Abstract
Background
It is generally well-known that smoking has a substantial impact on general health, and cardiovascular health in particular. The purpose of this study was to analyze the effects of different smoking status on the burden and characteristics of coronary artery plaques in Chinese men.
Methods
Our study enrolled 1920 individuals with suspected coronary artery disease undergoing 256-detector-row computed tomography scan after clinical assessment. These study participants were stratified into three groups: never smoker, current smoker, and former smoker, according to their smoking status. Thereafter, the associations of different smoking status with the coronary artery plaques were assessed using both univariable and multivariable logistic regression.
Results
The prevalences of any plaque, significant stenosis and coronary artery calcium score (CACS) ≥ 10 were highest in the current smokers (all p < 0.05). The proportion of calcified plaques was the lowest and the prevalence of non-calcified plaques was the highest in current smokers (p = 0.004). The higher pack-years group had significantly elevated percentages of any plaque, significant stenosis, ≥ 2/LM vessel disease and CACS ≥ 10 than the lower pack-years group (all p < 0.001). The percent of calcified plaques was lower and the percent of non-calcified plaques was higher in the higher (> 20) pack-years group than in the lower pack-years group (≤ 20) (p = 0.024). Current smoking with higher pack-years was the independent risk factor for any plaque, significant stenosis, CACS ≥ 10, non-calcified and mixed plaques (all p < 0.05) after multivariate adjustments.
Conclusions
The current smokers had the most serious burden of coronary artery plaques and the highest percentage of non-calcified plaques. Current smoking with higher pack-years was a significant risk factor for coronary artery plaque burden and non-calcified and mixed plaques.
Keywords: Chinese men, Cigarette smoking, Coronary artery calcium score, Coronary artery plaques, Non-calcified plaques
INTRODUCTION
Smoking is one of the most serious dangers to the overall health of the worldwide population.1 Many previous studies have found a relationship between cigarette smoking and coronary artery disease (CAD).2,3 Smoking is closely related to elevated levels of cholesterol, vascular calcification, platelet aggregation, thrombotic, coronary vasomotor reactivity and inflammation.4-6 A significant positive correlation between smoking dose and the risk of CAD, and smoking as little as one to four cigarettes a day increased the risk of CAD.7 Researches have found that smoking cessation could substantially improve cardiovascular health and reduce health care costs, even in the short term.8,9
Coronary artery angiography (CAG) is the gold standard for diagnosing CAD, but CAG cannot determine the characteristics of plaques. CAG would be difficult to use as a general screening tool in China because of its highly invasive nature, radiation exposure, and cost. However, using the 256-detector-row coronary computed tomography angioplasty (CCTA) technique involves a shorter scanning time, potentially improved image quality, and minimized radiation dose.10 CCTA as a mechanism for general routine health evaluation is not discouraged.11 In fact, CCTA as a screening tool in China for assessing individuals of suspected CAD is the most feasible and effective method to reflect widespread epidemiology and characteristics of CAD.
In the developing world, cigarettes smoking is still increasing rapidly; of the total worldwide smoking population, those living in China approximately account for 33% of all smokers.12 In China, men have higher rates of smoking and smoke more cigarettes per day. The association of cigarette smoking with CAD has been reported in other countries, but those results may be not applicable to a Chinese population. The association has not been sufficiently investigated in China. In this study, we have assessed the association of different smoking status (never, current, former) with the prevalence, severity and characteristic of CAD and coronary artery calcium score (CACS) in adult male patients with suspected CAD undergoing CCTA in China. The purpose of our investigation is to provide further evidence in understanding the effects of current smoking on the progress of CAD, as compared to those who have never smoked and former smokers in China.
METHODS
Study population
This prospective study included consecutive adult males (≥ 18 years of age) in China undergoing CCTA and CACS measurement in our institution from September 2011 to February 2013. CCTA and measurement of CACS were performed when CAD was suspected but not confirmed after clinical assessment (including cardiac symptoms, risk factors, electrocardiogram changes, and a positive stress test). Study participants had to provide detailed information about their smoking status, which included never, current, or former smoker in the study. Never smokers are defined as those participants who never smoked in their lifetime. Current smokers are defined as those participants who smoked every day for the past 30 days. Lastly, former smokers were those who had smoked more than 100 cigarettes in a lifetime but did not currently smoke. Those participants reported the ages of their cigarette smoking onset and cessation.13 Pack-years consumed was calculated with the formula: [years smoked] × [number of cigarette packs consumed per day] (assuming a pack contains 20 cigarettes). We excluded individuals who had known CAD or myocardial infarction, percutaneous coronary intervention or coronary artery bypass grafting, heart failure, severely impaired renal function (glomerular filtration rate < 30 ml/min) or chronic liver disease, active inflammatory disease or autoimmune disease, poor image quality, and insufficient medical records. Finally, 1920 individuals were enrolled. All patients gave written inform consent, and the study was approved by the ethics committee in The First Affiliated Hospital of China Medical University.
Assessment of CAD risk factors
All patients were systematically asked about their demographic information by reliable professionals. Body weight, height, and blood pressure were measured, and body mass index (BMI) was calculated as weight (kg)/height (m)2. Hypertension was defined as a previously established diagnosis and/or antihypertensive medication, systolic blood pressure ≥ 140 mmHg, and diastolic blood pressure ≥ 90 mmHg. Diabetes mellitus was defined as a previously established diagnosis and/or antidiabetic treatment, and fasting glucose ≥ 126 mg/dl. A family history of CAD was defined as a first-degree male relative < 55 years of age, or a first-degree female relative < 65 years of age. Additionally, medication use was recorded in detail.
Total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) were measured after at least a 12-h fasting period within 7 days of CCTA.
Acquisition of images
Computed tomography scans were performed using a 256-detector-row CCTA (Brilliance; Philips Medical System, The Netherlands). Individuals with a heart rate ≥ 75 beats per minute were treated orally with up to 100 mg metoprolol for several hours (except for contraindications of beta-blockers) before CCTA imaging to achieve a higher image quality. First, after a scout radiograph of the chest (lateral and anteroposterior), a noncontrast CACS scan was performed, and the image section thickness was 2.5 mm by triggering at a heart rate depending on the percentage of the R-R interval. The sections were collected from the level of the carina and proceeded to the level of the diaphragm. Thereafter, retrospective electrocardiogram-gated contrast-enhanced CCTA was performed. The CCTA scan was initiated 20 mm above the level of the left main artery to 20 mm below the inferior myocardial apex during a single breath-hold. Depending on the individual’s weight, a bolus of 50-80 ml of iopamidol or iohexol was intravenously injected at 4-5.5 ml/s into the antecubital vein, followed by 50 ml of saline. A standard scan protocol was applied, with 256 × 0.625 mm section collimation, 0.27 s for rotation time, 120 KV tube voltage, and 800-1100 mA tube current. In all scans, electrocardiogram-gate dose modulation was used. The electrocardiograms of individuals were simultaneously collected to allow for retrospective segmental data reconstruction. The images of all individuals were initially reconstructed at 75% of the R-R interval of the cardiac cycle. If motion artifacts were found, reconstruction of additional phases was performed. The best R-R interval image quality was chosen for interpretation. The dose range of radiation for CCTA was estimated to be 10-18 mSv.
Image analysis
All images were analysed separately by two experienced radiologists and one cardiologist who were blinded to the patients’ characteristics. Consensus on interpretation was performed to achieve a final CCTA diagnosis. All scans were evaluated by a three-dimensional workstation (Brilliance; Philips Medical Systems). The CACS was measured using the scoring system previously described by Agatston et al.
The three readers were permitted to use any/all available post-processing image reconstruction algorithms, including two-dimensional axial or three-dimensional maximal intensity projection, multiplanar reformat, cross-sectional analysis, or the volume-rendered technique. A 16-segment coronary artery tree model was used in the analysis of coronary arteries.14 In each coronary segment, plaques were defined as any tissue structure > 1 mm2, which existed either within the coronary artery lumen or was adjacent to the coronary artery lumen, and could be discriminated from surrounding pericardial tissue, epicardial fat, or the vessel lumen itself. For evaluating the degree of stenosis, the coronary lumen was semi-automatically traced at the maximal stenosis site and was compared with the mean value of a proximal and distal reference site. The image quality was evaluated and classified as follows: good, with no artifact; adequate, with the presence of artifacts but feasible for evaluating the degree of stenosis and plaque characteristics; or poor, with the presence of artifacts and not feasible for evaluating the degree of stenosis and plaque characteristics. If an image was graded as poor, the image was not included.
Coronary lesions ≥ 50% were defined as significant stenosis. All detected plaques were classified as calcified, non-calcified, or mixed. The calcified component of a stenosis was defined as a lesion with radiodensity greater than the luminal contrast. The non-calcified component of a stenosis was defined as a lesion with radiodensity greater than that of neighbouring soft tissue and lower than the luminal contrast. Plaques that contained calcified tissue greater than 75% of the plaque area were classified as calcified plaques, less than 25% as non-calcified plaques, and 25-75% as mixed plaques.15
Statistical analysis
Baseline characteristics are expressed as absolute counts and proportions for categorical variables, and as means ± standard deviations for continuous variables. Continuous variables were analysed by analysis of variance and categorical variables were analysed by the χ2 test.
The association of smoking status with coronary atherosclerosis was assessed by the χ2 test. Univariable and multivariable logistic regression were used to assess the association of current smoking, former smoking and never smoker with the significance of stenosis, CACS ≥ 10,16 and plaque characteristics. In multivariable analysis, the adjusted variables included age, BMI, family history of CAD, hypertension, diabetes mellitus, hyperlipidemia, stroke, TC, TG, LDL-C, and HDL-C. All analyses were performed using SPSS 15.0. The level of significance was set at p < 0.05.
RESULTS
Baseline characteristics
Our study involved 1920 male patients who were stratified into three groups according to their smoking status: never smoker (n = 864), current smoker (n = 851), and former smoker (n = 205). Table 1 shows the baseline characteristics of patients. Former smokers were the oldest and current smokers were the youngest (p < 0.001). The other characteristics and medication usage among the three groups were not significantly different.
Table 1. Baseline characteristics of the study population .
| Variables | Never smoker (n = 864) | Current smoker (n = 851) | Former smoker (n = 205) | p value |
| Age (years) | 55.63 ± 12.21 | 52.29 ± 10.31 | 56.76 ± 9.93 | < 0.001 |
| BMI | 25.38 ± 3.34 | 25.09 ± 3.77 | 25.11 ± 3.06 | 0.203 |
| hypertension | 286 (33.1) | 277 (32.5) | 80 (39.0) | 0.200 |
| Diabetes mellitus | 101 (11.7) | 103 (12.1) | 28 (13.7) | 0.739 |
| Family history of CAD | 33 (3.8) | 40 (4.5) | 10 (4.9) | 0.679 |
| Hyperlipidemia | 84 (9.7) | 93 (10.9) | 26 (12.7) | 0.419 |
| stroke | 17 (2.0) | 16 (1.9) | 6 (2.9) | 0.625 |
| LDL-C (mmol/l) | 3.81 ± 0.66 | 2.85 ± 0.77 | 2.79 ± 0.95 | 0.625 |
| HDL-C (mmol/l) | 1.10 ± 0.35 | 1.09 ± 0.29 | 1.06 ± 0.29 | 0.672 |
| TC (mmol/l) | 4.33 ± 1.10 | 4.46 ± 0.93 | 4.36 ± 1.19 | 0.195 |
| TG (mmol/l) | 1.64 ± 1.57 | 1.83 ± 1.49 | 1.57 ± 1.11 | 0.126 |
| History of medication | ||||
| Aspirin | 118 (13.7) | 131 (15.4) | 35 (17.1) | 0.373 |
| Beta blocker | 76 (8.8) | 69 (8.1) | 23 (11.2) | 0.367 |
| CCB | 89 (10.3) | 92 (10.8) | 27 (13.2) | 0.493 |
| ACEI/ARB | 94 (10.9) | 78 (9.2) | 22 (10.7) | 0.476 |
| Statins | 48 (5.6) | 41 (4.8) | 15 (7.3) | 0.355 |
| Antihyperglycemic/insulin | 77 (8.9) | 68 (8.0) | 27 (13.2) | 0.066 |
Values are mean ± standard deviation or n (%).
ACEI, angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker; BMI, body mass index; CAD, coronary artery disease; CCB, calcium channel blocker; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; TC, cholesterol; TG, triglycerides.
The finding of CCTA and CACS
The prevalence, degree, characteristics, and CACS of coronary artery plaques are shown in Table 2. The prevalences of any plaque, significant stenosis and CACS ≥ 10 were highest in the current smokers group (all p < 0.05). The proportion of calcified plaques was the lowest in current smokers and highest in former smokers, and the prevalence of non-calcified plaques was the highest in current smokers and the lowest in former smokers (p = 0.004).
Table 2. The finding of CCTA and CACS .
| Variables | Never smoker (n = 864) | Current smoker (n = 851) | Former smoker (n = 205) | p value |
| Any plaque | 553 (64.0) | 590 (69.3) | 130 (63.4) | 0.043 |
| ≥ 2/lM vessels disease | 374 (43.3) | 411 (48.3) | 95 (46.3) | 0.113 |
| Significant stenosis | 262 (30.3) | 325 (38.2) | 70 (34.1) | 0.003 |
| CACS ≥ 10 | 305 (35.3) | 351 (41.2) | 80 (39.0) | 0.040 |
| The number of all plaques | 2745 | 3232 | 880 | |
| Average numbers of plaques | 3.18 ± 3.16 | 3.80 ± 3.45 | 4.29 ± 4.18 | 0.059 |
| Average number and relative percentage of plaques | 0.004 | |||
| Calcified plaque | 1087 (39.6) | 1179 (36.5) | 369 (41.9) | |
| Non-calcified plaque | 818 (29.8) | 1036 (32.1) | 232 (26.4) | |
| Mixed plaque | 840 (30.6) | 1017 (31.5) | 279 (31.7) |
Values are mean ± standard deviation or n (%).
CACS, coronary artery calcium score; CCTA, coronary computed tomography angioplasty.
The current smokers were further categorized into higher (n = 397, > 20 pack-years) and lower (n = 454, ≤ 20 pack-years), with pack-years groups using the median of pack-years consumed as a cutoff point. The higher pack-years group had significantly higher percentages of any plaque, significant stenosis, ≥ 2/LM vessels disease and CACS ≥ 10 than lower pack-years group (all p < 0.001). The percent of calcified plaques was higher in lower than higher pack-years group, and the percent of non-calcified plaques was higher in higher than lower pack-years group (p = 0.024) (Table 3).
Table 3. The finding of CCTA and CACS in current smoker with lower pack-years group and higher pack-years group .
| Variables | Current smoker with lower pack-year (n = 454, ≤ 20 pack-years) | Current smoker with higher pack-year (n = 397, > 20 pack-years) | p value |
| Any plaque | 277 (61.0) | 313 (78.8) | < 0.001 |
| ≥ 2/lM vessels disease | 191 (42.1) | 219 (55.2) | < 0.001 |
| Significant stenosis | 142 (31.3) | 183 (46.1) | < 0.001 |
| CACS ≥ 10 | 154 (33.9) | 197 (49.6) | < 0.001 |
| The number of all plaques | 1471 | 1761 | |
| Average numbers of plaques | 3.24 ± 3.09 | 4.44 ± 4.21 | 0.071 |
| Average number and relative percentage of plaques | 0.024 | ||
| Calcified plaque | 569 (38.7) | 610 (34.6) | |
| Non-calcified plaque | 440 (29.9) | 596 (33.8) | |
| Mixed plaque | 462 (31.4) | 555 (31.5) |
Values are mean ± Standard deviation or n (%).
Abbreviations are in Table 2.
Univariate and multivariate logistic regression analysis
In univariate and multivariate analyses, smoker with lower pack-years was the significant risk factor for significant stenosis and non-calcified plaques (all p < 0.05); smoker with higher pack-years was the stronger risk factor for any plaque, significant stenosis, CACS ≥ 10, non-calcified and mixed plaques (all p < 0.05). After adjusting, the smoker with higher pack-years was not a significant risk factor for calcified plaques (Table 4).
Table 4. Univariate and multivariate logistic regression models for variables of current smoker and former smoker associated with coronary artery plaque .
| Never smoker (n = 864) | Former smoker (n = 205) | Current smoker with lower pack-year (n = 454, ≤ 20 pack-years) | Current smoker with higher pack-year (n = 397, > 20 pack-years) | |
| OR (95%CI) | OR (95%CI) | OR (95%CI) | OR (95%CI) | |
| Any plaque | ||||
| Univariate | 1 (ref) | 0.885 (0.124-6.325) | 0.238 (0.043-1.314) | 1.382 (1.053-1.576)* |
| Multivariate | 1 (ref) | 1.258 (0.791-2.000) | 0.918 (0.573-1.469) | 1.598 (1.399-1.897)* |
| ≥ 2/LM vessels disease | ||||
| Univariate | 1 (ref) | 0.883 (0.655-1.190) | 1.141 (0.743-1.752) | 0.937 (0.661-1.328) |
| Multivariate | 1 (ref) | 0.589 (0.347-1.000) | 0.769 (0.377-1.569) | 0.702 (0.386-1.276) |
| Significant stenosis | ||||
| Univariate | 1 (ref) | 1.402 (0.537-1.704) | 1.703 (1.498-1.993)* | 1.509 (1.398-1.650)* |
| Multivariate | 1 (ref) | 0.711 (0.448-1.127) | 1.058 (1.042-1.075)* | 1.830 (1.345-2.491)* |
| CACS ≥ 10 | ||||
| Univariate | 1 (ref) | 0.828 (0.623-1.100) | 1.018 (0.682-1.521) | 1.531 (1.025-1.738)* |
| Multivariate | 1 (ref) | 0.984 (0.938-1.031) | 0.592 (0.312-1.124) | 1.071 (1.051-1.093)* |
| Calcified plaque | ||||
| Univariate | 1 (ref) | 1.651 (1.512-1.828)* | 1.050 (0.749-1.471) | 1.565 (1.428-1.746)* |
| Multivariate | 1 (ref) | 0.811 (0.464-1.416) | 0.817 (0.512-1.303) | 1.009 (0.967-1.052) |
| Non-calcified plaque | ||||
| Univariate | 1 (ref) | 0.827 (0.590-1.160) | 1.601 (1.473-1.763)* | 1.629 (1.502-1.864)* |
| Multivariate | 1 (ref) | 0.831 (0.481-1.434) | 1.034 (1.019-1.049)* | 1.363 (1.018-1.826)* |
| Mixed plaque | ||||
| Univariate | 1 (ref) | 0.904 (0.645-1.268) | 0.677 (0.531-1.117) | 1.548 (1.416-1.723)* |
| Multivariate | 1 (ref) | 0.695 (0.397-1.215) | 0.636 (0.400-1.012) | 1.063 (1.046-1.084)* |
* Indicates vs. never smoker p < 0.05. The adjusted variables included age, BMI, family history of CAD, hypertension, diabetes mellitus, hyperlipidemia, stroke, TC, TG, LDL-C, HDL-C. Abbreviations are in Table 1 ,OR, odds ratio.
DISCUSSION
In our study, we have here reported the associations between smoking status and the prevalence, severity, characteristic and CACS of CAD. We found that current smokers suffer the higher incidence of CAD, more advanced lesions and higher CACS compared with never and former smokers. The incidence of calcified plaques was significantly lower and the percentage of non-calcified plaque was remarkably higher in the current smokers. The current smokers with higher pack-years (> 20 pack-years) had a higher percentage of non-calcified plaques, a lower percentage of calcified plaques and more serious coronary artery burden than those with lower pack-years (≤ 20 pack-years). Moreover, the status of current smoker with higher pack-years was the real risk predictor for coronary artery burden, non-calcified and mixed plaques. In total, current smoking increased the burden of coronary artery plaque and produced an effect on plaque characteristics in a dose-dependent manner.
In China, men comprise over 70 percent of the total smoking population. In the study, women have a lower rate of cigarette smoking, so the study population did not include women. Cigarette smokers have a more atherogenic lipid profile than non-smokers, and smokers also have lower levels of HDL-C, higher levels of oxidized LDL and products of lipid peroxidation,17-19 which may be important mechanisms by which smoking promotes atherosclerotic plaques.20 The ARIC study found a significant association between cigarette smoking and LDL-C in predicting CAD events.21 However, the levels of serum lipid were not different in different smoking status in the study, which was consistent with a study of Japanese and Korean men.16 However, this may be relevant to the selection of study population. Since the levels of lipid were no different in the study, it is more helpful to analyze the effect of cigarette smoking on CAD.
In the present study, the coronary artery plaque burdens were the heaviest (including degree and CACS of plaques) in current smokers than never or former smokers. The effect of current smoking was dose-dependent on the burden of CAD, the higher prevalence and CACS, and more serious lesions of coronary artery plaques were in higher pack-years than in the lower pack-years group. This observation was concordant with prior reports as well.7,22,23 We found the prevalence, severity and CACS of CAD were significantly lower in former rather than current smokers in the study. Some researches had reported the adverse effects of cigarette smoking occurred rapidly, and the risk of cardiovascular disease was reduced by half within one year of smoking cessation.24-26 The benefits of smoking cessation are not limited to younger smokers, whereby individuals older than 60 years of age also exhibited significantly reduced CAD risk.23 Smoking cessation resulted in substantial benefits for people with established CAD,27 serious heart disease and heart failure.28,29 In our study, current smoker with higher pack-years was the significant risk factor for the severity and CACS of CAD after adjustment, but former smoker was not. This result strongly supported the idea that smoking cessation can provide ample benefits. Additionally, smoking cessation may be highly cost-effective, and should even be considered therapeutic.28,30 Physicians play a vital role in helping patients stop smoking. Even a brief word of medical advice by a physician can increase the quit rate by 70%.31 So we hope physicians and healthcare providers could place an emphasis on giving smoking cessation advice or intervention to their patients.
In this study, current smokers had the highest prevalence of non-calcified plaques and the lowest prevalence of calcified plaques, compared with never or former smokers. The current smoker with higher pack-years was the strongest predictor for the presence of non-calcified and mixed plaques, but former smoker was not a predictor for plaque characteristics. It is generally understood that plaque morphology can play an important role in the degree of plaque vulnerability. Previous studies have confirmed that non-calcified plaques are associated with the occurrence of acute coronary syndrome as opposed to calcified plaques,32,33 and smoking was the significantly strongest predictor for non-calcified plaques which is consistent with the result of our study.34,35 Mixed plaques compared with non-calcified and calcified plaques were most frequently observed rather than thin-cap fibroatheromas, which tend to cause plaque rupture.36 One report suggested that non-calcified plaques may regress more easily while undergoing target medical therapies.37 So the coronary artery plaque burdens were reduced after smoking cessation, which partly may be caused by reducing the burden of non-calcified plaques.
The current study had several limitations. The smoking status of individuals was based on self-reporting, which could cause a possible selection bias. The study population was composed of Chinese men suspected of having CAD, which could restrict the generalizability of our results to similar care settings and ethnic groups because the results of our study may not apply to women. Because former smokers were few, we did not consider the effects of the time of smoking cessation on CAD. Additionally, unmeasured confounders may have affected our analysis. In cross-sectional analysis, we did not find a longitudinal relationship between smoking status and cardiovascular outcomes. In spite of these limitations, the association of current and former smoker with CAD in Chinese men has an important clinical significance to help us to better understand the role of smoking status in the progression of coronary artery plaques.
CONCLUSIONS
In conclusion, the current smokers had the most serious coronary artery burden and a higher percentage of non-calcified plaques than never and former smokers. The current smoker with higher pack-years (> 20 pack-years) was the strongest predictor for coronary artery burden, non-calcified and mixed plaques. The results have highlighted the adverse effects of smoking cigarette on coronary artery plaques, and further confirmed that the adverse cardiovascular effects of smoking may be slowed down or even reversed by smoking cessation.
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