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SARI, İBRAHİM

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SARI

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İBRAHİM

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2014 - 20152
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Subject: DYSFUNCTION × Subject: ASSOCIATION ×

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    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.
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    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.