Biomedical subjects

Huseyin Oflaz

Publications and source records attributed to Huseyin Oflaz.

30 records · Page 2Linked to original sources

PubMed2004

Angiotensin-converting enzyme gene polymorphism, left ventricular remodeling, and exercise capacity in strength-trained athletes.

The mechanisms that regulate the development of human physiological cardiac hypertrophy remain poorly understood. The renin-angiotensin system, which is modulated by genetic polymorphism, plays an important role in the regulation of vascular tone and myocardial hypertrophy. Although a few studies have analyzed the association of angiotensin-converting enzyme (ACE) polymorphism and left ventricular (LV) hypertrophy in isotonic exercise-trained subjects who developed eccentric cardiac hypertrophy, there has been no research done in power athletes who developed concentric cardiac hypertrophy. We have hypothesized that ACE genotypic modulation characteristics may affect LV mass in power athletes. This study included 29 elite Caucasian wrestlers (mean age, 22.6 years) and 51 age-matched sedentary subjects. According to the absence or presence of the insertion segment in the polymerase chain reaction (PCR) product, the subjects were classified as homozygous deletion-deletion (DD), insertion-insertion (II), or heterozygous insertion-deletion (ID). The association of LV hypertrophy with ACE gene insertion/deletion (I/D) polymorphism was analyzed. Left ventricular mass and index were determined by echocardiography. Angiotensin-converting enzyme genotyping was performed on peripheral leukocytes using the polymerase chain reaction technique. The study and control group subjects were similar in height and weight. Left ventricular hypertrophy in the athletes was more apparent than in the controls. Angiotensin-converting enzyme genotype II frequency was 17.2% (5) in the athletes, 17.6% (9) in the controls; ID frequency was 51.7% (15) in the athletes, 56.8% (29) in the controls; and the DD frequency was 31% (9) in the athletes and 25.4% (13) in the controls. Left ventricular mass and mass index were found to be higher in genotype DD (126.2 +/- 2.9g/m2) than genotype II (85.5 +/- 4.0g/m2) or genotype ID (110.1 +/- 2.3g/m2) in the athletes (P < 0.001). Furthermore, maximal oxygen consumption in genotype DD was found to be higher than in II and ID. An association was found between ACE gene I/D polymorphism and LV hypertrophy in strength-trained athletes.

Adult↗

PubMed2004

Alveolar hemorrhage associated with warfarin therapy: a case report and literature review.

A 75-year-old man was admitted to our clinic with the complaints of palpitation, fever, severe dyspnea, dizziness and bloody sputum associated with coughing. Chest radiographs revealed that the lungs were bilaterally infiltrated. A high resolution computed tomographic study of the thorax disclosed diffuse alveolar hemorrhage, of which presence was proved by histopathological study of bronchoalveolar lavage material. The hemorrhage occured at 8th day of 5 mg daily warfarin therapy, which was given for frequent atrial fibrillation attacks was controlled by fresh frozen plasma and vitamin K. Alveolar hemorrhage is difficult to diagnose and has high mortality if the treatment was not started as soon as possible. This is the first report of alveolar hemorrhage caused by 5 mg daily warfarin therapy. We propose that the patient's age, nutritional status, used drugs should be taken into consideration for true management of patients with atrial fibrillation.

Aged↗

PubMed2004

Endothelial dysfunction and increased carotid intima-media thickness in patients with autosomal dominant polycystic kidney disease.

BACKGROUND: Cardiovascular problems are a major cause of morbidity and mortality in patients with autosomal dominant polycystic kidney disease (ADPKD). Endothelial dysfunction (ED) and intima-media thickness (IMT) are predictors for the development and progression of atherosclerosis. In the present study, ED and IMT were investigated in patients with ADPKD. METHODS: Fifteen hypertensive and 16 normotensive patients with ADPKD with preserved renal function, 16 patients with essential hypertension, and 24 healthy subjects were included in the study. Endothelial function of the brachial artery was evaluated by means of high-resolution vascular ultrasound. Endothelial-dependent dilatation (EDD) was assessed by establishing reactive hyperemia, and endothelial-independent dilatation was determined by using sublingual isosorbide dinitrate. Carotid IMT was measured by means of high-resolution vascular ultrasound. RESULTS: EDD was significantly worse in hypertensive patients with ADPKD compared with patients with essential hypertension (9.1% +/- 4.1% versus 12.4% +/- 4.6%; P < 0.05) and even in normotensive patients with ADPKD compared with healthy subjects (13.1% +/- 5.2% versus 18.1% +/- 8.1%; P < 0.01). Moreover, carotid IMT was significantly greater in both hypertensive (0.71 +/- 0.10 mm; P < 0.01) and normotensive (0.57 +/- 0.14 mm; P < 0.001) patients with ADPKD compared with healthy subjects (0.45 +/- 0.10 mm). CONCLUSION: Both hypertensive and normotensive patients with ADPKD show significant ED and increased IMT, which are predictors of atherosclerosis.

Adult↗

PubMed2004

Endothelial dysfunction in patients with asthma: the role of polymorphisms of ACE and endothelial NOS genes.

OBJECTIVES: Polymorphisms of the angiotensin converting enzyme (ACE) and endothelial nitric oxide (eNOS) genes have been implicated in asthma pathogenesis. Angiotensin II and NO have important roles in maintaining vascular tone. In this study, the relationship between endothelial dysfunction and ACE and eNOS gene polymorphisms was investigated in patients with asthma. METHODS: This cross-sectional, controlled study was conducted at the Yedikule Chest Disease Hospital and Cardiology Center in a University Hospital. Forty-nine patients with asthma (18 male, 31 female; mean age: 33+/-12 years) and 49 age- and sex-matched healthy controls (20 male, 29 female; mean age: 30+/-8 years) were included. Pulmonary function tests and flow-mediated dilatation of the brachial artery [endothelium dependent dilatation (EDD)] were examined by high-resolution ultrasonography. The ACE and eNOS genotypes were determined by PCR. RESULTS: Asthma patients showed lower EDD (12+/-6% vs. 22+/-6%, p<0.001) as compared to controls. The EDD was correlated with both predicted value of FEV1 (r=0.31, p=0.04) and predicted value of FVC (r=0.37, p=0.013). Conversely, EDD values in patients with moderate asthma were significantly lower than those in patients with mild asthma (10.1+/-5.2% vs. 14.1+/-5.7%, p=0.017). However, the ACE and eNOS genotype distribution was not significantly different between controls and asthma groups. Furthermore, EDD was not associated with both gene polymorphism of ACE and eNOS. CONCLUSION: Patients with asthma have decreased vasodilatatory response to shear stress (EDD). Decreased EDD is correlated with the severity of asthma, but not with the distribution of ACE and eNOS genotypes.

Adult↗

PubMed2004

Evaluation of endothelial function in subclinical hypothyroidism and subclinical hyperthyroidism.

Subclinical hypothyroidism and subclinical hyperthyroidism are two frequently occurring conditions for which exact therapeutic approaches have not yet been established. The aim of this study was to compare the endothelial function and carotid artery intimae-media thickness (IMT) of these two groups of patients to euthyroid subjects and to assess the effects of these conditions on endothelial function. Study groups comprised of 25 subclinical hypothyroid patients (mean age, 32.28 +/- 9.67 years), 13 subclinical hyperthyroid patients (mean age, 35.69 +/- 9.67 years), and 23 euthyroid subjects (mean age, 35.87 +/- 7.93 years). They were evaluated for flow-mediated dilatation (FMD), and carotid artery IMT. The groups were matched strictly for atherosclerotic risk factors. The subclinical hypothyroid group was found to have significantly lower FMD values. No significant differences were observed between the groups with respect to other vascular parameters. The only discriminative factor between the groups was the state of their thyroid function. Therefore, subclinical hypothyroidism may have adverse effects on endothelial function independent from other well-known atherosclerotic risk factors.

Adult↗

PubMed2004

Carotid atherosclerosis is a predictor of coronary calcification in chronic haemodialysis patients.

BACKGROUND: Coronary artery calcification scores (CACS) calculated by electron beam computed tomography (EBCT) have been correlated with atherosclerotic burden in the non-uraemic population. However, the validity of this test in chronic haemodialysis patients (HD) is currently uncertain. In the present cross-sectional study, associations between carotid atherosclerosis and coronary calcification in HD patients are investigated. METHODS: We studied 79 chronic HD patients (39 male, 40 female; mean age, 45+/-12 years). The mean time on HD was 68+/-54 months (range, 6-187 months). In these patients, we measured serum calcium, phosphorus, total cholesterol, cholesterol subgroups and iPTH levels. EBCT, echocardiography, and high-resolution B-mode carotid Doppler ultrasonography were also performed. RESULTS: Plaque-positive HD patients had significantly higher CACS than plaque-negative patients (851+/-199 vs 428+/-185, mean+/-SE, P = 0.006). Coronary calcification scores were correlated with serum phosphorus (r = 0.37; P = 0.001). Only 8 of the 24 HD patients without coronary calcification had carotid plaques (33%), whereas 34 of the 53 patients with coronary calcification had carotid plaques (64%) (P = 0.015). Carotid plaque scores were correlated with CACS (r = 0.40; P = 0.001). A stepwise linear regression (model r = 0.72; P<0.001) revealed that CACS (log-transformed data of CACS) was associated with age (P<0.001), time on dialysis (P = 0.004), serum phosphorus level (P = 0.016) and carotid plaque scores (P = 0.037). CONCLUSIONS: Atherosclerosis is independently associated with coronary artery calcification and with hyperphosphataemia in chronic HD patients. CACS appeared to be predictive of both coronary atherosclerosis and carotid atherosclerosis.

Calcinosis↗

PubMed2003

Gene polymorphisms of endothelial nitric oxide synthase enzyme associated with pulmonary hypertension in patients with COPD.

In this cross-sectional controlled study, we aimed to investigate the role of polymorphisms of the angiotensin-converting enzyme (ACE) and endothelial nitric oxide synthase (eNOS) genes on pulmonary hypertension (PH) in patients with chronic obstructive pulmonary disease (COPD). Forty-two (41 male, 1 female, mean age: 62 +/- 7 years) COPD patients and 40 (all male, mean age: 60 +/- 8 years) healthy controls were included. Respiratory function tests, arterial blood gases, and echocardiographic examinations were performed. ACE and eNOS genotypes were determined using PCR. The ACE and eNOS genotype distribution was not significantly different between COPD patients and controls. On comparing pulmonary artery pressures in different eNOS genotypes, the mean pulmonary artery pressure (Ppa) in patients with the BB genotype was significantly higher than in patients with the nonBB genotypes (41.3 +/- 17.7 mmHg vs. 27.3 +/- 11.2 mmHg, P = 0.02). However, there was no difference in ACE genotype distributions between COPD patients with and without pulmonary hypertension. In stepwise linear regression analysis for predicting pulmonary artery pressure, PaO2 and polymorphism of eNOS gene were found to be independent variables. In conclusion, BB-type polymorphism of the eNOS gene has been associated with PH in addition to hypoxemia. However, ACE gene polymorphism was not found to be associated with PH.

Blood Pressure↗

PubMed2003

The effect of calcineurin inhibitors on endothelial function in renal transplant recipients.

Endothelial dysfunction is of vital importance, as it may cause ischemia and dysfunction in various organs. Despite, this problem has been well documented in patients with end-stage renal disease (ESRD), there is not enough data considering this issue following renal transplantation. One of the potential causes of endothelial dysfunction in renal transplant recipients may be administration of calcineurin inhibitors. The aim of this study is to evaluate the effects of two different calcineurin inhibitors [cyclosporin A (CsA) and tacrolimus (FK506)] on endothelial function in renal transplant patients. Forty-four renal transplant recipients [22 on FK506 (group I) and 22 on CsA (group II)] were studied. Endothelial functions of the brachial artery were evaluated by using high resolution vascular ultrasound. Endothelium-dependent and -independent vasodilations were assessed by establishing reactive hyperemia and using sublingual nitroglycerine (NTG), respectively. Results are presented as percentage change from baseline values. Significant endothelial dysfunction was noted in renal transplant patients treated with CsA. While endothelium-dependent vasodilation was 12.1 +/- 5.1% in group I and it was 6.5 +/- 3.7% in group II (p < 0.001). The increase in brachial artery diameter after sublingual NTG was 20.1 +/- 6.3 and 12.7 +/- 5.6% in groups I and II, respectively. This indicates that the endothelium-dependent and -independent vasodilation of the patients on FK506 is better preserved than the patients on CsA therapy. Besides, blood flow volume (BFV) increase was 51.2 +/- 39.4 and 43.9 +/- 24.3%, in groups I and II, respectively, in reactive hyperemia period (p > 0.05). Post-transplant course of renal transplant recipients is complicated by endothelial dysfunction. This problem is more prominent in patients on CsA therapy, which can predispose these patients to more frequent cardiac complications.

Adult↗

PubMed2003

Endothelial function is more impaired in hemodialysis patients than renal transplant recipients.

BACKGROUND: Endothelial dysfunction (ED) is a common precursor and denominator of cardiovascular events including development of atherosclerosis. In this cross-sectional, controlled study, we aimed to investigate ED measured by ischemia-induced forearm vasodilatation in chronic hemodialysis (HD) patients and renal transplant recipients (rTX). PATIENTS AND METHODS: Thirty-nine HD patients, 39 rTX and 38 normotensive healthy controls were included. There was no difference in age and gender distribution among the study groups. The mean time spent on dialysis and transplantation were 74 +/- 46 and 68 +/- 39 months. Serum high sensitive C-reactive protein (hs-CRP) and plasma fibrinogen levels were measured. Endothelium dependent post-ischemic vasodilatation of brachial artery was used to evaluate ED. RESULTS: The hs-CRP and plasma fibrinogen levels were significantly increased in HD patients when compared with rTX. On high resolution ultrasonographic examination, post-ischemic vasodilatation values in HD patients (9.55 +/- 6.47%) were significantly lower than rTX (14.39 +/- 8.06%, p = 0.007) and controls (20.42 +/- 6.10%, p < 0.001). Renal transplant recipients also had significantly lower post-ischemic vasodilatation values than controls (p = 0.001). The hs-CRP levels were negatively correlated with endothelium-dependent dilatations in TX (r = -0.59, p = 0.001), however, this correlation was not detected in HDp. CONCLUSION: Patients with end-stage renal disease have ED. Endothelial function is more impaired in HD patients than rTX. Different mechanisms might be responsible for ED in HD patients and rTX.

Adult↗

PubMed2003

Left ventricular hypertrophy and endothelial dysfunction in chronic hemodialysis patients.

BACKGROUND: Endothelial dysfunction (ED), which is a risk factor for atherosclerosis, has been reported recently in chronic hemodialysis (CHD) patients. In this study, we aim to investigate the association of ED and presence of left ventricular hypertrophy (LVH) in CHD patients. METHODS: One hundred four CHD patients (47 men, 57 women; mean age, 45 +/- 12 years) and 49 age- and sex-matched controls were included. Mean time on dialysis therapy was 62 months. Echocardiographic examination and flow-mediated endothelium-dependent (EDD) and endothelium-independent dilatation (EID) of the brachial artery, measured by high-resolution ultrasonography, a noninvasive method for assessing endothelial function, were performed on a nondialysis day. RESULTS: LVH was detected in 72 CHD patients (69%). Patients with LVH had a lower EDD (9.3% +/- 6.1% versus 12.1% +/- 8.3%; P = 0.06), but the difference was not significant. Mean EID was significantly lower in CHD patients with LVH (13.6% +/- 7.6% versus 18.6% +/- 9.8%; P = 0.008). Left ventricular mass index (LVMI) correlated with both EDD (r = -0.22; P = 0.03) and EID (r = -0.32; P = 0.002). Patients with LVH had a greater rate of hypertension (35 of 72 versus 7 of 32 patients; P = 0.02) and lower hemoglobin levels (11.0 +/- 1.8 versus 11.8 +/- 1.6 g/dL [110 +/- 18 versus 118 +/- 16 g/L]; P = 0.05). CHD patients had a lower EDD (10.2% +/- 6.9% versus 20.9% +/- 7.6%; P < 0.001) and EID (15.0% +/- 8.5% versus 27.8% +/- 8.5%; P < 0.001) compared with controls. In linear regression analysis for predicting LVMI, presence of hypertension, hemoglobin level, and EID, but not EDD, were found to be independent variables. CONCLUSION: EID, which may reflect decreased elasticity of arteries, contributes to the development of LVH in CHD patients, in addition to hypertension and anemia.

Adolescent↗

PubMed2002

Can thrombolytic therapy provide beneficial effects additional to epicardial coronary artery recanalization? A study based on coronary pressure measurement.

BACKGROUND: Collaterals provide significant blood supply to the myocardium at risk and the presence of a preserved and adequate collateral network may limit microvascular damage during the occlusion of an epicardial coronary artery. The aim of this study was to evaluate whether thrombolytic therapy (TT) may produce beneficial effects at the level of microvascular circulation in addition to epicardial coronary artery recanalization by using quantitative intracoronary pressure measurement techniques in patients with recent acute myocardial infarction (AMI). MATERIALS AND METHODS: Thirty-six patients who presented with AMI and had preinfarction angina pectoris, more than 60% stenosis and thrombolysis in myocardial infarction (TIMI) grade II flow in the infarct-related artery and who underwent a stent implantation procedure within 10 days of AMI were included in this study. Seventeen of 36 patients had received TT (group 1) and 19 had not received TT due to presence of contraindications or late admission (group 2). Quantitative coronary angiography, TIMI frame count (TFC) assessment and intracoronary pressure measurements were performed before and after stent implantation for all patients. Myocardial fractional flow reserve (FFRmyo) was calculated as the ratio of mean distal coronary pressure to mean aortic pressure. During total occlusion with balloon inflation, distal pressure was recorded as coronary wedge pressure (CWP). Collateral flow index (CFI) was determined by the ratio of simultaneously measured CWP to mean aortic pressure. RESULTS: There were no differences between the two groups with respect to mean per cent stenosis and mean FFRmyo both before and after stent implantation. The mean CWP (25.1 +/- 8.6 mmHg compared with 17.2 +/- 6.2 mmHg, P < 0.01) and CFI (0.24 +/- 0.10 compared with 0.16 +/- 0.11, P < 0.01) were significantly higher and mean post-stent corrected TFC (18.8 +/- 3.7 compared with 22.4 +/- 3.1, P < 0.01) was significantly faster in the group of patients who had received TT compared to those who had not. CONCLUSIONS: We concluded that destruction degree of collateral circulation and distal microvasculature is lower in patients who had received TT, compared to patients who could not be treated with TT. Besides protective effect on collateral vessels, TT provides even more reperfusion and less destruction of the microvasculature.

Blood Pressure Determination↗

PubMedDate not supplied

Non-invasive evaluation of endothelial function in hypertensive elderly patients.

Impaired endothelium-dependent vasomotion is a diffuse disease process resulting in abnormal regulation of blood vessel tone and loss of several atheroprotective effects of the normal endothelium. The aim of the present study was to investigate the effects of aging and hypertension on endothelial function. Sixty-six geriatric subjects with ages over 60 (48 hypertensive and 18 healthy) and 40 middle-aged subjects (16 hypertensive and 24 healthy) were included in the study. Systemic vascular endothelial function was evaluated through measuring brachial arterial vasodilation, a physiologic answer to reactive hyperemia occured with increased blood flow in the vessel after transient ischemia (flow-mediated dilation, FMD%), and with carotid artery intima-media thickness (IMT) measurement, using high-resolution ultrasonography. Endothelial independent vasodilation was also measured after administration of sublingual isosorbide dinitrate (isosorbide dinitrate mediated dilation, IDNMD%). FMD% was significantly decreased in elderly and/or hypertensive (HT) patients (geriatric HT: 9.5 +/- 4.7%, geriatric non-HT: 12.7 +/- 5.5%, middle-aged HT: 12.9 +/- 4.3% and middle-aged non-HT: 18.9 +/- 8.1%) (geriatric HT versus geriatric non-HT (P = 0.02), geriatric HT versus middle-aged HT (P = 0.01), geriatric non-HT versus middle-aged non-HT (P = 0.008)). Both FMD% and IDNMD% were inversely correlated with age, baseline vessel diameter and carotid artery intima-media thickness. FMD% was also inversely correlated with diastolic blood pressure. No correlation was found between FMD% and systolic blood pressure, serum cholesterol and triglyceride levels. Endothelium dependent (EDD) and independent dilatation of large arteries decreased with aging even in the healthy elderly, and FMD further declined in HT elderly patients, indicating that age and hypertension independently impair endothelial function. Positive correlations with age and hypertension, and significant inverse correlation with FMD, makes carotid artery IMT a possible indicator of endothelial function.

Adult↗