Does acute inhalation of nicotine alter left ventricular diastolic function in chronic smokers with coronary artery disease?
Acute cigarette smoking significantly impairs left ventricular diastolic function in patients with coronary artery disease, independent of its atherogenic effects.
In 28 chronic smokers (11 women, 17 men, 53 +/- 10 years old) with coronary artery disease (greater than 75% stenosis), left ventricular (LV) relaxation and filling behavior was assessed before and after inhalation of 0.9 mg nicotine (1 cigarette) by echocardiography. The following acute nicotine-mediated changes were noted (one-sided Wilcoxon test): heart rate increased from 67 to 81 beats/min (p greater than .001); the early diastolic flow (E wave) integral decreased from 49 to 39 mm (p less than .001); the late diastolic flow integral (A wave) increased from 36 to 41 mm (p less than .01). Consecutively, the ratio between E and A wave flow integrals decreased from 1.4 to 0.9 (p less than .001); the atrial contribution to LV filling rose from 42 to 53% (p less than .001); and the isovolumetric relaxation period increased from 89 to 122 ms (p less than .001). In cigarette smokers with coronary artery disease acute administration of nicotine hence causes a shift of mitral blood flow from early (E wave) to late (A wave) diastole and a prolongation of the isovolumetric relaxation time. Thus, cigarette smoking significantly affects LV diastolic function independently of its role as a risk factor for coronary atherosclerosis.
Störk et al. (Sat,) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: