Cevdet Erdöl

The effects of lipid-lowering therapy on low-density lipoprotein auto-antibodies: relationship with low-density lipoprotein oxidation and plasma total antioxidant status

BackgroundOxidized low-density lipoprotein (Ox-LDL) is believed to play an important role in the progression of atherosclerosis. Oxidative modification of low-density lipoprotein (LDL) is a prerequisite for rapid accumulation of LDL in macrophages and for the formation of foam cells. Because of high antioxidant levels in plasma, LDL oxidation is suggested to occur mainly in the subendothelial space of the arterial wall, where there is the concomitant presence of large amounts of reactive oxygen species generated by endothelial cells and activated leukocytes. After Ox-LDL formation, antibodies against this form of LDL may occur. Auto-antibodies against Ox-LDL (AuAb-Ox-LDL) show directly in in-vivo LDL oxidation. Many studies have indicated that the amount of antibodies in serum is positively correlated to the rate of progression of atherosclerotic plaques. Design and methodsIn this study the effect of lipid-lowering therapy on the levels of AuAb-Ox-LDL in patients with dyslipidemia was determined using atorvastatin (10 mg/day), and the relationship between the antibodies and plasma total antioxidant status (TAS) and LDL oxidation capacity was also investigated. Serum levels of AuAb-Ox-LDL, lipids, lipoproteins, TAS and susceptibility of LDL to oxidation were determined using lag time in 44 patients with dyslipidemia (29 with hypercholesterolemia and 15 with mixed-type hyperlipidemia). ResultsAfter lipid-lowering therapy, serum levels of AuAb-Ox-LDL were found to be significantly decreased, by 18.7%, while lag time and plasma TAS were increased (31.3% and 7.6% respectively) in patients with dyslipidemia. The percentage change in lag time was found to be negatively correlated to the percentage change in AuAb-Ox-LDL (r  = −0.31, P  < 0.05). The percentage change in lag time also showed a positive correlation with the percentage change in TAS (r  = 0.58, P  < 0.01). AuAb-Ox-LDL levels decreased by 21.7% in patients with hypercholesterolemia and by 12.6% in patients with mixed-type hyperlipidemia. Also AuAb-Ox-LDL levels in patients with hypercholesterolemia were higher than in those with mixed-type hyperlipidemia (367 ± 294 compared with 300 ± 176 mU/l). ConclusionIt was concluded that lipid-lowering therapy may contribute to the reduction in levels of AuAb-Ox-LDL and the increase in the antioxidant capacity of plasma LDL and TAS. It was also suggested that the measurement of antibodies against Ox-LDL during lipid-lowering therapy may be used as an important marker for representing in-vivo LDL oxidation and atherosclerotic processes.

Iron status and its relationship with lipid peroxidation in patients with acute myocardial infarction.

Aim — The aim of this study was to investigate iron status and its relationships with lipid peroxidation in patients with acute myocardial infarction (MI). Methods — The study included 30 male patients aged between 32 and 73 years (mean 55 ± 6) with acute MI.We measured the levels of plasma iron, transferrin (TF), ferritin (FER), ceruloplasmin (CER), cardiac enzymes, and erythrocyte malondialdehyde (e-MDA) in patients with acute MI on the admission and 1st, 3rd, 5th, 7th, 15th, 45th post MI day and investigated the variations of these parameters in acute MI. Results — The e-MDA level started to increase on the admission day and showed a peak value on the post MI 1st day (88 ± 23 and 98 ± 26 nmol/g Hb, respectively). Afterwards, the e-MDA level minimally changed until post MI 45th day, which showed a minimum level (57 ± 13 nmol/g Hb) (p < 0.05). In addition, the iron concentration of serum reached its maximum level on the 1st post MI day (99 ± 30 mg/dl, p < 0.05) and relatively decreased after the 3rd day. Courses of MDA and iron levels were similar. The FER level started to increase from the admission day of the patients (230 ± 375 mg/dl), showed a mean peak value on the 3rd day (296 ± 568 mg/dl) and decreased to a minimum level on the 45th day (121 ± 85 mg/dl) (p <0.05). Contrarily, the TF level started to decrease on the 1st day (221 ± 44 mg/dl), decreased minimum level on the 3rd day (211 ± 37 mg/dl) and continued approximately the same level until the 45th day (244 ± 45 mg/dl) (p < 0.05). The CER level started to increase from the first day of admission of the patients (43 ± 12 mg/dl), reached a maximum level on the 7th day (59 ± 12 mg/dl) and similar levels were observed until the 15th day. On the 45th day, the CER level was higher than on the first day (52 ± 13 mg/dl) (p < 0.05). Conclusion — There was an association of higher iron status with increased lipid peroxidation in patients with myocardial infarction.

Increased plasma fibronectin levels in patients with acute myocardial infarction complicated with left ventricular thrombus

Fibronectin is a polymorphic and multifunctional glycoprotein that plays a wide-ranging role in hemostasis. In this study, it was aimed to determine plasma fibronectin levels and evaluate its possible role in left ventricular (LV) thrombus formation following acute myocardial infarction (AMI). We have determined clinical, echocardiographic, and biochemical parameters in 97 consecutive patients (aged 59 +/- 13; 87 men/10 women) with first anterior AMI. Two-dimensional echocardiography was performed on Days 1, 3, 7, 15, and 30. Blood samples were obtained within 24-48 h after the onset of symptoms. The study also included 30 healthy control subjects. Plasma fibronectin levels were significantly higher in patients with AMI than control subjects (38 +/- 13 vs. 25.2 +/- 8.7 mg/dl, P=.0001). LV thrombus was detected in 20 (20.6%) of 97 patients. Plasma fibronectin levels were significantly higher in patients with LV thrombus (Group 2) than in patients without LV thrombus (Group 1) (44.5 +/- 11 vs. 36.1 +/-13.4 mg/dl, P=.01). Although univariate analysis showed that plasma fibronectin levels were higher in patients with thrombus, multivariate analysis showed that plasma fibronectin levels were not an independent predictor of LV thrombus formation (P=.059). In multivariate analyses, only peak creatine phosphokinase (CPK) level and LV wall motion score index (WMSI) were independent predictors of thrombus formation (P=.007 and P=.0001, respectively). These results suggest the increased plasma fibronectin levels may be one of the risk factors for LV thrombus formation after AMI. However, further studies concerning the relation between plasma fibronectin levels and LV thrombus formation are necessary.

Left ventricular diastolic function assessment by tissue Doppler echocardiography in relation to hormonal replacement therapy in postmenopausal women with diastolic dysfunction.

The objective of this study was to evaluate the effect of hormone replacement therapy (HRT) regimens on left ventricular diastolic function by using mitral pulsed wave Doppler (MPWD) and tissue Doppler velocities (TDE). Seventy-eight postmenopausal women with normotensive and impaired diastolic left ventricular filling were included in the study. All the patients began a six-cycle HRT course. This formulation consisted of E2 valerate plus Medroxy progesterone acetate (MPA). Left ventricular diastolic function at rest was evaluated by M-mode, two-dimensional, MPWD and TDE in 78 postmenopausal women with normal blood pressure before the treatment for 6 months of HRT. The M-mode, two-dimensional, and MPWD parameters assessed were heart rate, systolic blood pressure, diastolic blood pressure, left ventricular mass index, ejection fraction of the left ventricle (EF), septal (IVS) and posterior wall (PW) thickness, left ventricular end-systolic (LVESD) and end-diastolic (LVEDD) diameter, left atrial diameter, peak early diastolic velocity (E), peak atrial velocity (A), E/A ratio, E acceleration time, E deceleration time, diastolic filling period, and isovolumic relaxation time (IVRT). The TDE parameters assessed were peak early diastolic velocity (E′), peak late diastolic velocity (A′), peak systolic velocity, E′/A′ ratio, E′ acceleration time, E′ deceleration time, IVRT′, and E/E′ ratio. Quantitative data were analyzed using Student t test. Among the MPWD parameters, peak A velocity, E deceleration time, and IVRT significantly decreased, while peak E velocity and E/A ratio increased after a 6-month treatment. From the point of TDE parameters, E′ velocity and E′/A′ ratio increased, while A′ velocity, E′ deceleration time, E/E′ ratio and IVRT′ decreased. Some MPWD and TDE parameters were partially reversed after HRT. TDE velocities and especially E/E′ ratio may provide better and true information of the diastolic function. TDE parameters were independent from the preload and did not produce pseudonormal pattern. HRT may cause increase in the blood volume and produce pseudonormal pattern in transmitral flow. In that case, TDE may be a beneficial method for evaluation of diastolic function.

Plasma fibronectin level and its relationships with lipids, lipoproteins and C-reactive protein in patients with dyslipidaemia during lipid-lowering therapy

Objectives — The purpose of this study is to determine plasma fibronectin level and its relationships with plasma lipids, lipoproteins and C-reactive protein (CRP) levels in patients with dyslipidaemia during lipid-lowering therapy. Methods — Plasma levels of fibronectin, CRP, fibrinogen, lipids and lipoproteins in 38 patients with dyslipidaemia were determined before and after lipid-lowering therapy by using atorvastatin, 10 mg/day. Results — After lipid-lowering therapy, serum levels of fibronectin and CRP were found to be significantly decreased by 30.4% and 43,6%, respectively, while fibrinogen levels were increased 11.7% in patients with dyslipidaemia. Before the treatment, fibronectin was found to be positively correlated with CRP and total cholesterol (r=0.38, p<0.05 and r=0.33, p<0.05, respectively) and negatively correlated with high-density lipoprotein cholesterol (HDL-C) (r=–0.42, p<0.01) in patients with dyslipidaemia. High fibronectin levels (0.57±0.17 g/l) were found in patients with HDL-C below 35 mg/dl (0.57±0.09 g/l), compared to patients with HDL-C above 35 mg/dl (0.45±0.11 g/l). During the lipidlowering therapy, total cholesterol, low-density lipoprotein cholesterol (LDL-C), triglyceride and apo B levels were reduced while HDL-C and apo AI levels were increased. Conclusions — It was found that plasma fibronectin and CRP levels were decreased by lipid lowering therapy. Plasma fibronectin levels were associated with lipids, lipoproteins, CRP levels before treatment and these relationships disappeared after treatment. Consequently, it was suggested that reduction of plasma fibronectin levels, together with lipids and loss of its relationship with CRP, may play a role on the antiatherogenic effects of lipid-lowering therapy.OBJECTIVES The purpose of this study is to determine plasma fibronectin level and its relationships with plasma lipids, lipoproteins and C-reactive protein (CRP) levels in patients with dyslipidaemia during lipid-lowering therapy. METHODS Plasma levels of fibronectin, CRP, fibrinogen, lipids and lipoproteins in 38 patients with dyslipidaemia were determined before and after lipid-lowering therapy by using atorvastatin, 10 mg/day. RESULTS After lipid-lowering therapy, serum levels of fibronectin and CRP were found to be significantly decreased by 30.4% and 43.6%, respectively, while fibrinogen levels were increased 11.7% in patients with dyslipidaemia. Before the treatment, fibronectin was found to be positively correlated with CRP and total cholesterol (r=0.38, p<0.05 and r=0.33, p<0.05, respectively) and negatively correlated with high-density lipoprotein cholesterol (HDL-C) (r=-0.42, p<0.01) in patients with dyslipidaemia. High fibronectin levels (0.57 +/- 0.17 g/l) were found in patients with HDL-C below 35 mg/dl (0.57 +/- 0.09 g/l), compared to patients with HDL-C above 35 mg/dl (0.45 +/- 0.11 g/l). During the lipid-lowering therapy, total cholesterol, low-density lipoprotein cholesterol (LDL-C), triglyceride and apo B levels were reduced while HDL-C and apo AI levels were increased. CONCLUSIONS It was found that plasma fibronectin and CRP levels were decreased by lipid lowering therapy. Plasma fibronectin levels were associated with lipids, lipoproteins, CRP levels before treatment and these relationships disappeared after treatment. Consequently, it was suggested that reduction of plasma fibronectin levels, together with lipids and loss of its relationship with CRP, may play a role on the antiatherogenic effects of lipid-lowering therapy.

Assessment of left ventricular systolic and diastolic function by Doppler tissue imaging in patients with preinfarction angina

BACKGROUND The aim of this study was assessment of left ventricular (LV) systolic and diastolic function by pulsed wave Doppler tissue imaging (DTI) in patients with or without preinfarction angina in acute myocardial infarction. METHODS We prospectively evaluated 31 consecutive patients (4 women, 27 men; age 58 +/- 10 years) with a first acute myocardial infarction. LV systolic and diastolic function was assessed by classic methods and DTI on the third day during acute myocardial infarction. Patients were divided into 2 groups according to the presence (group 1; n = 10) or absence (group 2; n = 21) of preinfarction angina. Mitral inflow velocities and early diastolic mitral annular velocity (Em), late diastolic mitral annular velocity (Am), peak systolic mitral annular velocity, Em/Am, the ratio of early diastolic mitral inflow velocity (E) to Em, and myocardial performance index were calculated by DTI. RESULTS Group 1 had significantly higher Em and Em/Am than group 2 (11.3 +/- 3.34 cm/s vs 7.4 +/- 2.07 cm/s, P <.0001; 1.01 +/- 0.38 cm/s vs 0.6 +/- 0.2 cm/s, P =.001, respectively). The E/Em ratio and myocardial performance index were significantly lower in group 1 than in group 2 (5.1 +/- 2.92 vs 8.10 +/- 3.15, P=.018; 0.49 +/- 0.15 vs 0.65 +/- 0.24, P =.042, respectively). Wall-motion score index was lower in those with preinfarction angina than in those without (1.6 +/- 0.36 vs 1.9 +/- 0.39; P =.04, respectively). Peak systolic mitral annular velocity and Am were not statistically different between groups (9.4 +/- 1.84 vs 8.3 +/- 2.03, P =.172; 11.7 +/- 3.07 vs 12.1 +/- 3.34, P =.72, respectively). There were no significant differences between the 2 groups regarding transmitral E velocity, atrial contraction mitral inflow velocity (A), E/A ratio, isovolumetric relaxation time, and deceleration time of the mitral E wave (P =.91, P =.08, P =.58, P =.81, and P =.71, respectively). CONCLUSION LV diastolic function was better in patients with preinfarction angina than in patients without. This condition could not be detected by conventional mitral inflow Doppler velocities, but could be detected by DTI. This preliminary evidence shows that DTI is better than conventional mitral Doppler indices in the assessment of a favorable LV diastolic function in patients with preinfarction angina.

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)

Effect of coronary angiography on plasma endothelin-1 and nitric oxide concentrations.

Endothelium takes part in the regulation of vascular tone through the production of endothe lium-derived relaxing factor, nitric oxide (NO), and the contracting factor endothelin-1 (ET-1). Induction of ET-1 and NO is influenced by many stimuli including hypoxia and shear stress. Some of these stimuli may arise during coronary angiography (CAG). In this study, the authors aimed to show endothelial response in patients undergoing CAG by evaluating plasma ET-1 and NO end-products including nitrite and nitrate concentrations. Twenty-four male patients with a mean age of 54.3 years (age range: 37-70) were included in the study. The patients had no coronary atherosclerotic lesions established by CAG. The mean time of the CAG procedures was 24.8 minutes, with a range of 19-33 minutes. Immediately before blood sampling, systolic and diastolic blood pressures were recorded. The mean blood pressures before and after CAG were 140/90 and 150/95, respectively. End products of NO radical, nitrite and nitrate (NOx), in plasma were used as a marker for the production of NO radical. ET-1 concentrations were measured by ELISA method. Significant increases in ET-1 concentrations were observed during CAG while no change observed in NOx concentrations. Duration of the CAG procedure was found to be correlated with the percent increase of the plasma ET-1 concentrations during CAG (r = 0.45, p<0.05, Figure 1), but not with NOx concentrations. Plasma ET-1 concentrations in patients who were cigarette smoking were found higher than those of patients who were nonsmokers (1.26 ±0.38 and 2.97 ±0.87 fmol/L, respectively). It was concluded that endothe lial cells show increased ET-1 production as a response of some mechanical or emotional stimuli during CAG procedure that may play an important role in the regulation of vascular tonicity and some pathological processes. The authors suggest that duration and manipulation of CAG may be an important factor in plasma ET-1 concentrations.

Granulocytic sarcoma presenting as a right atrial mass

We describe a 48-year-old male who developed acute myelogenous leukaemia (AML) associated with a right atrial mass. The patient was admitted with fatigue, positional dyspnoea and headache. Transthoracic echocardiography (TTE) and transoesophageal echocardiography (TEE) revealed that the right atrium was filled with a mass. Peripheral blood smear revealed 85% blasts, and bone marrow examination showed 74% myeloid blasts and 27% monocytoid cells (monoblast and promonocytes). Immunophenotypic analysis of the bone marrow aspirates showed CD13, CD14 and CD33 positivity, consistent with acute myeloid leukaemia of M4 Fab subtype.The patient achieved remission (but not cure) accompanied by near resolution of the right atrial mass following intensive chemotherapy.

Relationship Between Changes in R-wave Amplitude During Left Ventriculography and the Seriousness of Coronary Heart Disease

Serious complications, such as myocardial infarction or death, may occur particularly in patients with severe coronary heart disease during coronary angiographies. Therefore, prediction of severe coronary heart disease before or during the initial steps of the procedure can provide a decrease in frequency of such complications. To predict the seriousness of coronary heart disease during left ventriculography, before, during, and after the application of contrast matter, electrocardiography (ECG) records were taken and R‐wave amplitudes were measured. Lead Oil was used for calculations. The patients were classified according to vessel lesions and were compared with the control group. Before and after left ventriculography, there was no significant difference between the groups with normal coronary arteries and one, two, or three vessel lesions. Although there was no significant difference obtained from the comparison of the control group and the groups with one‐vessel and two‐vessel lesions (9.7 mm, 9.2 mm, 10.1 mm, respectively, P > 0.05); there was statistical difference between the group with three‐vessel lesions and the control group during left ventriculography i6.4 mm, 9.7 mm, respectively, P < 0.05). Nonionic contrast material was used in all procedures. The decrement of R‐wave amplitude that is observed during left ventriculography can predict three‐vessel disease, which is a more serious condition for the patients. These patients should be monitored more carefully during coronary angiographies. A.N.E. 2002;7(2):114–119