Araştırma Çıktıları

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Subject: search.filters.subject.endothelial dysfunction

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    Evaluation of the effects of chronic biomass fuel smoke exposure on peripheral endothelial functions: an observational study
    (TURKISH SOC CARDIOLOGY, 2011-01-01) Buturak, Ali; Genc, Ahmet; Ulus, Ozden Sila; Duygu, Egemen; Okmen, Arda Sanli; Uyarel, Huseyin
    Objective: To evaluate the effect of chronic biomass fuel (BMF) smoke exposure on peripheral endothelial functions. Methods: Forty-seven healthy subjects who have been exposed to BMF smoke since birth (mean age 31.6 +/- 6.8 years, 21 male) were enrolled in the present cross-sectional observational study. The control group consisted of 32 healthy subjects (mean age 27.9 +/- 4.4 years, 11 male). The carotid intima media thickness (CIMT), flow associated dilatation (FAD \%) and endothelium independent vasodilatation (GTN \%) were assessed in all subjects. The carotid CIMT was defined as the distance between the leading edge of the lumen intima and the media adventitia interfaces. FAD \% was defined as the percentage change in the internal diameter of the brachial artery during reactive hyperemia related to the baseline. GTN \% was defined as the change in diameter in response to the application of 400 mu g of glyceril trinitrate relative to the baseline scan at the end of the fourth minute. Statistical analysis was performed using Student's t-test, Chi-square test and Spearman rank order correlation analysis. Results: The average exposure time of the subjects to biomass fuel smoke was 31.7 +/- 6.6 years. They have been exposed to dung inhalation products meanly 8.3 +/- 1.8 months in a year seasonally. The average daily exposure time was 15.7 +/- 3.3 hours. CIMT values of the two groups were not statistically different from each other (0.47 +/- 0.09 vs. 0.49 +/- 0.06 mm, p=0.138). However, a markedly reduced FAD \% was determined in the study group (5.06 +/- 4.95 vs. 10.7 +/- 4.64, p < 0.001). And GTN \% of the BMF exposed group was significantly lower than the control group (14.41 +/- 8.47 vs. 21.85 +/- 7.87, p < 0.001). Conclusion: FAD \% and GTN \% are markedly reduced in the individuals who have been exposed to BMF smoke inhalation products. Therefore, chronic BMF smoke exposure may be a risk factor for the development of endothelial dysfunction. (Anadolu Kardiyol Derg 2011
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    The Effect of Smoking on Endothelial Dysfunction in Autosomal Dominant Polycystic Kidney Disease Patients with Preserved Renal Function
    (TAYLOR \& FRANCIS LTD, 2021-01-01) Gul, Cuma Bulent; Yildiz, Abdulmecit; Sag, Saim; Oruc, Aysegul; Ersoy, Alparslan; Gullulu, Sumeyye
    Background In autosomal dominant polycystic kidney disease (ADPKD), endothelial dysfunction (ED) is common and occurs much earlier than kidney function impairment. The impact of smoking on ED in ADPKD patients has not been previously studied. The aim of this study was to investigate the potential contribution of smoking habits to ED and subclinical atherosclerosis in these patients. Methods This case-control study included 54 ADPKD patients with preserved renal function and 45 healthy control subjects. ED was assessed using ischemia-induced forearm flow-mediated dilatation (FMD). Carotid intima-media thickness (CIMT) was measured from 10 mm proximal to the right common carotid artery. Clinical demographic characteristics and laboratory data were recorded for the patients and control group. Regression analysis was used to determine independent associations of ED and CIMT. Results FMD was significantly lower in the ADPKD patients (19.5 +/- 5.63 vs. 16.56 +/- 6.41, p = .018). Compared with nonsmoker ADPKD patients, smoker patients had significantly lower FMD values (18.19 +/- 6.52 vs. 13.79 +/- 5.27, p = .013). In multiple regression analysis, age (beta = -0.294, 95\% CI: -0.392: -1.96, p = .001) for FMD and smoking (beta = 1.328, 95\% CI: 0.251, 2.404, p = .017) for CIMT were independent predictors. Conclusions Patients with ADPKD had more impaired endothelial function and subclinical atherosclerosis compared with control subjects. Smoking may increase the risk of subclinical atherosclerosis in ADPKD patients.