Background: The aim of this study was to investigate the acute effects of passive smoking on left ventricular (LV) function in healthy volunteers.
Methods: Sixty-one healthy nonsmoking volunteers were enrolled in this study. LV M-mode, two-dimensional, conventional Doppler, and color tissue Doppler echocardiography were performed, and carboxyhemoglobin (COHb) levels were obtained from subjects before and immediately after exposure to passive smoking for 30 min in a smoking room. The differences between baseline and post-smoke exposure measurements of transmitral E and mitral annular Em velocities, heart rate, systolic blood pressure, diastolic blood pressure, and COHb levels were assessed.
Results: Mean COHb levels were statistically higher after exposure. There were no changes in LV systolic function and volumes. LV diastolic function changed significantly immediately after passive smoking. The transmitral E wave (0.89 ± 0.12 vs 0.70 ± 0.14 m/sec, P = .001), the pulmonary venous D wave (0.52 ± 0.12 vs 0.49 ± 0.13 m/sec, P = .01), and the transmitral E/A ratio 1.79 ± 0.48 vs 1.47 ± 0.32, P = .001) decreased, while the transmitral A wave did not change. The mitral annular Em velocity decreased (12.5 ± 2.1 vs 11.7 ± 1.9 cm/sec, P = .001), the Am velocity increased (6.3 ± 2.1 vs 6.8 ± 1.6 cm/sec, P = .001), and the Em/Am ratio decreased (2.28 ± 0.82 vs 1.78 ± 0.42, P = .001). Color Doppler echocardiography determined diastolic impairment in only women, whereas color tissue Doppler echocardiography demonstrated diastolic dysfunction in both genders. Acute deleterious effects of passive smoking on color Doppler echocardiographic parameters were more prominent in women. Change in E was related to changes in heart rate and systolic blood pressure and with COHb levels, while change in Em was related only to COHb levels.
Conclusions: Acute exposure to passive smoking impairs LV diastolic function in healthy volunteers. The mechanism whereby passive smoking affects diastolic function is probably complex; however, carbon monoxide exposure and an increment in COHb level may be among the causes.
Copyright © 2011 American Society of Echocardiography. Published by Mosby, Inc. All rights reserved.