Assessment of atrial electromechanical delay and P wave dispersion in patients with chronic obstructive pulmonary disease.

OBJECTIVE: Chronic obstructive pulmonary disease (COPD) is associated with atrial fibrillation (AF) and reduced forced expiratory volume (FEV1) is an independent predictor for new onset AF. The aims of this study were (1) to analyze the atrial electromechanical delay (AEMD) and P wave dispersion which are two predictors of AF development in patients with COPD and without any cardiovascular disease, and (2) to assess the relationship of those with pulmonary functions as quantified by FEV1 measurements. METHODS: The study included 41 patients with COPD (33 male; mean age: 51 years) and 32 healthy controls. P wave dispersion was calculated as the difference between the maximum and minimum P wave duration in a 12-lead surface electrocardiography (ECG) recording. AEMD, defined as the time interval from the P wave onset on the ECG to the initiation of the late diastolic (Am) wave using a tissue Doppler examination, was measured from the lateral mitral annulus (LAEMD), septal annulus (SAEMD), and tricuspid lateral annulus (TAEMD). RESULTS: P wave dispersion was significantly longer in the COPD group than those in the controls (76±19 ms vs. 45±10 ms; p<0.001). All of the AEMD measurements demonstrated significant prolongation in patients with COPD (LAEMD: 74±9 ms vs. 64±11 ms; SAEMD: 66±10 ms vs. 57±12 ms; and TAEMD: 65±9 ms vs. 46±7 ms; p<0.001 for all). The only correlation with FEV1 was observed in the TAEMD values of the COPD group (rs: -401; p<0.009). CONCLUSION: Both P wave dispersion and AEMD parameters were significantly longer in COPD patients without any established structural or functional cardiac abnormalities, indicating an increased tendency for AF development, beginning from the initial stages of the disease.

Changes in inflammatory mediators as a result of intermittent hypoxia in obstructive sleep apnea syndrome.

BACKGROUND: Inflammation plays an important role in obstructive sleep apnea syndrome (OSAS). The objective of this study was to investigate the relationship of serum C-reactive protein (CRP), pentraxin-3 (PTX-3), procalcitonin (ProCT), interleukin-33 (IL-33) and its soluble receptor ST2 (sST2) with the syndrome severity and to show theirs importance as biomarkers. METHODS: This study comprises a total of 84 identical (sex and age wise) cases. Full-night polysomnography was performed in each patient. OSAS diagnosis and severity index being based on the widely used criterion known as Apnea Hypopnea Index(AHI). Subgroups were as follows: 24(AHI < 5) controls, 28 mild-moderate OSAS(AHI 5-30) and 32 severe OSAS(AHI > 30). RESULTS: PTX-3, IL-33 and sST2 receptors were significantly higher in OSAS groups than the control group (P < .001). However, both CRP and ProCT levels were similar in all subjects. There was a positive correlation between PTX-3 and BMI (r = 0.446; P < .01), ODI (r = 0.555; P < .01), IL-33 (r = 0.348; P = .001) and sST2 (r = 326; P = .002), while there was a negative correlation with minimum SaO2 (r = -0.672; P < .01) in patient group. PTX-3 as a predictor of OSAS showed highest specificity (%91.7) and sensitivity (%91.7) (P < .001). CONCLUSIONS: PTX-3 can be a new indicator reflecting the inflammatory state in patients with OSAS. Since patients with OSAS could have more hypoxic state during sleep, we found higher PTX-3 level in those patients and a negative correlation between PTX-3 and minimum SaO2 , which could explain that PTX-3 levels can increase with the severity of disease. Our results suggest that PTX-3 as an inflammatory biomarker may play a crucial role as an indicator of syndrome severity in OSAS.