Atrial electromechanical delay, neutrophil-to-lymphocyte ratio, and echocardiographic changes in patients with acute and stable chronic obstructive pulmonary disease

• Published in: Journal of research in medical sciences 2022-01, Vol.27 (1), p.64-64
• Main Authors: Yilmaz, Abdurrahman, Can, Sema, Perincek, Gokhan, Kahraman, Ferdi
• Format: Article
• Language: English
• Subjects: atrial electromechanical delay; Care and treatment; chronic obstructive pulmonary disease; echocardiography; Electrocardiogram; Electrocardiography; Ethylenediaminetetraacetic acid; Lung diseases; Lymphocytes; Original; prolongation
• ISSN: 1735-1995; 1735-7136
• DOI: 10.4103/jrms.JRMS_176_20

BackgroundAtrial electromechanical delay (AEMD) is the time interval between the beginning of P wave on surface electrocardiography and starting of the late diastolic wave on tissue Doppler imaging. We investigated the prolongation of AEMD, echocardiographic changes, and correlation of these findings with neutrophil-to-lymphocyte ratio (NLR) in patients with chronic obstructive pulmonary disease (COPD). Materials and MethodsThe study consisted of 105 (49 females and 56 males; mean age: 65.1 ± 9) patients with COPD exacerbation and 104 (21 females and 83 males; mean age: 64.8 ± 9.6) stable COPD outpatients. Demographics, body mass index, pulmonary function tests, and transthoracic echocardiography of the patients were evaluated. Echocardiography was performed in the first 6 h for stable COPD outpatients and in the first 24 h for COPD exacerbation patients. Diameters of right ventricle (RV), left ventricle (LV) and left atrium, aortic root diameters, left ventricular ejection fraction (LVEF), Emax, Amax, Emax/Amax, tricuspid annular plane systolic excursion (TAPSE), Ea, Aa, Ea/Aa, Emax/Ea, and tricuspid regurgitation velocity (TRV) were evaluated. AEMD measurements were obtained from lateral/tricuspid, lateral/mitral, and septal annulus from apical four-chamber views with tissue Doppler imaging and corrected for heart rate. Complete blood count including NLR was also assessed. ResultsThe mean age of patients in exacerbation period (65.1 ± 9) was higher than the stable group (64.8 ± 9.6). RV basal and mid diameters (P < 0.001), Amax (P < 0.001), Ea tricuspid (P = 0.040), Aa tricuspid (P < 0.001), TRV, and systolic pulmonary artery pressure (P < 0.001) were higher; TAPSE and tricuspid Emax/Amax (P < 0.001) were significantly lower in patients with COPD exacerbation. LV end-diastolic diameter (P = 0.002) and LVEF (P = 0.005), Emax/Amax mitral (P < 0.001), Ea/Aa mitral (P < 0.001), and Ea/Aa septal (P < 0.001) were significantly lower; Amax mitral (P = 0.002), Aa mitral (P < 0.001), Aa septal (P < 0.001), and systolic motion mitral (P = 0.011) were significantly higher in patients with exacerbation. AEMD lateral/tricuspid (P < 0.001), lateral/mitral (P < 0.001), and septal (P < 0.001) were significantly higher in patients with COPD exacerbation. Neutrophil and lymphocyte count (P < 0.001) and NLR (P = 0.003) were significantly higher in the acute group. A weak correlation of NLR with LV end-diastolic diameter (P = 0.003; r = 0.357), Emax/Ea mitral (P = 0.019; r