Effects of Passive Smoke on Blood Vessels
August 15, 1998
Effects of Passive Smoke on Blood Vessels
ABSTRACT & COMMENTARY
Synopsis: These authors have clearly demonstrated objective evidence of aortic dysfunction occurring with passive cigarette smoking.
Source: Stefandis C, et al. J Am Coll Phys 1998;128:426-434.
Many reported epidemiological studies have clearly demonstrated the untoward clinical effects of active smoking and passive smoke inhalation on the incidence of heart attacks, strokes, and carcinoma of the lung. These catastrophic clinical effects have, at least partially, been attributed to the effects of active smoking on endothelium-mediated vascular control,1-3 to the induction of coronary artery vasoconstriction,4-7 and to the physiologic increases in stiffness of both muscular and elastic artery segments.8-11 Passive smoke exposure has also been demonstrated to be associated with dose-related impairment of vascular dilatation secondary to endothelial abnormalities and with coronary artery vasoconstriction.12,13
By virtue of its elastic properties, the aorta greatly influences left ventricular performance and coronary artery blood flow. Previous studies have demonstrated that aortic elastic properties deteriorate acutely during active smoking,14 but objective abnormalities in aortic function have not been previously demonstrated during passive smoke inhalation. Stefandis and colleagues from the University of Athens carefully studied 48 male smokers; 16 were assigned to passive smoke inhalation studies, and the remainder were randomly assigned to either active smoking or sham smoking studies. All patients underwent diagnostic catheterization-aortic elastic properties were studied by measuring the aortic pressure-diameter relation before and for 20 minutes after passive, active, or sham smoking. Instantaneous diameters of the thoracic aorta were measured with high-fidelity ultrasonic dimension catheters. No changes in aortic elasticity were seen in the sham smoking group. Passive smoking was associated with unfavorable acute deterioration of aortic elastic properties, which occurred promptly after the initiation of passive smoking and was maintained for at least 20 minutes. Active smoking resulted in similar changes, although somewhat more intense than occurred with the passive smoking group.
COMMENT BY HAROLD L. KARPMAN, MD
Symptomatic coronary artery disease (i.e., unstable angina, acute myocardial infarctions, sudden death, etc.) occurs with higher frequency in active cigarette smokers and, in addition, is an important consequence of exposure to environmental tobacco smoke. Obviously, any effect upon aortic function may have important clinical implications because of the increased risk of compromising performance of the left ventricle and by disturbing coronary artery blood flow if aortic dysfunction occurs.
Stefandis et al have clearly demonstrated objective evidence of aortic dysfunction occurring with passive cigarette smoking, adding further support to the growing legislative attempts to control cigarette smoking in the workplace and in areas of public gatherings such as restaurants, airplanes, and office buildings. Knowing that the aorta and the coronary arteries are so significantly affected by passive cigarette smoking lends further support and credence to the legislative measures that are now being taken to control cigarette smoking. In addition, we particularly applaud the current administration's efforts via the Food and Drug Administration to control cigarette smoking in schools since, because of multiple social and peer pressures, students are particularly susceptible to this ghastly habit.
References
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