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ABSTRACT: Augmentation index (AIx), a measure of wave reflection, is regulated by a number of factors, including endothelial function and vascular smooth muscle tone. The relationship between local endothelium-derived factors and AIx is well known; however, association between endothelial damage markers and AIx has not been sufficiently studied. This study investigates whether endothelial damage markers-von Willebrand factor (vWF) soluble thrombomodulin (sTM)--are associated with wave reflections. We studied 46 (48.5 +/- 10.6, years) never-treated patients with hypertension (HT) and an age-matched control group of 40 (47 +/- 8.6, years) normotensive individuals. von Willebrand factor and sTM levels were determined in all subjects. We evaluated the aortic AIx of the study population using applanation tonometry (Sphygmocor, AtCor Medical, Sydney, Australia). The heart rate-corrected augmentation index (AIx@75) was estimated as a marker of wave reflections. Endothelial damage markers and AIx@75 were significantly higher in hypertensive patients than in controls. In the whole population, the vWF level (beta = 0.24, p = 0.01) was an independent determinant of AIx@75 in multivariate analysis. However, the sTM level was not associated with AIx@75. We found that the vWF level was an independent determinant of AIx@75. Our results suggest that increased an vWF level contributes significantly to increased wave reflections.
Clinical and Experimental Hypertension 01/2010; 32(1):29-34. · 1.07 Impact Factor
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ABSTRACT: The Seventh Report of the Joint National Committee on the Prevention, Detection, Evaluation, and Treatment of High Blood Pressure classifies blood pressure (BP) as normal, prehypertension, and hypertension. Although it has been shown that there is a relationship between hypertension and arterial stiffness, there is not sufficient data about arterial stiffness in patients with prehypertension. The present study was designed to evaluate arterial stiffness and wave reflections in subjects with prehypertension. We evaluated arterial stiffness and wave reflections of 45 subjects with prehypertension and an age-matched control group of 40 normotensive individuals, using applanation tonometry (Sphygmocor, AtCor Medical, Sydney, Australia). Aortic pulse wave velocity (PWV) was measured as indices of elastic-type aortic stiffness. The heart rate-corrected augmentation index (AIx@75) was estimated as a composite marker of wave reflections and arterial stiffness. Aortic PWV (10 +/- 2.5 vs. 8.6 +/- 1.7, m/s, p = 0.004) and AIx@75 (21 +/- 8.3 vs. 10 +/- 9.1, %, p = 0.0001) were significantly higher in subjects with prehypertension than in the control group. In multiple linear regression analysis, we found that the presence of the prehypertension was a significant predictor of aortic PWV (beta = 0.26, p = 0.009) and AIx@75 (beta = 0.46, p = 0.0001). Our results suggest that arterial functions were impaired even at the prehypertensive stage.
Clinical and Experimental Hypertension 01/2010; 32(2):84-9. · 1.07 Impact Factor
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ABSTRACT: 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 micromol/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 (beta = -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.
Heart and Vessels 09/2009; 24(5):366-70. · 2.05 Impact Factor
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Omer Gedikli M.D,
Merih Baykan M.D,
Kubra Kaynar M.D,
Gulsum Ozkan M.D,
Levent Korkmaz M.D,
Serkan Ozturk M.D,
Ismet Durmus M.D,
Sahin Kaplan M.D,
Sukru Celik M.D,
Omer Gedikli,
Merih Baykan,
Kubra Kaynar,
Gulsum Ozkan,
Levent Korkmaz, Serkan Ozturk,
Ismet Durmus,
Sahin Kaplan,
Sukru Celik
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ABSTRACT: Objective: The evidence of structural and functional cardiac abnormalities has been demonstrated by echocardiography in patients with chronic kidney disease (CKD). This study investigated whether left ventricular (LV) asynchrony is present in patients with CKD and normal QRS duration. Methods: Tissue synchronization imaging (TSI) was performed in 25 (56 ± 14 years) patients with CKD and narrow QRS complexes and 25 (51 ± 12 years) control subjects. LV asynchrony was identified on TSI images and the time to regional peak systolic velocity (Ts) in LV was measured by the six-basal–six-midsegmental model. Four TSI parameters of systolic asynchrony were computed when Ts was measured in ejection phase. Results: The standard deviation of Ts of 12 LV segments (33.6 ± 17.8 vs 16.7 ± 10 ms, P = 0.0001), standard deviation of Ts of the six basal LV segments (30 ± 20 vs 17.6 ± 9.6 ms, P = 0.008), maximal difference in Ts between any two of the 12 LV segments (102 ± 45 vs 54 ± 32 ms, P = 0.0001), and maximal difference in Ts between any two of the six basal LV segments (78 ± 50 vs 46 ± 22 ms, P = 0.007) were prolonged in patients with CKD compared with controls. The prevalence of LV systolic asynchrony was significantly higher in patients with CKD compared with controls (44% vs 12%, P = 0.01). The standard deviation of Ts of 12 LV segments were significantly associated with LV diameters, LV volumes, LV mass, blood pressure levels, and renal functions in univariate analysis. Conclusion: The results of this study indicate that LV systolic asynchrony may develop in patients with CKD.
Echocardiography 04/2009; 26(5):528 - 533. · 1.24 Impact Factor
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ABSTRACT: 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).
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).
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.
Serum relaxin is decreased in patients with HT. However, low endogenous relaxin is not related to cardiovascular function.
Blood pressure 02/2009; 18(1-2):68-73. · 1.26 Impact Factor
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ABSTRACT: Arterial stiffness increases in hypertensive individuals. Arterial stiffness is associated with impairment of systolic and diastolic myocardial function in hypertension (HT). However, the relationship between arterial stiffness and serum heart-type fatty acid-binding protein (H-FABP) levels, a sensitive marker of myocardial damage, has not been previously examined in patients with HT. We investigate the relationship between serum H-FABP levels and arterial stiffness in patients with newly diagnosed HT.
We studied 46 (48.5 +/- 10.6, years) never-treated patients with HT and age-matched control group of 40 (47 +/- 8.6, years) normotensive individuals. H-FABP levels were determined in all subjects. We evaluated arterial stiffness and wave reflections of study population, using applanation tonometry (Sphygmocor). Carotid-femoral pulse wave velocity (PWV) was measured as indices of elastic-type, aortic stiffness. The heart rate-corrected augmentation index (AIx@75) was estimated as a marker of wave reflections.
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 than control group. H-FABP levels were increased in hypertensive patients compared with control group (21.1 +/- 14.8 vs. 12.9 +/- 8.5, ng/ml, P = 0.002). In multiple linear regression analysis, we found that the body mass index (beta = 0.42, P = 0.0001) and carotid-femoral PWV (beta = 0.23, P = 0.03) were significant determinants of H-FABP levels.
Arterial stiffness is associated with serum H-FABP levels, a sensitive marker of myocardial damage, in patients with newly diagnosed HT.
American Journal of Hypertension 08/2008; 21(9):989-93. · 3.18 Impact Factor
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ABSTRACT: Background Arterial stiffness increases in hypertensive individuals. Arterial stiffness is associated with impairment of systolic and diastolic myocardial function in hypertension (HT). However, the relationship between arterial stiffness and serum heart-type fatty acid–binding protein (H-FABP) levels, a sensitive marker of myocardial damage, has not been previously examined in patients with HT. We investigate the relationship between serum H-FABP levels and arterial stiffness in patients with newly diagnosed HT.
American Journal of Hypertension 07/2008; 21(9):989-993. · 3.18 Impact Factor
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ABSTRACT: Mad honey poisoning is well known in the eastern Black Sea region of Turkey. The cause of the poisoning is the toxin grayanotoxin, found in honey obtained from the nectar of Rhododendron species on the mountains in the region. A 60-year-old man was brought to the emergency department with dizziness and syncope after eating a few spoonfuls of honey. While the patient was being treated, bradycardia and asystole developed. The patient was given 0.5 mg of atropine, and asystole began and ended. The patient was transferred to the catheter laboratory and a temporary pacemaker was implanted. Mad honey poisoning related asystole has not been previously reported, and the rapid response to atropine is significant.
Emergency Medicine Journal 09/2007; 24(8):592-3. · 1.44 Impact Factor
