Atrial electromechanical delay, neutrophil?to?lymphocyte ratio, and echocardiographic changes in patients with acute and stable chronic obstructive pulmonary disease
Abstract
Background: 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 nvestigated 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 Methods: 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 ransthoracic echocardiography of the patients were evaluated. Echocardiography was performed in the first 6 h for stable COPD utpatients 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. Results: 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), 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 orrelation of NLR with LV end?diastolic diameter (P = 0.003; r = 0.357), Emax/Ea mitral (P = 0.019; r = 0.285), Emax tricuspid (P = 0.045; r = ?0.244), and systolic motion septal (P = 0.003; r = 0.352) was detected in patients with stable COPD. Conclusion: In COPD exacerbation patients, prolongation of AEMD intervals was determined. Acute period of COPD ay trigger atrial dysrhythmias including atrial fibrillation and flutter, multifocal atrial tachycardia, premature beats, and both systolic and diastolic dysfunctions frequently.
Demographics, body mass index, pulmonary function tests, and ransthoracic echocardiography of the patients were evaluated. Echocardiography was performed in the first 6 h for stable COPD utpatients 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. Results: 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), 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 orrelation of NLR with LV end?diastolic diameter (P = 0.003; r = 0.357), Emax/Ea mitral (P = 0.019; r = 0.285), Emax tricuspid (P = 0.045; r = ?0.244), and systolic motion septal (P = 0.003; r = 0.352) was detected in patients with stable COPD. Conclusion: In COPD exacerbation patients, prolongation of AEMD intervals was determined. Acute period of COPD ay trigger atrial dysrhythmias including atrial fibrillation and flutter, multifocal atrial tachycardia, premature beats, and both systolic and diastolic dysfunctions frequently.
Keywords
Atrial electromechanical delay, chronic obstructive pulmonary disease, echocardiography, prolongation