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- J Lipid Atheroscler
- v.13(2); 2024 May
- PMC11140247
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J Lipid Atheroscler. 2024 May; 13(2): 184–193.
Published online 2024 Feb 22. doi:10.12997/jla.2024.13.2.184
PMCID: PMC11140247
PMID: 38826178
Seong Soon Kwon,1 Seug Yun Yoon,2 Kyoung-Ha Kim,2 Byoung-Won Park,1 Min-Ho Lee,1 Hyoungnae Kim,3 and Duk Won Bang
1
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Abstract
Objective
Serum hemoglobin (Hb) level affects the viscosity of blood. Several studies have reported that Hb level is associated with adverse cardiovascular outcome. However, there is a paucity of evidence on the association between serum Hb level and the risk of subclinical atherosclerosis. Thus, the objective of this study was to investigate the relationship between Hb level and risk of carotid plaque in a health checkup cohort.
Methods
This retrospective study analyzed a total of 3,805 individuals without history of cardiovascular disease (CVD) who underwent carotid ultrasonography (USG) between January 2016 and June 2018. Participants were divided into 4 groups based on Hb quartiles in each of male and female. Carotid plaque score was calculated based on USG reports. Multivariable logistic regression analysis was performed for each index of quartile groups regarding the risk of carotid plaque.
Results
Of 3,805 individuals (mean age, 52.62±10.25 years; 2,674 [70.28%] males), mean Hb level was 15.11±0.75 g/dL in male and 13.35±0.74 g/dL in female. When the Q1 group was compared to the Q4, increasing quartile of Hb was associated with the presence of significant carotid plaque (plaque score ≥3) in male (adjusted odds ratio [OR], 1.538; 95% confidence interval [CI], 1.182–2.001; p=0.001) and female (adjusted OR, 1.749; 95% CI, 1.058–2.676; p=0.01).
Conclusion
A high Hb level is associated with an increased risk of carotid plaques in individuals without history of CVD. This finding may support the need for early screening of CVD in individuals with high Hb levels.
Keywords: Hemoglobin, Atherosclerosis, Risk factors
INTRODUCTION
Since changes in hemoglobin (Hb) level can affect hemodynamics of the heart, Hb level is closely related to various cardiovascular outcomes. There is some evidence suggesting that high levels of Hb might be associated with an increased risk of developing atherosclerosis, although the exact relationship between the two is not fully understood yet.
Potential mechanisms explaining an association of high Hb levels with an increased cardiovascular disease (CVD) risk include increased peripheral platelet activation and increased oxidative stress from increased iron accumulation.1 On the other side, low Hb levels could potentially lead to increased left ventricular (LV) mass and LV filling pressure ultimately predisposing to development of CVD.2
Studies investigating the relationship between Hb level and CVDs have shown inconsistent results. One study has reported that increasing Hb level is associated with a lower severity of atherosclerosis.3 However, the average Hb in that study was 9.1 g/dL for men and 8.4 g/dL for women, indicating severe anemia. Therefore, it is difficult to apply results of that study to the general population whose Hb levels are within the normal range. Another study has reported that low Hb level is associated with an increased risk of major adverse cardiovascular events.4 However, since patients were limited to men over 70 years of age, it was difficult to generalize results of that study. Another previous study has suggested that people with high Hb levels might be more likely to have increased arterial stiffness, a risk factor for atherosclerosis.5 There is also evidence that both lower and higher Hb levels were associated with a higher risk of stroke6 and all cause mortality.7 However, there is a paucity of evidence on the association between Hb level and risk of subclinical atherosclerosis, especially in the general population without overt CVD. Carotid ultrasonography (USG) is a fast and non-invasive method to detect subclinical atherosclerotic change of artery. It is a useful tool to assess future risk of CVD.8 Therefore, the aim of this study was to evaluate the association between Hb level and risk of carotid plaque in a health checkup cohort.
MATERIALS AND METHODS
1. Study population
We performed a single-center, retrospective study that a total of 4,306 individuals aged over 20 years old who underwent carotid USG as part of the medical health checkup program in the Health Promotion Center of Soonchunhyang University Seoul Hospital between January 2016 and June 2018. Among them, 129 participants with a history of CVD or stroke were excluded. To confine the analysis to subjects with Hb level in the normal range, polycythemia9 (Hb greater than 16.5 g/dL in male and 16 g/dL in female) and anemia10 (Hb less than 13 g/dL in male and 12 g/dL in female) subjects were excluded. Finally, 3,805 subjects were eligible for inclusion in the present study. All participants were stratified into 4 groups based on Hb quartiles in each of male and female (Q1 was the lowest Hb level and Q4 was the highest level) (Fig. 1).
Fig. 1
Patient enrollment flowchart. Hb level is expressed as median (minimum–maximum) value.
Hb, hemoglobin (g/dL); CVD, cardiovascular disease.
This study followed the principles of the Helsinki declaration, and the study protocol was approved by the Institutional Review Board (IRB) of the of Soonchunhyang University Seoul Hospital (IRB No. 2023-01-005). The requirement for informed consent was waived by the IRB owing to its retrospective nature.
2. Variables and definitions
Demographic information were obtained from the medical records. Previous medical history and health behaviors such as smoking status were evaluated using a self-report questionnaire completed during an interview. Body mass index (BMI) was calculated as weight divided by the square of height (kg/m2). Obesity was defined as BMI ≥25 kg/m2 according to the World Health Organization standards for Asians. Blood pressure (BP) measurements were performed by experienced nurses for all subjects on the right arm after a rest ≥5 minutes using automated oscillometric manometers and appropriate cuff sizes. For all subjects, blood tests were performed after at least 8 hours of fasting without intake of caffeine, alcohol, or smoking. Participants who smoked at least one cigarette per day at the time of the health screening were defined as current smokers. Fasting blood samples were collected in an EDTA-2K tube, a heparin sodiumtube and a siliconized tube. Hb was measured using absorption spectrophotometry at Alinity HQ Analyzer® (Abbott). Presence of diabetes mellitus was defined as either fasting blood glucose level ≥126 mg/dL, or Hb A1c level ≥6.5%, or current use of any glucose lowering medications. Hypertension was defined as either current use of antihypertensive medication or having a measured BP ≥140/90 mmHg at health screening examinations. Dyslipidemia was defined based on the information the patient filled out in the self-report questionnaire. Serum creatinine level was measured using a calibration traceable to an isotope dilution mass spectrometry reference. Estimated glomerular filtration rate (eGFR) was calculated with the Chronic Kidney Disease Epidemiology Collaboration equation based on serum creatinine level.11
3. Carotid USG examination
A high-resolution B-mode USG (EPIQ 5C or IE 33 USG systems; Philips) equipped with an 11.0 MHz linear array transducer was used for carotid USG. Common carotid artery intima-media thickness (IMT) was measured from the level of the common carotid artery (1 cm proximal to the dilation of the carotid bulb) far wall in a region free of plaque. A new segment was selected if a plaque was found at that location. The leading edge of the lumen-intima interface and the media-adventitia interface of the B-mode frame were measured in order to calculate IMT. Software (Q-lab; Philips Medical Systems) that could automatically assess IMT at 64 places in a 10-mm segment was used. The value given was the arithmetic mean of IMT calculated. Mean carotid IMT was determined as the average of all measurements of both left and right arteries. Carotid plaque was defined as local thickening of the IMT of >50% compared to the surrounding vessel wall, an IMT >1.5 mm, or local thickening >0.5 mm.12 Extracranial carotid arteries were divided into 3 sectors on each side: common carotid artery, carotid bifurcation, and internal carotid artery. To define plaque burden, the carotid plaque score was calculated as a total number of sites with plaques ranging from 0 to 6 (right and left sided common carotid artery, carotid bifurcation, and internal carotid artery).13 A carotid plaque score of 3 or above was considered significant. All measurements were performed with the same device by the same experienced sonographer (SM Yoon, a registered diagnostic cardiac sonographer with 10 years of experience.). The intra-class correlation coefficient for carotid plaque score was 0.937 (95% confidence interval [CI], 0.890–0.964, p<0.001).
4. Data analysis
The expression for continuous variables is mean ± standard deviation (SD). A Student’s t-test was used to compare them. The expression for categorical variables is numbers and percentages. A χ2 test was used to compare them. Nonparametric variables are expressed as median and interquartile range using a Mann-Whitney U test. We had no missing data except for high-sensitive C-reactive protein (hs-CRP) (10.26%). Thus, we replaced missing data of hs-CRP with values obtained using multiple imputation with missing at random assumption. Multivariable logistic regression model was used to assess relationships between exposures and outcomes in each of male and female. Initially, Hb level was treated as a continuous variable. Thereafter, it was analyzed according to quartiles (Q) (Q1 lowest, Q4 highest). To evaluate the relationship between Hb and significant carotid plaque (plaque score ≥3), we adjusted for the following covariables: age, smoking, history of hypertension, diabetes, dyslipidemia, obesity, fasting blood sugar, low-density lipoprotein (LDL) cholesterol, triglyceride, hs-CRP, and eGFR. In addition to categorical analysis, association between Hb level as a continuous variable and the risk of significant carotid plaque was graphically presented with restricted cubic spline derived with equally distributed 3 knots based on a logistic regression model). In sensitivity analysis, we used various definitions of significant carotid plaque and showed associations with Hb level. Statistical significance was defined at p<0.05. All analyses were conducted using the R language version 4.2.2 (R Foundation for Statistical Computing).
RESULTS
1. Baseline characteristics of the study population
Baseline characteristics of participants according to quartiles of Hb level are presented in Table 1. The study cohort was divided into the following Hb quartile groups: Q1) 13–14.6 g/dL, Q2) 14.7–15.1 g/dL, Q3) 15.2–15.6 g/dL, and Q4) 15.7–16.5 g/dL. Of 3,805 individuals (mean age, 52.62±10.25 years; 2,674 [70.28%] males), mean Hb level was 15.11±0.75 g/dL in male and 13.35±0.74 g/dL in female. Mean carotid plaque score was 1.74±1.45. Subjects in higher quartiles of Hb group were younger. They had higher prevalence of current smoker and obesity than lower quartiles of Hb group. Blood test results showed that those in higher quartiles of Hb group had higher total cholesterol, LDL cholesterol, and triglyceride level, whereas they had lower levels of high-density lipoprotein cholesterol than those in lower quartiles of Hb group.
Table 1
The baseline characteristics of study population according to the Hb level
| Characteristics | Total (n=3,805) | Q1 (Hb 13–14.6) (n=984) | Q2 (Hb 14.7–15.1) (n=925) | Q3 (Hb 15.2–15.6) (n=931) | Q4 (Hb 15.7–16.5) (n=965) | p-value |
|---|---|---|---|---|---|---|
| Age (yr) | 52.62±10.25 | 54.46±10.49 | 52.15±10.16 | 51.69±10.33 | 52.08±9.76 | <0.001 |
| Sex (male) | 2,674 (70.28) | 689 (70.02) | 637 (68.86) | 664 (71.32) | 684 (70.88) | 0.667 |
| Current smoker | 784 (20.6) | 180 (18.29) | 171 (18.49) | 206 (22.13) | 227 (23.52) | 0.007 |
| Hypertension | 1,050 (27.6) | 264 (26.83) | 257 (27.78) | 256 (27.5) | 273 (28.29) | 0.909 |
| Diabetes mellitus | 410 (10.78) | 118 (11.99) | 93 (10.05) | 98 (10.53) | 101 (10.47) | 0.538 |
| Dyslipidemia | 413 (10.85) | 130 (13.21) | 96 (10.38) | 95 (10.2) | 92 (9.53) | 0.046 |
| BMI (kg/m2) | 24.56±3.17 | 24.02±3.08 | 24.44±3.09 | 24.76±3.18 | 25.01±3.26 | <0.001 |
| Obesity | 1,591 (41.81) | 349 (35.47) | 370 (40) | 408 (43.82) | 464 (48.08) | <0.001 |
| SBP (mmHg) | 123 (112–132) | 120 (110–130) | 122 (112–131) | 123 (112–132.5) | 125 (115–133) | <0.001 |
| DBP (mmHg) | 75 (68–82) | 72 (66–80) | 74 (68–82) | 76 (69–82) | 77 (70–84) | <0.001 |
| hs-CRP (mg/L) | 0.13±0.35 | 0.14±0.53 | 0.12±0.29 | 0.11±0.19 | 0.13±0.28 | 0.129 |
| Hb (g/dL) | 14.59±1.10 | 13.63±0.84 | 14.34±0.85 | 14.87±0.83 | 15.53±0.83 | <0.001 |
| eGFR (mL/min/1.73 m2) | 93.49±13.07 | 93.47±13.83 | 93.66±13.09 | 93.91±12.61 | 92.95±12.67 | 0.396 |
| FBS (mg/dL) | 96.21±19.45 | 96.33±20.05 | 96.07±18.23 | 96.12±19.69 | 96.32±19.75 | 0.987 |
| HbA1c (%) | 5.63±0.73 | 5.67±0.71 | 5.62±0.68 | 5.60±0.75 | 5.61±0.76 | 0.177 |
| Total cholesterol (mg/dL) | 193 (169–217) | 187 (162–211) | 193 (168–215) | 194 (171.5–218) | 199 (175–222) | <0.001 |
| LDL cholesterol (mg/dL) | 127 (105–150) | 121 (97–144) | 126 (105–148) | 128 (107–152) | 133 (109–156) | <0.001 |
| HDL cholesterol (mg/dL) | 55 (46–66) | 57 (48–68) | 55 (47–67) | 55 (47–65) | 53 (44–63) | <0.001 |
| Triglyceride (mg/dL) | 114 (81–165) | 103 (75–149) | 111 (80–155) | 116 (82–168.5) | 128 (91–182) | <0.001 |
| Carotid IMT (mm) | 0.57±0.10 | 0.58±0.10 | 0.57±0.10 | 0.57±0.10 | 0.58±0.10 | 0.049 |
| Carotid plaque score | 1.74±1.45 | 1.41±1.32 | 1.84±1.51 | 1.83±1.46 | 1.89±1.47 | <0.001 |
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Values are presented as number (%), median (range), or mean ± standard deviation.
Hb, hemoglobin; BMI, body mass index; SBP, systolic blood pressure; DBP, diastolic blood pressure; hs-CRP, high-sensitive C-reactive protein; eGFR, estimated glomerular filtration rate; FBS, fasting blood sugar; HbA1c, glycated hemoglobin; LDL, low-density lipoprotein; HDL, high-density lipoprotein; IMT, intima-media thickness.
2. Risk of significant carotid artery plaque according to Hb level
Supplementary Fig. 1. shows differences in carotid plaque score among subjects from quartiles 1 to 4. When we classified carotid plaque score into 0, 1, 2, and ≥3, the number of subjects with significant carotid plaque (score ≥3) was the lowest in the Q1 group, with the number being constantly higher in higher quartiles of Hb in both with male and female. Carotid plaque was most frequently found at the bifurcation site on both sides regardless of Hb quartiles (Supplementary Table 1).
In a logistic regression model adjusted for confounding factors, when the Q1 group was set as a reference, it was observed that in male, as the quartile of Hb level increased, the risk of significant carotid plaque increased in a stepwise fashion. In female, the risk of significant carotid plaque was not robust in the Q2 and Q3 group, but significantly associated with Q4 group. Compared to Q1 group, Q4 group showed 1.54 times higher risk of significant carotid plaque (adjusted odds ratio [OR], 1.538; 95% CI, 1.182–2.001; p=0.001) in male and 1.75 times higher risk of significant carotid plaque (adjusted OR, 1.749; 95% CI, 1.144–2.676; p=0.01) in female. When Hb level was analyzed as a continuous variable, 1-SD increment in Hb level was associated with a 23% higher risk of significant carotid plaque (adjusted OR, 1.230; 95% CI, 1.085–1.394, p=0.001) in male and 29% higher risk of significant carotid plaque (adjusted OR, 1.288; 95% CI, 1.058–1.569; p=0.012) in female (Table 2). Restricted cubic spline analysis showed similar results. In male, the risk of significant carotid plaque increased progressively with increasing Hb level, while in female, there was no significant change in risk at lower percentiles of Hb, but an increased risk was observed as the percentiles increased (Figs. 2 and and33).
Table 2
Multivariable logistic regression analysis for the association of hemoglobin to the risk of significant carotid plaque
| Exposures | Male | Female | |||
|---|---|---|---|---|---|
| Adjusted OR* (95% CI) | p-value | Adjusted OR* (95% CI) | p-value | ||
| Quartiles of hemoglobin | |||||
| Q1 | Ref. | - | Ref. | - | |
| Q2 | 1.448 (1.113–1.884) | 0.006 | 1.442 (0.929–2.238) | 0.103 | |
| Q3 | 1.461 (1.121–1.902) | 0.005 | 1.547 (0.996–2.403) | 0.052 | |
| Q4 | 1.538 (1.182–2.001) | 0.001 | 1.749 (1.144–2.676) | 0.010 | |
| Hemoglobin as continuous variable (Per 1 SD increment) | 1.230 (1.085–1.394) | 0.001 | 1.288 (1.058–1.569) | 0.012 | |
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Significant carotid plaque was defined as carotid plaque score ≥3.
OR, odds ratio; CI, confidence interval; SD, standard deviation; eGFR, estimated glomerular filtration rate; FBS, fasting blood sugar; LDL, low-density lipoprotein; hs-CRP, high-sensitive C-reactive protein.
*Adjusted for age, smoking, history of hypertension, diabetes, dyslipidemia, obesity, eGFR, FBS, LDL cholesterol, triglyceride, and hs-CRP.
Fig. 2
Restrictive cubic spline curve for the relationship between hemoglobin and significant carotid plaque in male. (A) Unadjusted; (B) Adjusted. Adjusted curve is derived from multivariable logistic regression model with adjusting for age, smoking, history of hypertension, diabetes, dyslipidemia, obesity, estimated glomerular filtration rate, fasting blood sugar, low-density lipoprotein cholesterol, triglyceride, and high-sensitive C-reactive protein.
CI, confidence interval.
Fig. 3
Restrictive cubic spline curve for the relationship between hemoglobin and significant carotid plaque in female. (A) Unadjusted; (B) Adjusted. Adjusted curve is derived from multivariable logistic regression model with adjusting for age, smoking, history of hypertension, diabetes, dyslipidemia, obesity, estimated glomerular filtration rate, fasting blood sugar, low-density lipoprotein cholesterol, triglyceride, and high-sensitive C-reactive protein.
CI, confidence interval.
3. Sensitivity analysis
We performed a sensitivity analysis to determine the association of Hb with differently defined significant carotid plaque. When using the carotid plaque score from 1 to 4 as a definition of significant carotid plaque, consistent results were observed regardless of the score in male, whereas in female there was no significant correlation at scores 1 and 2. However, when defined as scores 3 and 4 or higher, significant results were found (Table 3).
Table 3
Sensitivity analysis of the association between the hemoglobin (as continuous variable) and various definition of significant carotid plaque
| Carotid plaque score | Male | Female | ||
|---|---|---|---|---|
| Adjusted OR (95% CI)* | p-value | Adjusted OR (95% CI)* | p-value | |
| ≥1 | 1.008 (1.003–1.012) | 0.002 | 1.168 (0.956–1.428) | 0.129 |
| ≥2 | 1.221 (1.060–1.407) | 0.006 | 1.188 (0.968–1.456) | 0.099 |
| ≥3 | 1.230 (1.085–1.394) | <0.001 | 1.288 (1.058–1.569) | 0.012 |
| ≥4 | 1.111 (1.094–1.129) | <0.001 | 1.215 (1.036–1.425) | 0.017 |
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OR, odds ratio; CI, confidence interval.
*Adjusted for age, smoking, history of hypertension, diabetes, dyslipidemia, obesity, estimated glomerular filtration rate, fasting blood sugar, low-density lipoprotein cholesterol, triglyceride, and high-sensitive C-reactive protein.
DISCUSSION
In the present study, we examined the relationship between Hb and significant carotid plaque in individuals who had undergone a general health checkup. As a result, we found that increased Hb level was related to significant carotid artery plaque. This finding was consistent in sensitivity analyses.
Because the diagnostic criteria and prevalence of anemia and erythrocytosis are very different in men and women, we analyzed each gender separately. Many studies that evaluated the relationship between Hb and cardiovascular outcome analyzed men and women separately.5,6,14 Our result was consistent regardless of gender.
Blood viscosity is important for flow. When its viscosity increases, the force applied to the vessel wall also increases, causing vessel damage.15 The most important contributor to an increased viscosity is a high haematocrit.16 There is an evidence that erythrocytosis is associated with cardiovascular morbidity/mortality, and all-cause mortality in large population-based cross-sectional study.17 Higher level of hematocrit is also associated with increased short-term mortality compared to a normal hematocrit in ST-segment elevation myocardial infarction.18
Results of this study indicate that Hb can potentially affect the development and progression of atherosclerosis. Multiple mechanisms could explain how Hb is directly involved in and contributes to the progression of atherosclerosis. When red blood cells collide with the arterial wall, they can cause local hemolysis and membrane lipid retention, releasing heme-Fe++ that is toxic to the endothelial wall. This damage to the endothelium is associated with development and progression of atherosclerosis.19 Furthermore, Hb can induce the secretion of pro-inflammatory transcription factors such as NF-κB.20 It is well known that atherosclerosis is an inflammatory process.21 In our study, hs-CRP level was higher in higher quartiles of the Hb group, suggesting the involvement of an inflammatory process in the development of atherosclerosis.
In one large cohort study, Hb levels showed a U-shaped relationship with all-cause mortality.22 In our study, all subjects are within normal range Hb level. Thus, it was not a U-shaped relationship. A gradually increasing risk of significant carotid plaque was found when Hb increased. However, this relationship was not well-established. More studies are needed to confirm the link between Hb level and atherosclerosis.
It is well known that individuals with obese and poor metabolic profiles have high Hb level.23,24 In our study, BMI, BP and cholesterol profiles also tended to be worse in the high Hb group. However, even after adjusting the variables included in the metabolic syndrome, Hb level was confirmed to be a significant factor in carotid plaque. Additionally, increasing Hb level can be caused by a variety of underlying conditions such as lung disease25 which can increase the risk for atherosclerotic CVD.26 Despite this limitation, since Hb is an easily measurable parameter, it is convenient to evaluate patients’ cardiovascular risk indirectly in clinical practice.
In our study, we did not present a clear cut-off value of Hb to predict increased carotid plaque and only confirmed tendency according to quartile of Hb. We performed ROC analysis to suggest the optimal Hb level, but there are limitations due to the low area under the curve value. Even in a large-scale study related to Hb level, analysis was only performed by stratifying into quantile of Hb, and a clear cutoff value was not presented.7,27 Perhaps this is because Hb level can be very different depending on the study population. Additional research is needed to confirm the cutoff value in the future.
Our study had some limitations. First, since this was a retrospective cross-sectional study, causal inferences could not be drawn. To clarify the relationship between Hb and progression of atherosclerosis, a prospective longitudinal study is needed to confirm the occurrence of major adverse cardiovascular events according to the degree of Hb level. Second, because our data had no information about specific medication, we could not examine the effect of medication such as statin that could modify carotid plaque and lipid profiles. This study also lacked information on other exposures, including alcohol intake, physical activity. Therefore, we cannot rule out the possibility of residual confounding variables for some measured and unmeasured factors. Finally, in our study, only the carotid plaque score could be counted. It has been reported that assessment of plaque burden by volume measurement is a better parameter of atherosclerosis than a simple assessment of the presence or absence of plaques.28 However, the presence of carotid plaques has been reported to be an independent marker of CVD events in asymptomatic individuals.29 In the future study, a new 3-dimensional volumetric USG method for accurate quantification of atherosclerotic plaque volume30 is needed.
In conclusion, our study suggests that a high Hb level is associated with an increased risk of carotid plaques in individuals without history of CVD. This finding may support the need for early screening for CVD in individuals with high Hb levels. It can be used as a basis for recommending preemptive medical treatment and lifestyle modifications to these patients.
Footnotes
Funding: This research was supported by the Soonchunhyang University research fund.
Conflict of Interest: The authors have no conflicts of interest to declare.
Data Availability Statement: The data underlying this article cannot be shared publicly to protect the privacy of individuals that participated in the study. The data will be shared on reasonable request to the corresponding author.
All authors take responsibility for all aspects of the reliability and freedom from bias of the data presented and their discussed interpretation.
Contributed by
Author Contributions:
Conceptualization: Yoon SY, Kim KH, Park BW.
Data curation: Kwon SS.
Formal analysis: Kwon SS, Kim H.
Methodology: Kwon SS, Yoon SY.
Resources: Kwon SS.
Supervision: Bang DW.
Visualization: Kwon SS.
Writing - original draft: Kwon SS.
Writing - review & editing: Yoon SY, Kim KH, Park BW, Lee MH, Kim H, Bang DW.
SUPPLEMENTARY MATERIALS
Supplementary Table 1:
Distribution of carotid artery plaque according to hemoglobin quartiles
Click here to view.(29K, xls)
Supplementary Fig. 1:
Carotid plaque score according to quartile of the hemoglobin level. Carotid plaque score was classified into 0,1,2, and ≥3. Quartiles were described as Q1 to Q4 (Q1 as the lowest).
Click here to view.(692K, ppt)
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