Atrial electromechanical delay, neutrophil-to-lymphocyte ratio, and echocardiographic changes in patients with acute...

Atrial 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).

The 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), E_max, A_max, E_max/A_max, tricuspid annular plane systolic excursion (TAPSE), Ea, Aa, Ea/Aa, E_max/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.

The 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), A_max (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 E_max/A_max (P < 0.001) were significantly lower in patients with COPD exacerbation. LV end-diastolic diameter (P = 0.002) and LVEF (P = 0.005), E_max/A_max mitral (P < 0.001), Ea/Aa mitral (P < 0.001), and Ea/Aa septal (P < 0.001) were significantly lower; A_max 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), E_max/Ea mitral (P = 0.019; r = 0.285), E_max tricuspid (P = 0.045; r = -0.244), and systolic motion septal (P = 0.003; r = 0.352) was detected in patients with stable COPD.

In COPD exacerbation patients, prolongation of AEMD intervals was determined. Acute period of COPD may trigger atrial dysrhythmias including atrial fibrillation and flutter, multifocal atrial tachycardia, premature beats, and both systolic and diastolic dysfunctions frequently.