 |
 |
|
Home |
Current Issue |
Past Issues |
In the Clinic |
ACP Journal Club |
CME |
Collections |
Audio/Video |
Mobile |
Subscribe |
Tools |
Help |
ACP Online
|
15 March 1998 | Volume 128 Issue 6 | Pages 426-434
Background: The aorta acts as both a conduit and an elastic buffering chamber that modulates left ventricular function and coronary blood flow. Previous studies have shown that active smoking has unfavorable effects on aortic elasticity.
Objective: To study the association between passive smoking and the elastic properties of the human aorta.
Design: Comparison of nonsmokers during passive smoking studies and smokers during active smoking or sham smoking studies.
Setting: Academic medical center.
Participants: 16 male nonsmokers were assigned to passive smoking studies, and 32 current, long-term, male smokers were randomly assigned to either active smoking (16 patients) or sham smoking (16 patients) studies.
Intervention: All participants underwent diagnostic catheterization. In the passive smoking group, environmental tobacco smoke was vented into an exposure chamber for 5 minutes (mean carbon monoxide level, 30 parts per million). Each participant in the active smoking group smoked one filtered cigarette (1.0 mg of nicotine) under standardized conditions within 5 minutes; each participant in the sham smoking group performed a similar pattern of inhalation with one unlit cigarette.
Measurements: Aortic elastic properties were studied by measuring the aortic pressure-diameter relation before and for 20 minutes after passive, active, or sham smoking. Instantaneous diameter of the thoracic aorta was measured with a high-fidelity ultrasonic dimension catheter. Instantaneous aortic pressure and diameter were measured at the same site.
Results: Both passive and active smoking were associated with changes in the aortic pressure-diameter relation (change in mean distensibility in the passive smoking group, from 2.02 to 1.59 x 10–6 cm2 · dyne–1 [for comparisons of time course between passive and sham smoking groups, P < 0.001]; change in mean distensibility in the active smoking group, from 2.08 to 1.51 x 10–6 cm2 · dyne (–1) [for comparisons of time course between active and sham smoking groups, P < 0.001]). These changes represent decreases of 21% and 27%, respectively. No changes in aortic elasticity were seen in the sham smoking group.
Conclusions: Both passive and active smoking are associated with an acute deterioration in the elastic properties of the aorta. This association between exposure to tobacco smoke and aortic elasticity indicates that aortic function deteriorates during passive or active smoking.
The aorta acts as both a conduit and an elastic buffering chamber. By virtue of its elastic properties, this vessel influences left ventricular performance and coronary blood flow [14-23]. Conceivably, any adverse effect of smoking on aortic performance could compromise left ventricular function and coronary blood flow. Previous studies from our laboratory have shown that aortic elastic properties deteriorate acutely during active smoking [24]. In the current study, we investigated aortic elastic properties during passive smoking by using a high-fidelity method suitable for determining the association between aortic pressure and diameter [24-26].
Potential participants were male patients who underwent diagnostic cardiac catheterization for evaluation of chest pain. Patients with left main-vessel or three-vessel coronary artery disease, arterial hypertension, valvular heart disease, congenital heart disease, left ventricular systolic dysfunction, chronic obstructive pulmonary disease, history of cerebrovascular accident, and diabetes mellitus were excluded from the study. According to these criteria, 16 nonsmokers and 32 current, long-term smokers (
Study Protocol
Design
The participants did not consume caffeine-containing beverages or meals and refrained from smoking for at least 12 hours before the study. Diagnostic cardiac catheterization and studies of aortic performance were performed during the same catheterization session. After diagnostic catheterization, the participants were allowed to relax in the supine position. An exposure chamber was placed over the heads of the persons in the passive smoking group. Thirty minutes after the last infusion of contrast medium, baseline hemodynamic measurements were obtained. For the passive smoking group, environmental tobacco smoke was then vented into the exposure chamber for 5 minutes; an average carbon monoxide level of 30 parts per million was maintained. The exposure chamber was subsequently removed and patients were allowed to inhale smoke-free room air. Carbon monoxide levels were measured by using a portable carbon monoxide analyzer (Model T15, Langan Products, San Francisco, California).
After baseline measurements, the participants in the active smoking group each smoked one filtered cigarette containing 1.0 mg of nicotine under standardized conditions: Every 15 seconds, a puff lasting 5 seconds was taken, and the whole cigarette had to be smoked within 5 minutes. The participants in the sham smoking group performed a similar pattern of inhalation with one unlit cigarette. All variables except cardiac output were measured at baseline and at 1, 2, 3, 4, 5, 10, 15, and 20 minutes after the initiation of passive, active, or sham smoking. Cardiac output was measured by thermodilution at baseline and at 5, 10, and 20 minutes after initiation of passive, active, or sham smoking.
Measurement of Aortic Diameters and Pressures
Instantaneous aortic diameters were measured at the descending thoracic aorta by a Y-shaped intravascular catheter that was developed in our laboratory and uses sonometry to measure diameter (Figure 1). Aortic pressures were obtained simultaneously at the same point of the aorta by a 3-French catheter-tip micromanometer (Model SPC-330, Millar Instruments, Houston, Texas), as described elsewhere [24-26]. ARTICLE
Unfavorable Effects of Passive Smoking on Aortic Function in Men
Among other underlying mechanisms, tobacco smoke's effect on the mechanical properties of the arterial wall may play an important role in its catastrophic cardiovascular effects. Previous studies have shown that active smoking influences endothelium-mediated vascular control [1-3], induces coronary artery vasoconstriction [4-7], and increases the stiffness of both muscular and elastic arteries [8-11]. Other investigators have demonstrated that passive smoking is associated with dose-related impairment of endothelium-dependent dilatation and with coronary artery vasoconstriction [12, 13].
Methods
Top
Methods
Results
Discussion
Author & Article Info
References
Study Group
1 pack per day for 1 year) were enrolled in the study. The nonsmokers were assigned to passive smoking studies, and the smokers were randomly assigned to either active (16 patients) or sham (16 patients) smoking studies. Cardiovascular agents were withheld for at least five half-lives before the study. The institutional ethical committee approved the study protocol, and each patient provided written informed consent.
|
Data Acquisition
A VF-1 mainframe (Crystal Biotech, Hopkinton, Massachusetts) was fitted with appropriate modules for measuring aortic diameter and pressure and acquiring an electrocardiogram. Signals were digitized every 5 milliseconds. The digitized data were stored and processed by using Microsoft Excel software (Redmond, Washington).
Estimation of Aortic Elastic Properties and Pressure-Diameter Relation
The slope of the pressure-diameter loop and aortic distensibility were used as measures of aortic elasticity [24-31].
Statistical Analysis
Slope of the Pressure-Diameter Loop
The aortic pressure-diameter loop is derived by plotting digitized data for the pressure (ordinate) and the diameter (abscissa) during a single cardiac cycle (Figure 2). The line of this plot during cardiac systole is not identical to the line during cardiac diastole because diameter lags behind pressure as a result of the viscoelastic nature of the aortic wall. Thus, this plot assumes the shape of a clockwise hysteretic loop, the ascending portion of which corresponds to systole and the descending portion of which corresponds to diastole. Multiple loops were obtained for all participants during the study. To characterize the loop, linear regression analysis of pressure versus diameter was done separately in each loop to determine the slope (that is, the regression coefficient b of the following regression equation: pressure = 
+ b x diameter) of the regression line. The slope of this regression line (DeltaP/DeltaD) is an index of aortic elasticity because it gives an inverse measure of the changes in aortic diameter that occur during the cardiac cycle as a response to the changes in distending pressure. With a given change in aortic pressure, a vessel with deteriorated elastic properties responds with a relatively small change in aortic diameter (thus, the slope of the pressure-diameter regression line will be high). In contrast, with a given change in aortic pressure, a vessel with improved elastic properties responds with a relatively large change in aortic diameter (thus, the slope of the pressure-diameter regression line will be low).
|
The pressure-diameter loop operates along a hypothetical line of elasticity. Shifting of the pressure-diameter loop to a different hypothetical line of elasticity provides valuable information on the mechanisms involved in the changes in aortic elastic properties (Figure 3).
|
Aortic Distensibility
Aortic distensibility was calculated from the following formula: Distensibility = 2Deltad/(d x DeltaP) x 10–6 cm2 · dyne–1, where d is diastolic aortic diameter, Deltad is the difference between the systolic and diastolic aortic diameters (pulsatile change in aortic diameter), and DeltaP is the difference between the systolic and diastolic aortic pressures (pulse pressure).
Large distensibility values represent improved aortic elastic properties, and small values represent deteriorated properties.
Data Analysis
To obtain individual patient values of aortic pressure and diameter and derived variables at every time point, as well as values of the slope of the pressure-diameter loop regression line, analyses were done on 10 consecutive heartbeats and results were averaged. No values were missing for any variable at any time point. Data are expressed as the mean ±SD. Repeated-measures analysis of variance (averaged F) was used to detect statistically significant changes in variables within the groups (passive, active, and sham smoking) during the study period, to compare these variables between the passive and sham smoking groups and between the active and sham smoking groups, and to determine whether the time course of these variables differed between the passive and sham smoking groups and between the active and sham smoking groups. To test the univariate homogeneity of variance between the passive and sham smoking groups and between the active and sham smoking groups, the Cochran and Bartlett-Box tests were used. The Box M test was used to assess the equality of the variance-covariance matrices. Greenhouse-Geisser 
correction was used in the repeated-measures analysis of variance when the Box M test was significant [32]. Normality assumptions, tested by using the Kolmogorov-Smirnoff one-sample test and by calculating the ratio of skewness to the SE of skewness of the sample distribution, were satisfied. P values less than 0.05 were considered statistically significant. Data analysis was done with SPS software, version 7.0 (Chicago, Illinois).
Results
|
|---|
|
TopMethodsResultsDiscussionAuthor & Article InfoReferences |
|---|
Three participants in the passive smoking group, three in the active smoking group, and four in the sham smoking group had angiographically normal coronary arteries; the remaining participants had coronary artery disease. Age, baseline hemodynamic measures, and baseline aortic elasticity measures in the three groups are shown in Table 1.
|
Changes after Passive Smoking
Heart Rate, Cardiac Function, and Aortic Pressures
Passive smoking was associated with prompt increments in the mean heart rate; cardiac index; and systolic, diastolic, and pulse pressures. Most of these increments occurred during the first 5 minutes. The mean heart rate and cardiac index increased over time in the passive smoking group (peaks at 5 minutes, 76 beats/min [P < 0.001] and 3.6 L/min · m–2 [P = 0.001]; Table 2) and remained the same with sham smoking (P > 0.2 for both variables). These variables were similar in the passive and sham smoking groups (P = 0.2 for heart rate and P = 0.24 for cardiac index), but their time course differed between the two groups (P < 0.001 for heart rate and P = 0.002 for cardiac index). In both the passive and the sham smoking group, the systemic vascular resistance index did not change with time (P > 0.2 for both comparisons [Table 2]). This variable and its time course were similar in the passive and sham smoking groups (P > 0.2 for both variables).
|
The mean systolic and diastolic aortic pressures increased with passive smoking over time (peak at 4 minutes, 145.8 mm Hg for systolic pressure and 83.7 mm Hg for diastolic pressure; P < 0.001 for both variables [Figure 4 and Table 2]) and remained the same with sham smoking (P > 0.2 for both variables). Moreover, although the mean systolic and diastolic pressures were similar in the two groups (P = 0.1 for systolic pressure and P > 0.2 for diastolic pressure), both variables increased more rapidly in the passive smoking group (P < 0.001 for both variables). The mean pulse pressure increased over time in the passive smoking group (peak at 4 minutes, 62.1 mm Hg; P = 0.005 [Table 2]) and remained the same in the sham smoking group (P > 0.2). Although this variable was similar in the passive and sham smoking groups (P = 0.2), it increased more rapidly in the passive smoking group (P = 0.004).
|
Aortic Diameters
The mean systolic and diastolic aortic diameters during the study are shown in Figure 5. Both diameters increased with passive smoking over time (peak at 4 minutes, 23.98 mm for systolic diameter [P = 0.04] and 22.53 mm for diastolic diameter [P = 0.001]; Table 2) and remained the same with sham smoking (systolic diameter, P > 0.2; diastolic diameter, P = 0.2). Although these variables were similar in the passive and sham smoking groups (P > 0.2 for systolic and diastolic), the time course of diastolic diameter differed in these groups (P = 0.01) and the difference in the time course of systolic diameter was marginally insignificant (P = 0.06). Passive smoking was associated with a decrease in pulsatile change in aortic diameter over time (minimum, 1.43 mm at 5 minutes; P = 0.002 [Table 2]); in the sham smoking group, the pulsatile change remained the same (P > 0.2). This variable was similar in the passive and sham smoking groups (P = 0.2) but decreased more rapidly in the passive smoking group (P = 0.03). The clinical significance of the changes in aortic diameter seen with passive smoking can only be inferred by their contribution to the changes in aortic elasticity indexes described later in this article and by explanations of the mechanisms involved in these changes.
|
Aortic Pressure-Diameter Relation
The values of the slope of the aortic pressure-diameter relation (slope of the pressure diameter loops [Figure 2]) averaged over time were higher in the passive smoking group than in the sham smoking group (P = 0.02 [Table 2]), indicating reduced elastic properties in the passive smoking group. Passive smoking was also associated with an increase in the average slope of the aortic pressure-diameter relation over time (P < 0.001), a finding that suggests reduced elastic properties. In contrast, the slope remained the same in the sham smoking group (P > 0.2). Thus, the average change in diameter per unit change in pressure decreased in the passive smoking group from 0.029 (1/34.83 [that is, 1/slope]) to a minimum of 0.022 (1/44.86) at 4 minutes of passive smoking (22% decrease); the diameter also remained lower compared with the baseline diameter (data not shown). In addition, the mean slope increased more rapidly in the passive smoking group than in the sham smoking group (P < 0.001).
Figure 2 shows the pressure-diameter loops in the passive smoking group; these loops are not indicative of the group's mean changes in variables but were selected to illustrate loop behavior. The pressure-diameter loop shifted to another hypothetical line of elasticity (Figure 3). Similar shifting of the pressure-diameter loop to another hypothetical line of elasticity was seen in all participants in the passive smoking group. In contrast, the pressure-diameter loop did not shift in the sham smoking group (Figure 2).
Aortic Distensibility
The values of distensibility, averaged over time, were lower in the passive smoking group than in the sham smoking group (P = 0.04 [Figure 6 and Table 2]). Although average distensibility decreased over time in the passive smoking group (from 2.02 to a minimum of 1.59 x 10–6 cm2 · dyne–1 at 4 minutes [21% decrease]; P < 0.001), indicating reduction of aortic elastic properties, it remained the same in the sham smoking group (P > 0.2). Moreover, mean distensibility decreased more rapidly in the passive smoking group than in the sham smoking group (P < 0.001).
|
Changes after Active Smoking
Active smoking was associated with prompt increments in mean heart rate, cardiac index, and systolic and diastolic aortic pressures. Most of these increments were seen during the first 5 minutes of smoking. Figure 4 shows the mean systolic and diastolic aortic pressures during the study. Over time, mean heart rate (P < 0.001), cardiac index (P < 0.001), systolic blood pressure (P = 0.001), and diastolic blood pressure (P < 0.001) increased with active smoking (Table 2). These variables were similar in the active and sham smoking groups (heart rate, P = 0.1; cardiac index, P > 0.2; systolic pressure, P > 0.2; diastolic pressure, P > 0.2); however, the time course of these variables differed between the two groups (P < 0.001 for heart rate, cardiac index, and diastolic pressure; P = 0.001 for systolic pressure). Mean systemic vascular resistance index, pulse pressure, and systolic and diastolic diameters did not show statistically significant differences for all tests (for P values, see Table 2). The mean systolic and diastolic aortic diameters during the study are shown in Figure 5. Mean pulsatile change in aortic diameter decreased over time (P < 0.001; Table 2). This variable differed between the active and sham smoking groups (P < 0.001) and decreased more rapidly in the active smoking group than in the sham smoking group (P < 0.001).
The mean slope of the pressure-diameter relation and aortic distensibility (Figure 6) changed with active smoking over time; this finding suggests deterioration of aortic elastic properties (P < 0.001 for both comparisons [Table 2]). These variables differed between the active and sham smoking groups (slope, P < 0.001; distensibility, P = 0.003). Moreover, these variables changed more rapidly in the active smoking group than in the passive smoking group (P < 0.001 for both comparisons). In all participants in the active smoking group, the pressure-diameter loop shifted to another hypothetical line of elasticity (Figure 2).
Discussion
|
|---|
|
TopMethodsResultsDiscussionAuthor & Article InfoReferences |
|---|
Smoking and Arterial Mechanical Properties
Coronary and Large Arteries
The effect of cigarette smoking on vascular control may contribute to the many unfavorable health consequences of smoking. Active smoking causes immediate constriction of epicardial coronary arteries and increases coronary resistance vessel tone [4-7]. Moreover, it affects endothelium-mediated vascular control in clinically healthy persons [1-3]. Other investigators [8] have shown an acute deterioration of the mechanical properties of both the elastic common carotid artery and the muscular brachial artery after active smoking; a transitory increase in stiffness of radial and femoral arteries has also been shown [9-11]. In addition, passive smoking has been associated with dose-related impairment of endothelium-dependent dilatation in healthy adults and with mild coronary artery vasoconstriction in nonsmoking adults [12, 13].
Aorta
By showing that passive smoking has a similar unfavorable effect on aortic elastic properties, our current study extends the findings from our previous studies that have shown an acute deterioration in the elastic properties of the human aorta with active smoking [24]. Behavior of the pressure-diameter relation provides valuable information about the mechanisms involved in these changes. Estimation of aortic elastic properties is based on the expansion of aortic diameter in response to distending pressure. This relation is essentially linear: The greater the increase in distending pressure (from diastolic to systolic pressure), the greater the change in aortic diameter (from diastolic to systolic diameter); the pressure-diameter loop operates on the linear part of a hypothetical line of elasticity (Figure 3). Beyond a certain point, however, this relation is no longer linear: The hypothetical line of elasticity assumes a steeper slope, and larger changes in distending pressure lead to relatively smaller changes in aortic diameter (reduced deltaD/deltaP [inverse slope]). If the intrinsic properties of the aortic wall do not change, changes in blood pressure alone (which are called passive changes in aortic elastic properties) are characterized by the sliding of the pressure-diameter loop upward or downward along the same hypothetical line of elasticity. On the other hand, changes of the intrinsic aortic elastic properties (which are called active changes in the elastic properties of the vessel) are characterized by shifting of the pressure-diameter loop to the left or right of the initial hypothetical line of elasticity. Thus, the pressure-diameter loop operates on a different line of elasticity that has a steeper slope if the intrinsic elastic properties of the vessel have deteriorated [24-2629, 33, 34]. With respect to our findings for passive smoking, the aorta was distended at first (hence the increase in systolic and diastolic diameter) because of the elevation in blood pressure (passive change); this finding is consistent with those of previous studies of active smoking in other elastic-type arteries, such as the carotid artery [8]. Moreover, the shift of the pressure-diameter loop in another hypothetical line of [deteriorated, as indicated by the steeper slope] elasticity with passive or active smoking suggested the contribution of an active mechanism in these changes. Thus, the deterioration of aortic elastic properties was the net effect of the combination of two different mechanisms: 1) the passive distention of the aorta due to an increase in blood pressure and 2) the active stiffening of the vessel due to elevated muscular tone, in response to both passive and active smoking.
Smooth-muscle cells are the arterial-wall components that are subject to acute and active changes. Both active and passive smoking affect endothelium-mediated vascular control in clinically healthy persons [1-3, 12]. Active stiffening of the vessel caused by elevated muscular tone may be related to activation of the sympathetic nervous system [35, 36]. Other pharmacologic effects of active or passive smoking that may affect aortic tone include inhibition of prostacyclin production by endothelial cells [37], activation of platelets [38], and release of vasopressin [39]. Smooth-muscle cell function may also be affected by impaired nutrition of the aortic wall because of possible direct vasoconstriction of the vasa vasorum or impaired flow due to the increase in blood pressure [31].
Clinical Implications
Heart disease is an important consequence of exposure to environmental tobacco smoke. The unfavorable effects of passive smoking on aortic function may have important clinical implications, particularly through the resulting compromised performance of the left ventricle and disturbance in the balance of myocardial supply and demand. The potential applicability to large populations and the considerable duration of these effects throughout the day further stress the clinical significance of our findings.
Left Ventricular Performance
Aortic elastic properties are an important component of left ventricular afterload and constitute a major determinant of left ventricular power output [14-17]. Thus, passive smoking negatively affects left ventricular performance by stiffening the aorta. The importance of this influence may be more prominent in patients with left ventricular dysfunction or disease states, such as coronary artery disease or hypertension, in which aortic distensibility is already affected [18, 25-3040, 41].
Myocardial Oxygen: Supply and Demand
Exposure to tobacco smoke increases myocardial oxygen demand [2, 4, 5, 7-935, 42-45]. It also concomitantly reduces supply by causing direct vasoconstriction in the coronary bed [4-713, 44, 45]. Moreover, as our current findings indicate, coronary perfusion may be compromised with smoking because of an additional mechanism: Deterioration of aortic elastic properties adversely influences coronary flow [18-20]. It is conceivable that, when exposed to tobacco smoke, the left ventricle is forced to function under the deleterious combination of increased oxygen demand and decreased oxygen supply for a considerable period during the day.
Study Limitations
Both passive and active smoking caused an increase in heart rate and cardiac output. These changes may have contributed to the deterioration of aortic elastic properties and may represent an indirect mechanism by which exposure to tobacco smoke influences aortic elasticity. Several additional limitations of study deserve mention. All participants were men, most of whom had coronary artery disease. Thus, we can only speculate about whether aortic function in other groups, such as women or persons without coronary artery disease, responds similarly to tobacco smoke exposure. In addition, the aorta becomes stiffer with advancing age [25, 34]. It is reasonable to speculate that our findings may be applicable to populations older than the one that we studied. However, these findings may be more prominent in younger populations, especially children, in which a more elastic aorta has the "reserve" to deteriorate; an aorta stiffened by age may not have this reserve.
Conclusions
We show that both passive and active smoking are associated with an acute deterioration in aortic elastic properties. This change becomes evident soon after the initiation of passive or active smoking and is maintained for at least 20 minutes. This association between exposure to tobacco smoke and aortic elasticity indicates that aortic function deteriorates during passive or active smoking.
Drs. Vlachopoulos, Tsiamis, Diamantopoulos, Toutouzas, Giatrakos, Vaina, Tsekoura, and Toutouzas: Department of Cardiology, Athens Medical School, Hippokration Hospital, 114 Vassilissis Sophias Avenue, Athens 11527, Greece.
Author and Article Information
|
|---|
|
TopMethodsResultsDiscussionAuthor & Article InfoReferences |
|---|
References
|
|---|
|
TopMethodsResultsDiscussionAuthor & Article InfoReferences |
|---|
1. Celermajer DS, Sorensen KE, Georgakopoulos D, Bull C, Thomas O, Robinson J, et al. Cigarette smoking is associated with dose-related and potentially reversible impairment of endothelium-dependent dilation in healthy young adults. Circulation. 1993; 88:2149-55.
2. Kiowski W, Linder L, Stoschitzky K, Pfisterer M, Burckhardt D, Burkart F, et al. Diminished vascular response to inhibition of endothelium-derived nitric oxide and enhanced vasoconstriction to exogenously administered endothelin-1 in clinically healthy smokers. Circulation. 1994; 90:27-34.
3. Lekakis J, Papamichael C, Vemmos C, Nanas J, Kontoyannis D, Stamatelopoulos S, et al. Effect of acute cigarette smoking on endothelium-dependent brachial artery dilatation in healthy individuals. Am J Cardiol. 1997; 79:529-31.
4. Quillen JE, Rossen JD, Oskarsson HJ, Minor RL Jr, Lopez AG, Winninford MD. Acute effect of cigarette smoking on the coronary circulation: constriction of epicardial and resistance vessels. J Am Coll Cardiol. 1993; 22:642-7.
5. Moliterno DJ, Willard JE, Lange RA, Negus BH, Boehrer JD, Glamann DB, et al. Coronary artery vasoconstriction induced by cocaine, cigarette smoking, or both. N Engl J Med. 1994; 330:454-9.
6. Maouad J, Fernandez F, Hebert JL, Zamani K, Barrillon A, Gay J. Cigarette smoking during coronary angiography: diffuse or focal narrowing (spasm) of the coronary arteries in 13 patients with angina at rest and normal coronary arteriograms. Cathet Cardiovasc Diagn. 1986; 12:366-75.
7. Moreyra AE, Lacy CR, Wilson AC, Kumar A, Kostis JB. Arterial blood nicotine concentration and coronary vasoconstrictive effect of low-nicotine cigarette smoking. Am Heart J. 1992; 124:392-7.
8. Kool MJ, Hoeks AP, Struijker Boudier HA, Reneman RS, Van Bortel LM. Short- and long-term effects of smoking on arterial wall properties in habitual smokers. J Am Coll Cardiol. 1993; 22:1881-6.
9. Caro CG, Lever MJ, Parker KH, Fish PJ. Effect of cigarette smoking on the pattern of arterial blood flow: possible insight into mechanisms underlying the development of atherosclerosis. Lancet. 1987; 4:11-3.
10. Berlin I, Cournot A, Renout P, Duchier J, Safar M. Peripheral haemodynamic effects of smoking in habitual smokers. A methodological study. Eur J Clin Pharmacol. 1990; 38:57-60.
11. Giannattasio C, Mangoni AA, Stella ML, Carugo S, Grassi G, Mancia G. Acute effects of smoking on radial artery compliance in humans. J Hypertens. 1994; 12:691-6.
12. Celermajer DS, Adams MR, Clarkson P, Robinson J, McCredie R, Donald A, et al. Passive smoking and impaired endothelium-dependent arterial dilatation in healthy young adults. N Engl J Med. 1996; 334:150-4.
13. Brown RE, Nasher PJ Jr, Rossen JD, Winniford MD. Passive exposure to environmental tobacco smoke causes coronary vasoconstriction in humans [Abstract]. Circulation. 1993; 88(Suppl):l-260.
14. Urschel CW, Covell JW, Sonnenblick EH, Ross J Jr, Braunwald E. Effects of decreased aortic compliance on performance of the left ventricle. Am J Physiol. 1968; 214:298-304.
15. Murgo JP, Westerhof N, Giolma JP, Altobelli SA. Aortic input impedance in normal man: relationship to pressure wave forms. Circulation. 1980; 62:105-16.
16. Binkley PF, Boudoulas H. Measurement of myocardial inotropy. In: Leier CV, ed. Cardiotonic Drugs: A Clinical Review. New York: Marcel Dekker; 1991:37-41.
17. Kelly RP, Tunin R, Kass DA. Effect of reduced aortic compliance in cardiac efficiency and contractile function of in situ canine left ventricle. Circ Res. 1992; 71:490-502.
18. Bogren HG, Mohiaddin RH, Klipstein RK, Firmin DN, Underwood RS, Rees SR, et al. The function of the aorta in ischemic heart disease: a magnetic resonance and angiographic study of aortic compliance and blood flow patterns. Am Heart J. 1989; 118:234-7.
19. Watanabe H, Ohtsuka S, Kakihana M, Sugishita Y. Coronary circulation in dogs with an experimental decrease in aortic compliance. J Am Coll Cardiol. 1993; 21:1497-506.
20. Ohtsuka S, Kakihana M, Watanabe H, Sugishita Y. Chronically decreased aortic distensibility causes deterioration of coronary perfusion during increased left ventricular contraction. J Am Coll Cardiol. 1994; 24:1406-14.
21. Nichols WW, O'Rourke MF. Wave reflections. In: Nichols WW, O'Rourke MF, eds. McDonald's Blood Flow in Arteries. 3d ed. London: Edward Arnold; 1990:251-69.
22. Boudoulas H, Wooley CF. Aortic function. In: Boudoulas H, Toutouzas PK, Wooley CF, eds. Functional Abnormalities of the Aorta. Armonk, NY: Futura; 1996:3-36.
23. Belz GG. Elastic properties and Windkessel function of the human aorta. Cardiovasc Drugs Ther. 1995; 9:73-83.
24. Stefanadis C, Tsiamis E, Vlachopoulos C, Stratos C, Toutouzas K, Pitsavos C, et al. Unfavorable effect of smoking on the elastic properties of the human aorta. Circulation. 1997; 95:31-8.
25. Stefanadis C, Stratos C, Vlachopoulos C, Marakas S, Boudoulas H, Kallikazaros I, et al. Pressure-diameter relationship of the human aorta. A new method of determination by the application of a special ultrasonic dimension catheter. Circulation. 1995; 92:2210-9.
26. Stefanadis C, Dernellis J, Vlachopoulos C, Tsioufis C, Tsiamis E, Toutouzas K, et al. Aortic function in arterial hypertension determined by pressure-diameter relation: effects of diltiazem. Circulation. 1997; 96:1853-8.
27. Stefanadis C, Wooley CF, Bush CA, Kolibash AJ, Boudoulas H. Aortic distensibility abnormalities in coronary artery disease. Am J Cardiol. 1987; 59:1300-4.
28. Stefanadis C, Stratos C, Boudoulas H, Kourouklis C, Toutouzas P. Distensibility of the ascending aorta: comparison of invasive and non-invasive techniques in healthy men and in men with coronary artery disease. Eur Heart J. 1990; 11:990-6.
29. Stratos C, Stefanadis C, Kallikazaros I, Boudoulas H, Toutouzas P. Ascending aorta distensibility in hypertensive patients and response to nifedipine administration. Am J Med. 1992; 93:505-12.
30. Stefanadis C, Stratos C, Boudoulas H, Vlachopoulos C, Kallikazaros I, Toutouzas P. Distensibility of the ascending aorta in coronary artery disease and changes after nifedipine administration. Chest. 1994; 105:1017-23.
31. Stefanadis C, Vlachopoulos C, Karayannacos P, Boudoulas H, Stratos C, Fillipides T, et al. Effect of vasa vasorum flow on structure and function of the aorta in experimental animals. Circulation. 1995; 91:2669-78.
32. Everitt B, Hay D. Talking about Statistics. London: Edward Arnold; 1992:85-98.
33. Milnor WR. Hemodynamics. Baltimore: Williams & Wilkins; 1989:58-101.
34. Nichols WW, O'Rourke MF. Properties of the arterial wall. In: Nichols WW, O'Rourke MF, eds. McDonald's Blood Flow in Arteries. 3d ed. London: Edward Arnold; 1990:77-124.
35. Cryer PE, Haymond MW, Santiago JV, Shah SD. Norepinephrine and epinephrine release and adrenergic mediation of smoking-associated hemodynamic and metabolic events. N Engl J Med. 1976; 295:573-7.
36. Winninford MD, Wheelan KR, Kremers MS, Ugolini V, van den Berg E Jr, Niggernann EH, et al. Smoking-induced coronary vasoconstriction in patients with atherosclerotic coronary artery disease: evidence for adrenergically mediated alterations in coronary artery tone. Circulation. 1986; 73:662-7.
37. Nadler JL, Velasco JS, Horton R. Cigarette smoking inhibits prostacyclin formation. Lancet. 1983; 1:1248-50.
38. Davis JW, Hartman CR, Lewis HD Jr, Shelton L, Eigenberg DA, Hassanein KM, et al. Cigarette smoking-induced enhancement of platelet function: lack of prevention by aspirin in men with coronary artery disease. J Lab Clin Med. 1985; 105:479-83.
39. Benowitz NL. Drug therapy. Pharmacologic aspects of cigarette smoking and nicotine addiction. N Engl J Med. 1988; 319:1318-30.
40. Dart AM, Lacombe F, Yeoh JK, Cameron JD, Jennings GL, Laufer E, et al. Aortic distensibility in patients with isolated hypercholesterolaemia, coronary artery disease, or cardiac transplant. Lancet. 1991; 338:270-3.
41. Isnard RN, Pannier BM, Laurent S, London GM, Diebold B, Safar ME. Pulsatile diameter and elastic modulus of the aortic arch in essential hypertension: a noninvasive study. J Am Coll Cardiol. 1989; 13:399-405.
42. Czernin J, Sun K, Brunken R, Bottcher M, Phelps M, Schelbert H. Effect of acute and long-term smoking on myocardial blood flow and flow reserve. Circulation. 1995; 91:2891-7.
43. Deanfield JE, Shea MJ, Wilson RA, Horlock P, de Landsheere CM, Selwyn AP. Direct effects of smoking on the heart: silent ischemic disturbances of coronary flow. Am J Cardiol. 1986; 57:1005-9.
44. Nicod P, Rehr R, Winniford MD, Campbell WB, Firth BG, Hillis LD. Acute systemic and coronary hemodynamic and serologic responses to cigarette smoking in long-term smokers with atherosclerotic coronary artery disease. J Am Coll Cardiol. 1984; 4:964-71.
45. Aronow WS. Effect of passive smoking on angina pectoris. N Engl J Med. 1978; 299:21-4.
This article has been cited by other articles:
|
|
 |
|
  C Vlachopoulos, K Aznaouridis, and C Stefanadis Clinical appraisal of arterial stiffness: the Argonauts in front of the Golden Fleece Heart, November 1, 2006; 92(11): 1544 - 1550. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 X. Guo, M. J. Oldham, M. T. Kleinman, R. F. Phalen, and G. S. Kassab Effect of cigarette smoking on nitric oxide, structural, and mechanical properties of mouse arteries Am J Physiol Heart Circ Physiol, November 1, 2006; 291(5): H2354 - H2361. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. B Panagiotakos and C. Pitsavos Passive smoking's role in diabetes. BMJ, May 6, 2006; 332(7549): 1044 - 1045. [Full Text] [PDF]
|
|
|
|
 |
|
 R. R. Sankatsing, S. W. Fouchier, S. de Haan, B. A. Hutten, E. de Groot, J. J.P. Kastelein, and E. S.G. Stroes Hepatic and Cardiovascular Consequences of Familial Hypobetalipoproteinemia Arterioscler. Thromb. Vasc. Biol., September 1, 2005; 25(9): 1979 - 1984. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Barnoya and S. A. Glantz Cardiovascular Effects of Secondhand Smoke: Nearly as Large as Smoking Circulation, May 24, 2005; 111(20): 2684 - 2698. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Vlachopoulos, F. Kosmopoulou, D. Panagiotakos, N. Ioakeimidis, N. Alexopoulos, C. Pitsavos, and C. Stefanadis Smoking and caffeine have a synergistic detrimental effect on aortic stiffness and wave reflections J. Am. Coll. Cardiol., November 2, 2004; 44(9): 1911 - 1917. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. P Sargent, R. M Shepard, and S. A Glantz Reduced incidence of admissions for myocardial infarction associated with public smoking ban: before and after study BMJ, April 24, 2004; 328(7446): 977 - 980. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Liao, T. Y. Wong, R. Klein, D. Jones, L. Hubbard, and A. R. Sharrett Relationship Between Carotid Artery Stiffness and Retinal Arteriolar Narrowing in Healthy Middle-Aged Persons Stroke, April 1, 2004; 35(4): 837 - 842. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Westerbacka, A. Seppala-Lindroos, and H. Yki-Jarvinen Resistance to Acute Insulin Induced Decreases in Large Artery Stiffness Accompanies the Insulin Resistance Syndrome J. Clin. Endocrinol. Metab., November 1, 2001; 86(11): 5262 - 5268. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y.-p. Sun, B.-q. Zhu, A. E. Browne, R. E. Sievers, J. M. Bekker, K. Chatterjee, W. W. Parmley, and S. A. Glantz Nicotine Does Not Influence Arterial Lipid Deposits in Rabbits Exposed to Second-Hand Smoke Circulation, August 14, 2001; 104(7): 810 - 814. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Nelson The miseries of passive smoiong Human and Experimental Toxicology, February 1, 2001; 20(2): 61 - 83. [Abstract] [PDF]
|
|
|
|
 |
|
 F. A. Lederle, G. R. Johnson, S. E. Wilson, E. P. Chute, R. J. Hye, M. S. Makaroun, G. W. Barone, D. Bandyk, G. L. Moneta, R. G. Makhoul, et al. The Aneurysm Detection and Management Study Screening Program: Validation Cohort and Final Results Arch Intern Med, May 22, 2000; 160(10): 1425 - 1430. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Stefanadis, J. Dernellis, E. Tsiamis, L. Diamantopoulos, A. Michaelides, and P. Toutouzas Assessment of Aortic Line of Elasticity Using Polynomial Regression Analysis Circulation, April 18, 2000; 101(15): 1819 - 1825. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C Stefanadis, J Dernellis, E Tsiamis, C Stratos, L Diamantopoulos, A Michaelides, and P Toutouzas Aortic stiffness as a risk factor for recurrent acute coronary events in patients with ischaemic heart disease Eur. Heart J., March 1, 2000; 21(5): 390 - 396. [Abstract] [PDF]
|
|
|
|
 |
|
 J. J. van der Heijden-Spek, J. A. Staessen, R. H. Fagard, A. P. Hoeks, H. A. S. Boudier, and L. M. Van Bortel Effect of Age on Brachial Artery Wall Properties Differs From the Aorta and Is Gender Dependent : A Population Study Hypertension, February 1, 2000; 35(2): 637 - 642. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 O. T. Raitakari, M. R. Adams, R. J. McCredie, K. A. Griffiths, and D. S. Celermajer Arterial Endothelial Dysfunction Related to Passive Smoking Is Potentially Reversible in Healthy Young Adults Ann Intern Med, April 6, 1999; 130(7): 578 - 581. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Stefanadis, E. Tsiamis, J. Dernellis, and P. Toutouzas Effect of estrogen on aortic function in postmenopausal women Am J Physiol Heart Circ Physiol, February 1, 1999; 276(2): H658 - H662. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Smoking and the Aorta Journal Watch Cardiology, March 31, 1998; 1998(331): 11 - 11. [Full Text]
|
|
|
Article
