UNLABELLED: To examine the impact of acute nicotine consumption echocardiographic examination was performed in 22 healthy subjects (nine women, 13 men, 20 to 50 cigarettes/day over a minimum of five years) without any evidence of organic heart disease (normal 2D and Doppler echo, normal ECG at rest and during exercise) aged 20 to 51 years (mean +/- SD: 37 +/- 9 years) before and after cigarette smoking (0.9 mg nicotine). Left ventricular filling parameters were derived by transmitral pulsed Doppler ultrasound with the flow profile along the mitral valve being characterized by the early diastolic (E-wave) and late diastolic (A-wave) inflow into the left ventricle. The isovolumetric relaxation period was determined by simultaneous M-mode registrations over the aortic and mitral valve. During smoking the early diastolic peak velocity decreased from 56 to 52 cm/s (p less than .01) and the early diastolic flow integral fell from 64 to 56 mm (p less than .01). The A/E ratio of the peak velocities rose from 68 to 82% (p less than .001), the A/E ratio of the flow integrals increased from 46 to 56% (p less than .001) and the atrial contribution to ventricular filling rose from 33 to 36% (p less than .001). Furthermore during cigarette smoking the isovolumetric relaxation period rose from 70 to 77 ms (p less than .001). - CONCLUSION: In healthy subjects cigarette smoking causes an increase of the atrial contribution to ventricular filling and the isovolumetric relaxation period. Thus, acute nicotine consumption significantly impairs the energy-consumpting process of early diastolic relaxation, independently of its role as a risk factor for atherosclerosis.
UNLABELLED: To examine the impact of acute nicotine consumption echocardiographic examination was performed in 22 healthy subjects (nine women, 13 men, 20 to 50 cigarettes/day over a minimum of five years) without any evidence of organic heart disease (normal 2D and Doppler echo, normal ECG at rest and during exercise) aged 20 to 51 years (mean +/- SD: 37 +/- 9 years) before and after cigarette smoking (0.9 mg nicotine). Left ventricular filling parameters were derived by transmitral pulsed Doppler ultrasound with the flow profile along the mitral valve being characterized by the early diastolic (E-wave) and late diastolic (A-wave) inflow into the left ventricle. The isovolumetric relaxation period was determined by simultaneous M-mode registrations over the aortic and mitral valve. During smoking the early diastolic peak velocity decreased from 56 to 52 cm/s (p less than .01) and the early diastolic flow integral fell from 64 to 56 mm (p less than .01). The A/E ratio of the peak velocities rose from 68 to 82% (p less than .001), the A/E ratio of the flow integrals increased from 46 to 56% (p less than .001) and the atrial contribution to ventricular filling rose from 33 to 36% (p less than .001). Furthermore during cigarette smoking the isovolumetric relaxation period rose from 70 to 77 ms (p less than .001). - CONCLUSION: In healthy subjects cigarette smoking causes an increase of the atrial contribution to ventricular filling and the isovolumetric relaxation period. Thus, acute nicotine consumption significantly impairs the energy-consumpting process of early diastolic relaxation, independently of its role as a risk factor for atherosclerosis.
Authors: Abdullah M Alshehri; Ayman M Azoz; Hosam A Shaheen; Yahya A Farrag; Mohie Aldeen A Khalifa; Adel Youssef Journal: J Saudi Heart Assoc Date: 2013-04-06