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SARI, İBRAHİM

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SARI

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İBRAHİM

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Now showing 1 - 4 of 4
  • Publication
    Neutrophil to lymphocyte and platelet to lymphocyte ratio in patients with dipper versus non-dipper hypertension
    (TAYLOR & FRANCIS INC, 2014) ÇİNÇİN, AHMET ALTUĞ; Sunbul, Murat; Gerin, Fethullah; Durmus, Erdal; Kivrak, Tarik; Sari, Ibrahim; Tigen, Kursat; Cincin, Altug
    Background: Neutrophil to lymphocyte ratio (NLR) and platelet to lymphocyte ratio (PLR) are associated with worse outcome in various diseases. Non-dipping blood pressure pattern is associated with higher cardiovascular mortality. The aim of this study was to explore the association between NLR and PLR in patients with dipper versus non-dipper hypertension. Methods: The study included 166 patients with hypertension. Eighty-three patients (40 male, mean age: 49.1 +/- 10.5 years) had dipper hypertension, while 83 patients (41 male, mean age: 52.3 +/- 12.7 years) had non-dipper hypertension. Results: Baseline demographic characteristics were similar in both groups. Patients with non-dipper hypertension had significantly higher NLR compared to dipper hypertension (2.3 +/- 0.9 versus 1.8 +/- 0.5, p < 0.001). Patients with non-dipper hypertension had significantly higher PLR compared to dipper hypertension (117.7 +/- 35.2 versus 100.9 +/- 30.5, p = 0.001). In univariate analysis, hyperlipidemia, smoking, presence of diabetes, PLR more than 107 and NLR more than 1.89 were among predictors of dipper and non-dipper status. In logistic regression analyses, only hyperlipidemia (odds ratio: 2.96, CI: 1.22-7.13) and PLR more than 107 (odds ratio: 2.62, Cl: 1.13-6.06) were independent predictors of dipper and non-dipper status. A PLR of 107 or higher predicted non-dipper status with a sensitivity of 66.3% and specificity of 68.7%. Conclusion: We demonstrated that patients with non-dipper hypertension had significantly higher NLR and PLR compared to dipper hypertension, which has not been reported previously. Moreover PLR more than 107 but not NLR was independent predictor of non-dipper status.
  • Publication
    Acute sleep deprivation is associated with increased arterial stiffness in healthy young adults
    (SPRINGER HEIDELBERG, 2014) SARI, İBRAHİM; Sunbul, Murat; Kanar, Batur Gonenc; Durmus, Erdal; Kivrak, Tarik; Sari, Ibrahim
    Background Arterial stiffness and its hemodynamic consequences are known to be associated with increased cardiovascular morbidity and mortality. Pulse wave velocity (PWV) and augmentation index (AIx) are noninvasive indicators of the arterial stiffness and wave reflection. Sleep deprivation (SD) is known to be associated with increased incidence of adverse cardiovascular events. The aim of this study was to investigate whether there is an association between acute SD and arterial stiffness parameters in healthy adults, which has not been studied previously. Methods The study population consisted of 42 healthy volunteers (18 males, mean age 30.0 +/- 4.5 years). Measurements of arterial stiffness were carried out by using a Mobil-O-Graph arteriograph system. Arterial stiffness measurements were obtained both after a night with regular sleep (RS) and after a night with SD. Results Mean sleep time was significantly lower after the night of SD when compared after RS (0.73 +/- 1.39 versus 7.33 +/- 0.52 h, p < 0.001). Peripheral systolic blood pressure, peripheral pulse pressure, and cardiac output were significantly higher after SD when compared after RS (p = 0.032, 0.007, and 0.003, respectively). PWVwas significantly higher (5.33 +/- 0.46 versus 5.15 +/- 0.26 m/s, p = 0.001), and AIx was significantly lower (20.5 +/- 11.9 versus 26.0 +/- 8.4 %, p = 0.008) after the night of SD when compared after the RS. While PWV was significantly higher (p= 0.008), and AIx was significantly lower (p = 0.039) in male subjects, only PWVwas significantly higher (p = 0.009) in female subjects. Sleep time correlated with AIx (p = 0.034; r = 0.233) and inversely correlated with PWV (p = 0.044; r = -0.222). Conclusion In the present study, we demonstrated that even one night of SD is associated with increased arterial stiffness in healthy adults. The present findings suggest that adverse effects of SD on cardiovascular system might be at least in part due to increased arterial stiffness which needs to be tested with large-scale studies and in the chronic SD setting.
  • Publication
    Effect of acute sleep deprivation on left atrial mechanics assessed by three-dimensional echocardiography
    (SPRINGER HEIDELBERG, 2016) ÇİNÇİN, AHMET ALTUĞ; Cincin, Altug; Sari, Ibrahim; Sunbul, Murat; Kepez, Alper; Oguz, Mustafa; Sert, Sena; Sahin, Anil; Ozben, Beste; Tigen, Kursat; Basaran, Yelda
    Although sleep deprivation (SD) affects cardiovascular system in many ways, physio-pathological changes in cardiac chamber volume and function have not been described well. The aim of the present study was to investigate the effect of SD on left atrial (LA) and ventricular function with three-dimensional (3D) echocardiography. Thirty-two healthy individuals (12 females, mean age 33.25 +/- 8.18) were evaluated. Echocardiographic examination was performed once after a night of regular sleep and a night of sleep debt. Beside conventional parameters, 3D phasic volumes and function were measured using a commercially available 3D echocardiography system and offline analysis software. Mean sleep duration of the study group was 8.15 +/- 2.19 h in the day of regular sleep and 2.56 +/- 2.25 h in the day of sleep deprivation. There was a significant prolongation in deceleration time (180.83 +/- 15.34 vs. 166.44 +/- 26.12; p = 0.044) and increase in E/e' (6.95 +/- 1.26 vs. 6.38 +/- 0.85; p = 0.005). Among 3D measurements, the difference in left ventricular ejection fraction (EF), LA EF, LA reservoir function and LA active EF were not significant. Mean LA passive EF of the individuals was significantly lower after night shift (24.10 +/- 7.66 vs. 31.49 +/- 7.75; p = 0.006). Acute SD is associated with a reduction in LA passive emptying function in healthy adults. 3D-derived indices were sufficient to show subclinical diastolic dysfunction according to impairment in passive phase of LA ejection. Prospective large-scale studies are needed to enlighten this issue.
  • Publication
    Effect of acute sleep deprivation on heart rate recovery in healthy young adults
    (SPRINGER HEIDELBERG, 2015) ÇİNÇİN, AHMET ALTUĞ; Cincin, Altug; Sari, Ibrahim; Oguz, Mustafa; Sert, Sena; Bozbay, Mehmet; Atas, Halil; Ozben, Beste; Tigen, Kursat; Basaran, Yelda
    Sleep deprivation (SD) is known to be associated with increased incidence of adverse cardiovascular events, but underlying pathophysiological mechanism has not been clearly demonstrated. Autonomic nervous system plays an important role in the regulation of cardiovascular function, and impairment in this system is associated with increased cardiovascular mortality. The aim of the current study was to investigate the effect of acute SD on autonomic regulation of cardiac function by determining heart rate recovery (HRR). Twenty-one healthy security officers and nine nurses (mean age 33.25 +/- 8.18) were evaluated. Treadmill exercise test was applied once after a night with regular sleep and once after a night shift in hospital. The HRR was calculated as the reduction in heart rate from peak exercise to the 30th second (HRR30), 1st minute (HRR1), 2nd minute (HRR2), 3rd minute (HRR3), and 5th minute (HRR5). The change in blood pressure (BP) measurements was also determined. Exercise capacity of individuals with SD was significantly lower (10.96 +/- 1.01 vs. 11.71 +/- 1.30 metabolic equivalent task (MET)s; p = 0.002), and peak systolic BP was significantly higher (173.8 +/- 16.3 vs. 166.2 +/- 9.9; p = 0.019). There was a signicant difference in HRR30 (12.74 +/- 6.19 vs. 17.66 +/- 5.46; p = 0.003) and HRR1 (31 +/- 6.49 vs. 36.10 +/- 7.78; p = 0.004). The ratio of these indices to peak HR was also significantly lower with SD (HRR%(30) 8.04 +/- 4.26 vs. 10.19 +/- 3.21; p = 0.025 and HRR%(1): 18.66 +/- 4.43 vs. 20.98 +/- 4.72; p = 0.013). The difference in other indices of HRR was not significant. Our findings suggest that SD blunts cardiovascular autonomic response, and consequences of this relation might be more pronounced in subjects who are exposed to sleeplessness regularly or in subjects with baseline cardiovascular disease.