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(Circulation. 1997;95:31-38.)
© 1997 American Heart Association, Inc.

Articles

Unfavorable Effect of Smoking on the Elastic Properties of the Human Aorta

Christodoulos Stefanadis, MD; Eleftherios Tsiamis, MD; Charalambos Vlachopoulos, MD; Costas Stratos, MD; Konstantinos Toutouzas, MD; Christos Pitsavos, MD; Stelios Marakas, MD; Harisios Boudoulas, MD; Pavlos Toutouzas, MD

the Department of Cardiology, Hippokration Hospital, University of Athens, Greece, and the Department of Cardiology, Ohio State University, Columbus (H.B.).

	Abstract

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Background Smoking is a major risk factor for cardiovascular morbidity and mortality. Because previous studies have shown that smoking affects vasomotor response, we hypothesized that smoking may also acutely alter aortic elastic properties.

Methods and Results We studied 40 male current and long-term smokers who underwent diagnostic cardiac catheterization for chest-pain evaluation. Twenty subjects (age, 48±2 years, mean±SEM) were randomly assigned to smoking and 20 (age, 47±2 years) to sham smoking studies. Aortic elastic properties were studied with the determination of the aortic pressure-diameter relation before smoking, every minute for the first 5 minutes after the initiation of smoking or sham smoking, and every 5 minutes for the following 15 minutes. Instantaneous diameter of the thoracic aorta was measured with a special ultrasonic dimension catheter developed in our laboratory and previously validated. Instantaneous aortic pressure was measured at the same site as was diameter with a Millar micromanometer. Smoking was associated with significant changes in the aortic pressure-diameter relation that denote deterioration of the elastic properties and were maintained during the whole study period: the slope of the pressure-diameter loop became steeper (baseline, 35.43±1.38; minute 1, 45.26±1.65; peak at minute 10, 46.36±1.69 mm Hg/mm; P<.001) and aortic distensibility decreased (baseline, 2.08±0.12; minute 1, 1.60±0.08; nadir at minute 5, 1.54±0.07x10^-6 cm²·dyne^-1; P<.001). In contrast, no changes in aortic elasticity indexes were observed with sham smoking.

Conclusions Smoking is associated with an acute deterioration of aortic elastic properties. This effect of smoking may contribute to the unfavorable consequences of smoking on the cardiovascular system.

Key Words: aorta • arteries • elasticity • hemodynamics • smoking

	Introduction

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Smoking is a major and independent risk factor for cardiovascular morbidity and mortality.^{1 2} Many underlying mechanisms have been proposed for the hazardous effects of smoking, including promotion of atherogenesis, unfavorably changed lipid profile,³ increased blood viscosity, alterations in platelet function and promotion of thrombosis,^{4 5} and enhanced adrenergic activity.⁶ Previous studies have shown that smoking also induces coronary artery vasoconstriction^{7 8 9 10} and affects arterial elastic properties unfavorably, increasing stiffness of both muscular and elastic arteries.^{11 12 13 14}

It is well appreciated today that the aorta not only serves as a conduit but also plays an important role in modulating left ventricular function, coronary blood flow, and arterial function throughout the cardiovascular system.^{15 16 17 18 19 20 21 22 23 24} It follows that any unfavorable effect of smoking on aortic elastic properties will contribute to the adverse effects of smoking on the cardiovascular system. However, the acute effect of smoking on aortic elastic properties has not been defined. A recently introduced method suitable for the determination of the aortic pressure-diameter relation^{25 26} was used in the present study to investigate the acute effect of cigarette smoking on aortic elastic properties.

	Methods

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Study Population
Potential candidates for participation in the study were consecutive male smokers who underwent diagnostic cardiac catheterization for chest-pain evaluation. Patients with left main and 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, 40 male smokers were enrolled in the study. All subjects were current and long-term smokers (1 pack/d for 1 year). Twenty subjects were randomly assigned to smoking studies (smoking group; age, 48±2 years, mean±SEM) and 20 to sham smoking studies (control group; age, 47±2 years). Four patients in each group had angiographically normal coronary arteries, and the remainder had coronary artery disease (luminal stenosis 50% in diameter) in one or two of the major coronary arteries. Cardiovascular agents, including ß-adrenergic blockers, calcium channel blockers, and long-acting nitrates, were withheld for at least 5 half-lives before the study. The study protocol was approved by the institutional ethical committee, and written informed consent was obtained from each patient.

Study Protocol
Study Design
The subjects 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 on aortic elastic properties were performed in the same catheterization session. First, routine coronary arteriography and left ventriculography with nonionic contrast medium were performed. After diagnostic catheterization, the patients were allowed to relax in the supine position. Thirty minutes after the last infusion of contrast medium, baseline hemodynamic measurements were obtained. Thereafter, the subjects of the study group smoked one filtered cigarette containing 1.0 mg nicotine under standardized conditions: every 15 seconds, a puff of 5 seconds was taken, and the whole cigarette had to be smoked within 5 minutes. The subjects in the control group performed a similar pattern of inhalation with one unlit cigarette (sham smoking). Measurements were obtained every minute for the first 5 minutes after the initiation of smoking or sham smoking and every 5 minutes for 15 minutes after the cessation of smoking or sham smoking. Cardiac output was measured by thermodilution at baseline and at minutes 5, 10, and 20 after initiation of smoking or sham smoking.

Measurement of Aortic Diameters and Pressures
Instantaneous aortic diameters and pressures were recorded simultaneously and at the same point of the aorta. This technique has been described in detail recently.^{25 26} Aortic diameters were measured by a Y-shaped intravascular catheter that was developed in our laboratory^{25 26} and uses sonometry for the measurement of diameters. At each tip of the catheter, a piezoelectric crystal (5 MHz, 1 mm in diameter, Crystal Biotech) was attached. The technical characteristics of the device include^{25 26} (1) resolution for assessment of changes in diameter of 10 µm, (2) flat (±5%) frequency response in testing up to 40 Hz, (3) no measurable phase lag, and (4) minimal loading on the aortic wall (0.45 g per arm when the distance between the arms is 1 cm). The catheter for aortic diameter measurements was inserted in the following manner. A long (50-cm) 8F guiding sheath was inserted through a 9F introducer punctured into the right femoral artery and advanced to the proximal descending aorta. Once the catheter tip was in position, the guiding sheath was withdrawn to completely expose the Y-shaped end of the catheter, which allowed the spring-loaded arms to spread apart until they touched the aortic wall. By virtue of their flexibility, once the wires touch the aortic wall, they freely follow its movements during the cardiac cycle (Fig 1).

View larger version (31K): [in this window] [in a new window]   Figure 1. Schematic of study instrumentation. Diameter-measuring device and catheter-tip micromanometer are positioned at thoracic aorta and connected to a mainframe (VF-1). Instantaneous diameter and pressure contours are displayed in real-time mode on a computer monitor. Reproduced with permission.25

Aortic pressures were obtained simultaneously by a 3F catheter-tip micromanometer (model SPC-330, Millar Instruments, Fig 1) inserted through a 5F introductory sheath punctured into the left femoral artery. The catheter-tip micromanometer was advanced retrogradely, and its tip was located minimally below the level of the pair of crystals (Fig 1). Both aortic dimension and pressure catheters were positioned under fluoroscopy. Before the insertion of these catheters, the patient received an intravenous bolus infusion of 100 U/kg heparin and during the procedure, continuous infusion of heparin to maintain activated clotting time of >300 seconds.

Data Acquisition and Processing
A VF-1 mainframe (Crystal Biotech) was fitted with appropriate modules for acquisition of aortic diameters and pressures and ECG. Ultrasonic crystals, pressure micromanometer, and ECG leads were connected to a 5-MHz length-gauge module (LG-510), a dual-pressure module (BP-1), and an ECG module, respectively. Signals of aortic pressure, aortic diameter, and ECG collected by the VF-1 mainframe were displayed simultaneously in a real-time mode on a PC (IBM 486 DX) using a multichannel 12-bit analog-to-digital converter (Data Translation Inc) and commercially available data acquisition software (Dataflow, Crystal Biotech, Fig 1). Signals were digitized every 5 ms. The sensitivity of the LG-510 length-gauge module to which the crystals were connected was 100 mV/mm. The digitized data were stored and later processed by commercially available software (Microsoft Excel for Windows). For aortic pressure and diameter measurements and subsequent calculations, 10 consecutive beats were averaged.

Estimation of Aortic Elastic Properties
Aortic pressure-diameter relation, aortic distensibility, pressure-strain elastic modulus, and radial pulsation were used as indexes of aortic elastic properties.

Aortic pressure-diameter relation
Aortic pressure-diameter loops were obtained in all subjects before, during, and after smoking or sham smoking by plotting of the pressure (ordinate) and the diameter (abscissa) digitized data. Linear regression analysis of pressure versus diameter was performed in each patient separately to determine the slope (ie, the regression coefficient, b, of the regression equation: pressure=+bxdiameter) and the intercept (ie, the of the regression equation) of the regression line.

Aortic distensibility
Aortic distensibility was calculated from the formula^{25 26 27 28 29 30 31 32 33 34} : distensibility=2d/(dxP)x10^-6 cm²·dyne^-1, where d is diastolic aortic diameter, d is systolic-diastolic aortic diameter (pulsatile change in aortic diameter), and P is systolic-diastolic aortic pressure (pulse pressure).

Pressure-strain elastic modulus
Peterson's pressure-strain elastic modulus (E_P) of the aorta was calculated from the formula³⁵ : E_P=(Pxd)/dx10⁶ dyne·cm^-2.

Radial pulsation
Radial pulsation (or pulsation around mean radius) was obtained as one half the total radial excursion (systolic-diastolic) divided by mean radiusx100.³⁵

Analysis of Data and Statistical Analysis
Data are expressed as mean±SEM. For comparison of patient characteristics between the two groups, the unpaired t test was used. For changes during the study within each group, ANOVA was used. A value of P<.05 was considered statistically significant.

	Results

Top Abstract Introduction Methods Results Discussion References

 
Examples of simultaneous recordings of aortic pressure and diameter before and after 5 minutes of smoking or sham smoking are shown in Fig 2. From such recordings, systolic and diastolic aortic pressure, pulse pressure, systolic and diastolic aortic diameters, pulsatile diameter, aortic pressure-diameter relation, aortic distensibility, pressure-strain elastic modulus, and radial pulsation before, during, and after smoking or sham smoking were calculated.

View larger version (19K): [in this window] [in a new window]   Figure 2. Simultaneous recordings of aortic pressure and aortic diameter before and 5 minutes after initiation of smoking or sham smoking in a subject of smoking group (A) and in a subject of control group (B).

Baseline Characteristics
Ages were similar in the two groups. At baseline, hemodynamic and aortic elasticity indexes were not statistically different between the two groups (Table).

View this table: [in this window] [in a new window]   Table 1. Study Population: Baseline Characteristics

Changes After Smoking and Sham Smoking
Heart Rate, Cardiac Function, and Aortic Pressures
Systolic aortic pressures, diastolic aortic pressures, and pulse pressures before, during, and after smoking and sham smoking are shown in Fig 3. Smoking was associated with prompt increments in the mean heart rate, cardiac index, systolic and diastolic aortic pressures, and pulse pressure, predominantly during the first 5 minutes. The mean heart rate increased significantly with smoking (P<.001) and rose from a presmoking value of 68±2 to a maximum of 78±2 bpm at minute 5. Mean cardiac index increased significantly (P<.001) with smoking and rose from a presmoking value of 3.3±0.1 to a maximum of 3.6±0.1 L·min^-1·m^-2 at minute 5. Systemic vascular resistance index did not change with smoking (baseline, 2283±75 versus minute 5, 2311±69 dyne·s·cm^-5·m²; P=NS). The mean systolic aortic pressure increased with smoking (P<.001) and rose from 131.0±3.6 to a maximum of 141.5±4.0 mm Hg at minute 5. Likewise, the mean diastolic aortic pressure increased (P<.001) and rose from 75.7±2.0 to a maximum of 84.0±2.2 mm Hg at minute 5. The mean pulse pressure increased (P=.031) and rose from 55.4±2.2 to a maximum of 59.3±2.7 mm Hg at minute 2. No significant changes in mean heart rate, cardiac index, systemic vascular resistance index, systolic or diastolic aortic pressure, or pulse pressure were associated with sham smoking (Fig 3).

View larger version (22K): [in this window] [in a new window]   Figure 3. Mean±SEM systolic and diastolic aortic pressures and pulse pressure before, during, and after smoking and sham smoking.

Aortic Diameters
The mean systolic and diastolic aortic diameters and pulsatile change in diameter before, during, and after smoking and sham smoking are shown in Fig 4. Systolic aortic diameter did not show significant variations during the study. Diastolic diameter showed a trend, although it was not statistically significant (P=.052), to increase slightly during the first 5 minutes (peak at minute 5, 21.72±0.67 versus baseline, 21.34±0.61 mm), while afterward it showed a gradual return toward presmoking values. No significant changes in systolic and diastolic aortic diameters were associated with sham smoking.

View larger version (24K): [in this window] [in a new window]   Figure 4. Mean±SEM diastolic and systolic aortic diameters and pulsatile change in diameter before, during, and after smoking and sham smoking. Apart from deterioration in aortic elastic properties (see "Discussion"), the decrease in pulsatile change in aortic diameter with smoking may be partially related to increase in heart rate.

Smoking, however, was associated with a significant decrease in pulsatile change in aortic diameter (P<.001). Pulsatile change in diameter decreased significantly the first minute after smoking (from 1.58±0.07 to 1.30±0.05 mm), reached a minimum at minute 4 (1.23±0.05 mm), and remained significantly lower compared with baseline thereafter. No significant changes in pulsatile change in aortic diameter were observed with sham smoking (Fig 4).

Aortic Pressure-Diameter Relation
Aortic pressure-diameter loops were obtained in all patients before, during, and after smoking or sham smoking. Representative examples of aortic pressure-diameter loops are shown in Fig 5. The slopes and the values of intercepts are also shown.

View larger version (24K): [in this window] [in a new window]   Figure 5. Pressure-diameter loops of same cardiac cycles of patients of Fig 2 before and 5 minutes after initiation of smoking (A) and before and 5 minutes after initiation of sham smoking (B). Five minutes after initiation of smoking, loop has a steeper slope, indicating reduced elastic properties compared with baseline (ie, reduced d/P for any given segment of loop), while it has shifted to another hypothetical line of elasticity. Because of counterclockwise rotation of pressure-diameter loop (see "Discussion" and Fig 8 for details), little elevation in diastolic blood pressure results in relatively larger increase in diastolic aortic diameter. Conversely, 5 minutes after sham smoking, loop remains practically unchanged.

From each individual patient slope and intercept value, the mean slopes and the mean values of the intercepts of the pressure-diameter loops before, during, and after smoking and sham smoking were obtained. These parameters are shown in Fig 6. Smoking was associated with a significant increase in the mean slope (P<.001). Slope increased significantly at minute 1 after smoking (from 35.43±1.38 to 45.26±1.65 mm Hg/mm), reached a maximum at minute 10 (46.36±1.69 mm Hg/mm), and remained significantly greater compared with baseline thereafter. Smoking was associated with a significant decrease in the mean intercept (P<.001). Intercept decreased significantly at minute 1 after smoking (from -685.80±38.22 to -905.57±47.50 mm Hg), reached a minimum at minute 5 (-936.97±45.76 mm Hg), and remained significantly lower compared with baseline thereafter. These findings show that the pressure-diameter loop became steeper with smoking (Figs 5A and 6), denoting reduced elastic properties. No significant changes in the slope and the intercept of the pressure-diameter relation were observed with sham smoking (Figs 5B and 6).

View larger version (20K): [in this window] [in a new window]   Figure 6. Mean±SEM slope and intercept before, during, and after smoking and sham smoking.

In all subjects who smoked, shifting of the pressure-diameter loop to another hypothetical line of elasticity (see below, "Discussion") was observed with smoking, whereas no changes were observed with sham smoking.

Aortic Distensibility
The mean aortic distensibility before, during, and after smoking and sham smoking is shown in Fig 7. Smoking was associated with a significant decrease in distensibility (P<.001). Distensibility decreased significantly at minute 1 after smoking (from 2.08±0.12 to 1.60±0.08x10^-6 cm²·dyne^-1), reached a minimum at minute 5 (1.54±0.07x10^-6 cm²·dyne^-1), and remained significantly lower compared with baseline thereafter. No significant changes in distensibility were observed with sham smoking (Fig 7).

View larger version (11K): [in this window] [in a new window]   Figure 7. Mean±SEM aortic distensibility before, during, and after smoking and sham smoking.

Pressure-Strain Elastic Modulus
Smoking was associated with a significant increase in pressure-strain elastic modulus (P<.001). Pressure-strain elastic modulus increased significantly at minute 1 after smoking (from 1.02±0.05 to 1.31±0.06x10⁶ dyne·cm^-2), reached a maximum at minute 5 (1.35±0.06x10⁶ dyne·cm^-2), and remained significantly greater compared with baseline thereafter. No significant changes in pressure-strain elastic modulus were observed with sham smoking.

Radial Pulsation
Smoking was associated with a significant decrease in radial pulsation (P<.001). Radial pulsation decreased significantly at minute 1 after smoking (from 3.6±0.2 to 3.0±0.1%), reached a minimum at minute 4 (2.8±0.1%), and remained significantly lower compared with baseline thereafter. No significant changes in radial pulsation were observed with sham smoking.

	Discussion

Top Abstract Introduction Methods Results Discussion References

 
The present study demonstrates that smoking produced an acute decrease of the elastic properties of the aorta in habitual smokers. This effect of cigarette smoking was maintained for at least 20 minutes.

Smoking and Vasomotor Response
Apart from the several underlying mechanisms proposed for the catastrophic influence of smoking,^{3 4 5 6} an adverse effect on vascular control may play an important role. Previous studies have shown that smoking induces immediate constriction of epicardial coronary arteries and an increase in coronary resistance vessel tone.^{7 8 9 10} Other investigators focused on the study of arterial elastic properties and showed an acute increase of arterial wall stiffness. Kool et al,¹¹ using noninvasive methodology, showed an acute decrease in the distensibility of both the elastic common carotid artery and the muscular brachial artery. Other studies using indirect techniques^{12 13 14} also found transitory increase in stiffness of radial and femoral arteries after smoking.

Smoking and Aortic Elastic Properties
The present study demonstrates that smoking clearly influenced the elastic properties of the aorta. To the best of our knowledge, this is the first report dealing with the acute effect of smoking on aortic elastic properties. A deterioration in aortic elastic properties was observed at minute 1 after the initiation of smoking, and this reduction was still prominent 20 minutes later.

In our study, the slope of the pressure-diameter loop became steeper, indicating that with the same amount of change in distending pressure (ie, pulse pressure), less change in aortic diameter occurred. In addition, aortic distensibility decreased, pressure-strain elastic modulus increased, and radial pulsation decreased. All findings denote deterioration of aortic elastic properties with smoking. The effect of smoking on aortic elastic properties may be secondary to changes in aortic pressure, intrinsic elastic properties of the aorta, or both.

To better define whether the changes in aortic elastic properties were simply related to pressure changes, the aortic pressure-diameter relation was obtained and analyzed. Changes in blood pressure alone lead to passive changes in aortic elastic properties characterized by sliding of the pressure-diameter loop upward or downward along the same hypothetical sigmoid line of elasticity (Fig 8A). Conversely, changes in the intrinsic elastic properties of the vessel lead to active changes in the elastic properties of the vessel characterized by shifting of the pressure-diameter loop either to the left or to the right of the initial hypothetical sigmoid line of elasticity. If this shifting is associated with a counterclockwise rotation of the pressure-diameter loop, then the new hypothetical line of elasticity has a steeper slope, indicating reduced elastic properties (Fig 8B). With regard to our results, diastolic diameter showed a trend to increase with smoking; this increase might be considered a passive phenomenon, because an increase in aortic pressures was observed at the same time. This finding is consistent with previous studies in other elastic-type arteries, such as the carotid artery.¹¹ Conversely, the shift of the pressure-diameter loop in another hypothetical line of elasticity suggested a contribution of an active mechanism in these changes. Therefore, the aorta was at first distended (hence the increase in diastolic diameter) in a passive manner because of elevation in blood pressure. In addition, because of the active stiffening, the aorta was forced to function along a new hypothetical line of deteriorated elasticity, becoming less distensible, as indicated by the steeper slope of the pressure-diameter relationship (ie, reduced d/P for any given segment of the loop). Thus, the deterioration of aortic elastic properties was the net result of the combination of the passive distention of the aorta due to an increase in blood pressure and the active stiffening of the vessel due to elevated muscular tone.

View larger version (10K): [in this window] [in a new window]   Figure 8. A, Passive changes in aortic elastic properties are related to changes in blood pressure alone and characterized by sliding of pressure-diameter loop upward or downward along same hypothetical sigmoid line of elasticity. B, Active changes in elastic properties of vessel are related to changes in intrinsic elastic properties of vessel and characterized by shifting of pressure-diameter loop either to left or to right of initial hypothetical sigmoid line of elasticity. Moreover, if this shifting is associated with a counterclockwise rotation of the pressure-diameter loop, then the new hypothetical line of elasticity has a steeper slope, denoting reduced elastic properties. D indicates diameter; P, pressure.

Of the arterial wall components, the one that is subject to acute and active changes is the smooth muscle. Active stiffening of the vessel due to elevated muscular tone may be partially a result of activation of the sympathetic nervous system.^{6 36} In addition, smoking affects the endothelium-mediated vascular control in clinically healthy subjects.^{37 38} Other pharmacological effects of smoking that may affect aortic tone include inhibition of prostacyclin production by endothelial cells,³⁹ activation of platelets,⁴⁰ and release of vasopressin.⁴¹ Impaired nutrition of the aortic wall may be an additional mechanism affecting smooth muscle cell function. Previous studies from our laboratory^{32 34} showed that interruption of vasa vasorum supply of the aortic wall led to an acute decrease in aortic distensibility. Thus, possible direct vasoconstriction of the vasa vasorum or impairment of their flow due to the increase of blood pressure⁴² with smoking may lead to ischemia of the aortic wall and resultant stiffening of the vessel.

Aortic Elastic Properties: Clinical Implications
Left ventricular function
Aortic elastic properties are an important component of left ventricular afterload, constituting a major determinant of left ventricular power output.^{15 16 17 18} Thus, aortic stiffening with smoking burdens left ventricular performance. This effect may be more important in patients with left ventricular dysfunction or disease states, such as coronary artery disease or hypertension, in which aortic distensibility is already affected.^{19 25 29 30 31 33 43 44}

Myocardial oxygen supply/demand
Cigarette smoking causes an increase in myocardial oxygen demand by increasing heart rate and blood pressure.^{6 7 8 10 11 12 38 45 46} Conversely, it causes a concomitant reduction in supply by direct vasoconstriction in the coronary bed.^{7 8 9 10 45 46} Moreover, decreased aortic distensibility may compromise subendocardial flow.^{19 20 21} Thus, it is conceivable that in habitual smokers, the left ventricle is forced to perform under conditions of increased stress for a long period throughout the day, with a resultant increase in oxygen demand but with a concomitant decrease in supply.

Specific Comments
In the present study, long-term smokers were enrolled; thus, the results can be applied only to this specific population group. Recent studies, however, have shown that passive smoking is associated with dose-related impairment of endothelium-dependent dilatation in healthy adults.⁴⁷ It is our speculation, therefore, that passive smoking may also be an important factor affecting aortic elastic properties.

Conclusions
The present study demonstrates that smoking causes an acute decrease in aortic elastic properties. This decrease becomes evident even at minute 1 after the initiation of smoking, and it is maintained for at least 20 minutes. This acute effect of smoking may be a contributing factor to its deleterious consequences for human health.

	Acknowledgments

 
This study was supported by a grant from the Hellenic Heart Foundation.

	Footnotes

 
Reprint requests to Christodoulos Stefanadis, MD, FACC, FESC, 9 Tepeleniou St, Paleo Psychico, Athens 154 52, Greece.

Received May 20, 1996; revision received August 10, 1996; accepted September 4, 1996.

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