INTRODUCTION: The aim of this study was to evaluate the relationship between cigarette smoking and atrial rhythm disorders with the use of noninvasive methods. METHODS: The study population consisted of 50 healthy volunteer smokers and 40 healthy volunteer non-smokers who had normal echocardiographic parameters and similar sex and age profiles. P-wave dispersion (PWD) was calculated from the 12-lead surface ECG. Left ventricle (LV) end-systolic and end-diastolic diameters, LV ejection fraction, and interatrial and intraatrial electromechanical delay were measured by tissue Doppler imaging and conventional echocardiography. RESULTS: Isovolumetric relaxation time and deceleration time were significantly higher (91.5 ± 11 vs. 82.35 ± 8.6, p < 0.0001; 215.7 ± 37.1 vs. 175.3 ± 17.7, p < 0.0001, respectively), and HDL cholesterol was significantly lower in smokers (39.34 ± 7.5 vs.44.3 ± 8.07, p = 0.003). There were no significant differences between the groups with respect to Sm and Em values, Am value, and E/A and E/Em ratios. However, the Em/Am ratio was significantly lower in smokers (1.28 ± 0.21 vs. 1.44 ± 0.33, p < 0.006). Inter- and intraatrial electromechanical delay were significantly higher in smokers when compared with non-smokers (51.11 ± 1.54 vs. 27.30 ± 3.36, p < 0.0001, and 30.63 ± 3.2 vs. 12.24 ± 3.26, p < 0.0001, respectively). The amount of smoking was strongly correlated with interatrial electromechanical delay (r = 0.567, p < 0.0001), and a significant correlation was detected between PWD and interatrial electromechanical delay (r = 0.653, p = 0.001). CONCLUSION: We have demonstrated the relationship between inter- and intraatrial electromechanical delay and PWD. These parameters may be useful predictive markers for the development of AF in the asymptomatic period before cardiac rhythm disturbances occur. This finding may indicate that smokers have an increased risk of developing atrial rhythm disturbances.
INTRODUCTION: The aim of this study was to evaluate the relationship between cigarette smoking and atrial rhythm disorders with the use of noninvasive methods. METHODS: The study population consisted of 50 healthy volunteer smokers and 40 healthy volunteer non-smokers who had normal echocardiographic parameters and similar sex and age profiles. P-wave dispersion (PWD) was calculated from the 12-lead surface ECG. Left ventricle (LV) end-systolic and end-diastolic diameters, LV ejection fraction, and interatrial and intraatrial electromechanical delay were measured by tissue Doppler imaging and conventional echocardiography. RESULTS: Isovolumetric relaxation time and deceleration time were significantly higher (91.5 ± 11 vs. 82.35 ± 8.6, p < 0.0001; 215.7 ± 37.1 vs. 175.3 ± 17.7, p < 0.0001, respectively), and HDL cholesterol was significantly lower in smokers (39.34 ± 7.5 vs.44.3 ± 8.07, p = 0.003). There were no significant differences between the groups with respect to Sm and Em values, Am value, and E/A and E/Em ratios. However, the Em/Am ratio was significantly lower in smokers (1.28 ± 0.21 vs. 1.44 ± 0.33, p < 0.006). Inter- and intraatrial electromechanical delay were significantly higher in smokers when compared with non-smokers (51.11 ± 1.54 vs. 27.30 ± 3.36, p < 0.0001, and 30.63 ± 3.2 vs. 12.24 ± 3.26, p < 0.0001, respectively). The amount of smoking was strongly correlated with interatrial electromechanical delay (r = 0.567, p < 0.0001), and a significant correlation was detected between PWD and interatrial electromechanical delay (r = 0.653, p = 0.001). CONCLUSION: We have demonstrated the relationship between inter- and intraatrial electromechanical delay and PWD. These parameters may be useful predictive markers for the development of AF in the asymptomatic period before cardiac rhythm disturbances occur. This finding may indicate that smokers have an increased risk of developing atrial rhythm disturbances.
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