BACKGROUND: Cigarette smoking causes myocardial damage with several mechanisms such as sympathetic nervous system activation, oxidative stress, and endothelial dysfunction. Chronic smokers have an increased risk of morbidity and mortality associated with cardiac events. We aimed to compare the myocardial deformation parameters between chronic smokers and nonsmoker healthy population. METHOD: Forty-two healthy participants (mean age 33.48 ± 10.00 years) without smoking history, 40 participants (mean age 33.98 ± 9.27 years) who had been smoking were prospectively included. In addition to conventional echocardiographic measurements, global longitudinal strain (GLS) of left ventricle (LV), GLS of right ventricle (RV), left atrial strain, and strain rate were analyzed. RESULTS: Smokers had lower peak early diastolic velocity (E) and E/a (early diastolic velocity/late diastolic velocity) ratio in mitral inflow (70.0 ± 13.9 cm/sec vs 77.1 ± 13.3 cm/sec, P = .023; 1.4 ± 0.4 vs 1.7 ± 0.4, P = .011; respectively). Peak early diastolic velocity of mitral valve septal annulus (Em) and Em/Am ratio (peak early diastolic velocity of mitral valve/late diastolic velocity of mitral valve) (11.0 ± 2.1 cm/sec vs 12.1 ± 2.4 cm/sec, P = .023; 1.2 ± 0.3 vs 1.4 ± 0.4, P = .039; respectively) were lower in smokers. LV GLS and RV GLS were significantly lower in smokers (-17.6% ± 3.01 vs -19.2% ± 2.5; P = .013, -18.9% ± 4.4 vs -21.0% ± 4.5; P = .039; respectively). CONCLUSION: Impaired LV and RV deformation were found in chronic smokers in our study. Although there was no statistically significant difference with left ventricular ejection fraction, LV GLS which is the early indicator of LV systolic dysfunction was lower in chronic smokers. The assessment of early harmful effects of smoking on left and right ventricle might be evaluated with speckle tracking echocardiography.
BACKGROUND: Cigarette smoking causes myocardial damage with several mechanisms such as sympathetic nervous system activation, oxidative stress, and endothelial dysfunction. Chronic smokers have an increased risk of morbidity and mortality associated with cardiac events. We aimed to compare the myocardial deformation parameters between chronic smokers and nonsmoker healthy population. METHOD: Forty-two healthy participants (mean age 33.48 ± 10.00 years) without smoking history, 40 participants (mean age 33.98 ± 9.27 years) who had been smoking were prospectively included. In addition to conventional echocardiographic measurements, global longitudinal strain (GLS) of left ventricle (LV), GLS of right ventricle (RV), left atrial strain, and strain rate were analyzed. RESULTS: Smokers had lower peak early diastolic velocity (E) and E/a (early diastolic velocity/late diastolic velocity) ratio in mitral inflow (70.0 ± 13.9 cm/sec vs 77.1 ± 13.3 cm/sec, P = .023; 1.4 ± 0.4 vs 1.7 ± 0.4, P = .011; respectively). Peak early diastolic velocity of mitral valve septal annulus (Em) and Em/Am ratio (peak early diastolic velocity of mitral valve/late diastolic velocity of mitral valve) (11.0 ± 2.1 cm/sec vs 12.1 ± 2.4 cm/sec, P = .023; 1.2 ± 0.3 vs 1.4 ± 0.4, P = .039; respectively) were lower in smokers. LV GLS and RV GLS were significantly lower in smokers (-17.6% ± 3.01 vs -19.2% ± 2.5; P = .013, -18.9% ± 4.4 vs -21.0% ± 4.5; P = .039; respectively). CONCLUSION: Impaired LV and RV deformation were found in chronic smokers in our study. Although there was no statistically significant difference with left ventricular ejection fraction, LV GLS which is the early indicator of LV systolic dysfunction was lower in chronic smokers. The assessment of early harmful effects of smoking on left and right ventricle might be evaluated with speckle tracking echocardiography.