

Circulating levels of relaxin and its relation to cardiovascular function in patients with hypertension

Background. The role of endogenous relaxin on hypertensive cardiovascular damage remains unknown. We investigated the relaxin level and its relation to cardiovascular function in patients with never treated hypertension (HT). Methods. We studied 42 (47.8±10 years) never treated patients with HT and 40 age‐matched (47±8.6 years) normotensive individuals. Serum relaxin levels were determined in all subjects using enzyme‐linked immunosorbent assay. Left ventricular (LV) diameters were evaluated by transthoracic echocardiography. Ejection fraction and LV mass index were measured. Diastolic functions were evaluated with both conventional and tissue Doppler echocardiography. We evaluated central aortic pressures, heart rate‐corrected augmentation index (AIx@75), a marker of wave reflections, and aortic pulse wave velocity (PWV) as indices of elastic‐type aortic stiffness of the study population using applanation tonometry (SphygmoCor). Results. Relaxin levels were significantly lower in hypertensive patients as compared with controls (36.5±7.3 vs 49.7±39.8 pg/ml, p=0.03). The relaxin level was negatively correlated with brachial and central aortic pressure. However, serum relaxin was not significantly associated with LV diameters, ejection fraction, LV mass index, LV diastolic function, AIx@75 or aortic PWV in our study. Conclusion. Serum relaxin is decreased in patients with HT. However, low endogenous relaxin is not related to cardiovascular function.

Low total antioxidative capacity levels are associated with augmentation index but not pulse-wave velocity

It is well known the relationship between oxidative stress and vascular function. However, association between total antioxidative capacity and arterial stiffness was not studied in patients with hypertension (HT). This study investigated whether total antioxidative capacity is associated with arterial stiffness and wave reflections. We studied 46 (age 48.5 ± 10.6 years) never treated patients with HT and age-matched control group of 40 (age 47 ± 8.6 years) normotensive individuals. Total antioxidative capacity level was determined in all subjects. We evaluated arterial stiffness and wave reflections of the study population, using applanation tonometry (SphygmoCor). Carotid-femoral pulse-wave velocity (PWV) was measured as index of aortic stiffness. The heart rate-corrected augmentation index (AIx@75) was estimated as a composite marker of wave reflections and arterial stiffness. Carotid-femoral PWV (10.5 ± 2.2 vs 8.7 ± 1.6, m/s, P = 0.0001) and AIx@75 (22.7 ± 9.5 vs 15 ± 11, %, P = 0.001) were significantly higher in patients with HT compared with age-matched control subjects. Total antioxidative capacity level (274 ± 70 vs 321 ± 56 µmol/l, P = 0.001) was significantly lower in hypertensive patients than controls. In the whole population, total antioxidative capacity level negatively correlated with AIx@75 (r = −0.24, P = 0.02) in univariable analysis, but not with carotid-femoral PWV (r = −0.08, P = 0.43). Also, we found that total antioxidative capacity level (β = −0.21, P = 0.03) was an independent determinant of AIx@75 in multivariable analysis. Our results suggest that the decrease in the ability of antioxidant defenses contributes significantly to increased wave reflections.

Aortic pulse wave velocity in subjects with aortic valve sclerosis.

Background: Aortic stiffness is an independent risk factor for cardiovascular events and mortality. The measurement of pulse‐wave velocity (PWV) is the most simple, noninvasive, and robust method to determine aortic stiffness. Whether aortic stiffness contributes to aortic valve sclerosis (AVS) remains unknown. The aim of the present study was to examine the relationship between PWV and AVS in subjects free of clinically evident atherosclerotic disease. Methods: We enrolled 62 patients (48 men; age 65 ± 8 years) diagnosed with AVS and an additional 62 age‐, hypertension‐, diabetes mellitus‐, and history of smoking‐matched subjects without AVS. Applanation tonometry was applied to assess the augmentation index and aortic PWV. The subjects with symptomatic vascular disease were excluded from the study. AVS was defined by echocardiography as thickening and calcification of the normal trileaflet aortic valve without obstruction to the left ventricular outflow. Results: There was no significant difference between the two groups regarding the aortic PWV and augmentation index (11.7±3.3 vs 11.8±3.7, P=0.85; 28.0±9.4 vs 25.0±8.6, P=0. 17, respectively). The presence of AVS was significantly correlated with ejection fraction (r=0.211, P=0.011), male gender (r=0.362, P=0.0001), and age (r=0.200, P=0.026). Conclusions: The lack of an association between the aortic PWV and AVS suggests that AVS is a complex phenomenon consisting of several distinct processes, related to both atherosclerotic and nonatherosclerotic processes.

Factor V Leiden and its relation to left ventricular thrombus in acute myocardial infarction.

Objective — The genetic defect of coagulation factor V, known as factor V Leiden, produces a resistance to degradation by activated protein C (APC) and increases the risk of venous thrombosis. However, the role of factor V Leiden in the formation of left ventricular (LV) thrombus has not been studied.We investigated whether factor V Leiden is a risk factor for LV thrombus in patients with acute myocardial infarction (AMI). Methods and results — We have analyzed clinical, echocardiographic and biochemical data in 135 consecutive patients (aged 58 ± 13 years; 31 women) with first anterior AMI. Two-dimensional echocardiographic examination was performed on days I, 3, 7, 15 and 30; LV thrombus was detected in 33 (24.4%) of 135 patients with AMI. The study also included 95 control subjects. Healthy age and sex-matched subjects without a personal or family history of ischaemic heart disease, stroke or thromboembolic disease served as a control group. Blood samples from the patients and controls were analyzed for the factor V Leiden mutation by DNA analysis, using the polymerase chain reaction. In addition, concentrations of fibrinogen, von Willebrand factor (vWF), tissue plasminogen activator (t-PA), plasminogen activator inhibitor-I (PAI-1) and D-dimer were measured in 135 patients. There was no significant difference in the prevalence of factor V Leiden between patients and control subjects. The prevalence of the factor V mutation was 9% (3/33) in patients with thrombus, and 7.7% (8/103) in patients without thrombus. The prevalence of factor V Leiden was 7.3% (7/95) in control subjects. No significant differences in plasma fibrinogen (480 ± 195 vs. 444 ± 179 mg/dl, p = 0.6), D-dimer (471 ± 256 vs. 497 ± 293 ng/dl, p = 0.7), vWF (112 ± 18 vs. 103 ± 15%, p = 0.5), PAI-I (26.7 ± 9.8 vs. 28.1 ± 10.2 ng/dl, p = 0.6), and t-PA (19.8 ± 8.7 vs. 17.2 ± 9.1 ng/dl, p = 0.7), levels are found in patients with LV thrombus when compared with those without LV thrombus. Multivariate analyses showed that peak creatine kinase level (p = 0.002) and LV wall motion score index (p = 0.003) were independent predictors of LV thrombus formation. Conclusion — Factor V Leiden mutation is not a risk factor for LV thrombus formation in patients with AMI. (Acta Cardiol 2001; 56(1 ): 1-6)

Mitral Annular Calcification Is Associated with Pulse Wave Velocity but Not with Augmentation Index

Objective: To investigate the possible relationship between mitral annular calcification (MAC) and arterial stiffness. Subjects and Methods: Forty-two patients (mean age 68 ± 6 years) with MAC and an age-matched control group of 41 individuals (mean age 66 ± 6 years) were studied. Arterial stiffness and wave reflections of the study population were evaluated by using applanation tonometry (SphygmoCor). Aortic pulse wave velocity (PWV) was measured as an index of aortic stiffness. The heart rate-corrected augmentation index (AIx@75) was estimated as a composite marker of wave reflections and arterial stiffness. Results: Aortic PWV was significantly higher in patients with MAC (12.2 ± 2.3 m/s) than in controls (10.1 ± 1.3 m/s, p = 0.0001). However, AIx@75 was similar between the groups (28 ± 10 vs. 29 ± 10%, p = 0.59). Multivariate analysis involving the whole population revealed that brachial diastolic blood pressure (β = 1.87, p = 0.04) and MAC (β = 0.41, p = 0.0001) were independent determinants of aortic PWV. Conclusion: The data showed that MAC was significantly associated with increased arterial stiffness and that it was an independent determinant of aortic PWV.