Cardiology

Rarely tested or treated but highly prevalent: Hypercholesterolemia in emergency department observation unit patients with chest pain

a b s t r a c t

Background: Hypercholesterolemia (HCL) is common among Emergency Department (ED) patients with chest pain but is typically not addressed in this setting. This study aims to determine whether a missed opportunity for Emergency Department Observation Unit (EDOU) HCL testing and treatment exists.

Methods: We conducted a retrospective observational cohort study of patients >=18 years old evaluated for chest pain in an EDOU from 3/1/2019-2/28/2020. The electronic health record was used to determine demographics and if HCL testing or treatment occurred. HCL was defined by self-report or clinician diagnosis. Proportions of patients receiving HCL testing or treatment at 1-year following their ED visit were calculated. HCL testing and treatment rates at 1-year were compared between white vs. non-white and male vs. female patients using Multivariable logistic regression models including age, sex, and race.

Results: Among 649 EDOU patients with chest pain, 55.8% (362/649) had known HCL. Among patients without known HCL, 5.9% (17/287, 95% CI 3.5-9.3%) had a lipid panel during their index ED/EDOU visit and 26.5% (76/287, 95% CI 21.5-32.0%) had a lipid panel within 1-year of their initial ED/EDOU visit. Among patients with known or newly diagnosed HCL, 54.0% (229/424, 95% CI 49.1-58.8%) were on treatment within 1-year. After adjustment, testing rates were similar among white vs. non-white patients (aOR 0.71, 95% CI 0.37-1.38) and men vs. women (aOR 1.32, 95% CI 0.69-2.57). Treatment rates were similar among white vs. non-white (aOR 0.74, 95% CI 0.53-1.03) and male vs. female (aOR 1.08, 95% CI 0.77-1.51) patients.

Conclusions: Few patients were evaluated for HCL in the ED/EDOU or outpatient setting after their ED/EDOU en- counter and only 54% of patients with HCL were on treatment during the 1-year follow-up period after the index ED/EDOU visit. These findings suggest a missed opportunity to reduce cardiovascular disease risk exists by eval- uating and treating HCL in the ED or EDOU.

(C) 2023

  1. Introduction

Hypercholesterolemia (HCL) affects nearly 30% of the United States (US) population and is a major risk factor for atherosclerotic cardiovas- cular disease (ASCVD), the composite of obstructive coronary artery disease, stroke, transient ischemic attack, and peripheral artery disease

* Corresponding author at: Department of Emergency Medicine, Wake Forest School of Medicine, Medical Center Boulevard, Winston-Salem, NC, 27157 USA.

E-mail address: [email protected] (N.P. Ashburn).

[1-3]. Low-density lipoprotein cholesterol (LDL-C) is the principle driver of ASCVD and is the primary therapeutic target for mitigating ASCVD risk [2,4-8]. Traditionally, screening and treatment for HCL has been ini- tiated in primary care or cardiology clinic settings but not in the Emer- gency Department (ED) or Emergency Department Observation Unit (EDOU).

Chest pain, the most common symptomatic manifestation of ASCVD, is responsible for over 6.5 million Emergency Department (ED) visits in the US each year [9-12]. While these patients are being evaluated in the ED or EDOU, there may be an opportunity to reduce ASCVD risk by

https://doi.org/10.1016/j.ajem.2023.06.009

0735-6757/(C) 2023

testing for HCL and initiating lipid lowering therapy [13-15]. Currently, at the time of ED discharge, patients with acute chest pain are typically instructed to follow-up with their primary care physician or cardiologist with the assumption that lipid testing and therapy will be provided in the outpatient setting. However, it is unclear whether these patients ul- timately receive HCL care in the outpatient setting. Recognizing this po- tential gap in care, the Society for Academic Emergency Medicine (SAEM) and the American College of Emergency Physicians (ACEP) rec- ommend that emergency providers offer Preventive care for cardiovas- cular disease [16-19]. Despite these recommendations, it remains exceptionally uncommon for ED or EDOU providers to test for or treat HCL [20-22].

The goal of this study is to determine if current ED and EDOU care practices for patients with chest pain miss a key opportunity to evaluate for and treat HCL. To address this key evidence gap, this study aims to determine the proportion of patients who receive HCL testing and treat- ment in the ED or EDOU and in the outpatient setting within 1-year of EDOU discharge. Additionally, because non-white and female patients are historically less likely to receive preventive cardiovascular care [23-26], a secondary objective was to determine if HCL testing and treat- ment rates vary by race or sex.

  1. Methods
    1. Study design

We conducted a retrospective observational cohort study of patients being evaluated for acute chest pain in the ED and EDOU of Atrium Health Wake Forest Baptist from 3/1/2019 to 2/28/2020. The Wake For- est University Health Sciences Institutional Review Board approved the study protocol and granted a waiver of informed consent. The Strength- ening the Reporting of Observational Studies in Epidemiology (STROBE) guidelines helped direct the research and reporting processes [27].

    1. Study setting and population

Patients >=18 years old being evaluated for acute chest pain and pos- sible acute coronary syndrome in the EDOU at Atrium Health Wake For- est Baptist were included. The Atrium Health Wake Forest Baptist ED is located in the Piedmont Triad area of North Carolina and is staffed by board-certified or board-eligible emergency physicians 24 h per day. It has an annual volume of approximately 110,000 encounters. To be eligi- ble for EDOU care, the ED attending had to place the patient on the EDOU Chest pain protocol (Supplemental Appendix 1). Patients with ST-segment elevation myocardial infarction, hemodynamic instability (heart rate <40 or >120 beats per minute, systolic blood pres- sure <90 mmHg, or SpO2% <90% on room air or normal home oxygen flow rate) at any time during their ED encounter, high sensitivity cardiac troponin I (Beckman Coulter; Brea, CA) >=100 ng/L, or trauma were not eligible for EDOU care. This EDOU is a protocol-driven (Type 1) observa- tion unit. The EDOU is managed by emergency medicine physician as- sistants and nurse practitioners who are supervised by board-certified or board eligible emergency physicians. Patients undergo serial tropo- nin testing, Telemetry monitoring, and when appropriate, Stress testing or coronary computed tomography angiography.

    1. Data collection and variables

Index ED and EDOU Encounter data and outpatient clinic follow-up data through 1-year of the index visit were abstracted from the elec- tronic health record (EHR; Clarity-Epic Systems Corporation, Verona, WI) by trained data abstractors. HCL was defined by patient self- report to the treating ED clinical team or by clinician diagnosis either in the ED or during the 1-year follow-up period. Self-reported HCL was captured in the EHR as a structured risk stratification variable in the ED. Lipid panel measurements, including LDL-C, non-high-density

lipoprotein cholesterol (non-HDL-C), total cholesterol, high-density li- poprotein cholesterol (HDL\\C), and triglycerides, were extracted from the EHR. Data were entered into a Research Electronic Data CAP- ture (REDCap) database. Best practice guidelines for the chart review were used, including having trained data extractors, a data dictionary, digital extraction forms within REDCap, having regular performance re- view by the principal investigator (PI), and a random sample of entries reviewed by the PI [28,29]. Training consisted of in-person instruction with the PI, where actual encounters were reviewed to ensure familiar- ity with where and how to access the relevant data in the EHR and how to input the data into REDCap.

    1. Outcomes

Study outcomes were: 1) the proportion of patients with and with- out known HCL who were evaluated with a lipid panel in the ED/ EDOU or in an outpatient clinic during the 1-year follow-up period and 2) the proportion of patients with known or newly diagnosed HCL who were on a lipid lowering medication in the ED/EDOU or at any time during the 1-year follow-up period. We evaluated the missed op- portunity for EDOU-based HCL testing among all patients and among the subgroups of patients with and without known HCL. A missed test- ing opportunity was defined as a patient who did not receive a lipid panel during the ED/EDOU encounter or the 1-year outpatient follow- up period. We included patients with known HCL who did not receive a lipid panel in the ED/EDOU or 1-year follow-up period for this missed opportunity because response to therapy or medication compliance may be unknown. Similarly, a missed opportunity for EDOU-initiated HCL therapy was defined as a patient with known or newly diagnosed HCL who failed to receive any HCL therapy in the ED/EDOU or the 1- year outpatient period. Additional outcomes were LDL-C, non-HDL-C, total cholesterol, HDL\\C, and triglycerides measures among patients with lipid panel testing. Known HCL was defined as HCL that was diagnosed before their index ED/EDOU encounter based on patient self-report or medical record review. Newly diagnosed HCL included pa- tients with HCL diagnosed in the ED/EDOU or the 1-year outpatient follow-up period. Therapy for HCL was defined as being on any statin medication, ezetimibe, or PCSK9 inhibitor.

    1. Statistical analysis

Counts, percentages, and means with standard deviations were used to describe the study population. Rates of HCL testing and therapy dur- ing the ED and EDOU encounter, the 1-year follow-up period inclusive of the ED and EDOU encounter, and the missed opportunities for testing and therapy were calculated and reported with exact 95% confidence in- tervals (95% CI). Lipid panel results were reported with means and stan- dard deviations or medians and interquartile ranges, as appropriate. The two-sample t-test (with the corresponding 95% CI for the difference) or the Wilcoxon Rank Sum Test (with the corresponding Hodges-Lehmann estimator and 95% CI) was used to compare lipid measures among pa- tients receiving HCL therapy at 1-year to those who were not. Rates of HCL testing among white vs. non-white and male vs. female patients were compared at 1-year using Fisher’s exact tests. Similarly, HCL ther- apy rates among patients with a diagnosis of HCL at 1-year were also compared among these race and sex subgroups with Fisher’s exact test. To further evaluate the association of race and sex with receiving HCL testing and therapy, multivariable logistic regression was per- formed. Multivariable models included age (continuous), race (white vs. non-white), and sex (male vs. female). Unadjusted and adjusted odds ratios (aOR) with corresponding 95% CIs were calculated.

  1. Results

Among the 649 EDOU patients, 59.5% (386/649) were female and 43.8% (284/649) were non-white with a mean age of 59.8 +-

Table 1

Cohort characteristics.

Patient Characteristics

No Known HCL

Known HCL

Total

n = 287, n (%)

n = 362, n (%)

n = 649, n (%)

Age (mean +- SD) (years)

57.5 (12.9)

61.6 (11.6)

59.8 (12.3)

Sex

Female

166 (57.8)

220 (60.8)

386 (59.5)

Race

White 154 (53.7)

211 (58.3)

365 (56.2)

Non-white

133 (46.3)

151 (41.7)

284 (43.8)

Black

104 (36.2)

120 (33.2)

224 (34.1)

Other

29 (10.1)

31 (8.6)

60 (9.2)

Ethnicity

Hispanic or Latino

22 (7.7)

21 (5.8)

43 (6.6)

Comorbidities

Obesity (BMI >=30 kg/m2)

136 (47.4)

209 (57.7)

345 (53.2)

Diabetes

58 (20.2)

145 (40.1)

203 (31.3)

Hypertension

191 (66.6)

308 (85.1)

499 (76.9)

known CAD

20 (7.0)

61 (75.3)

81 (12.5)

Stroke

28 (9.8)

40 (11.1)

68 (10.5)

SD – standard deviation, BMI – body mass index, CAD – coronary artery disease.

12.3 years. At the time of the initial EDOU visit, 55.8% (362/649) had known HCL. During the 1-year follow-up period, 69.7% (452/649) were evaluated in an outpatient clinic for any reason. Table 1 describes the demographics of patients with and without known HCL at the time of the EDOU encounter.

In patients without known HCL, just 26.5% (76/287, 95% CI 21.5-32.0%) were evaluated with a lipid panel in the ED/EDOU or outpa- tient setting within 1-year. This testing consisted of 5.9% (17/287) hav- ing a lipid panel in the ED/EDOU and 21.3% (61/287) in the outpatient setting. Among patients without known HCL, 21.6% (62/287) were given a new diagnosis of HCL, resulting in a total of 65.3% (424/649) of patients having a diagnosis of HCL at 1-year. Fig. 1A demonstrates the missed HCL testing opportunities among patients without a known diagnosis of HCL.

Among patients with known HCL, 44.8% (162/362, 95% CI 40.0-50.0%) were evaluated with a lipid panel in the ED/EDOU or outpa- tient setting. The ED/EDOU ordered a lipid panel in 5.8% (21/362) of these patients while outpatient providers ordered a lipid panel in 40.1% (145/362). Fig. 1B shows the missed opportunity to evaluate pa- tients with known HCL using a lipid panel. For patients with known HCL during the ED/EDOU encounter, 48.1% (174/362, 95% CI 36.3-45.9%) were not on a lipid lowering agent at any point during the ED/EDOU encounter or follow-up period. The EDOU prescribed HCL treatment to just 0.3% (1/362) of patients with known HCL. For pa- tients with newly diagnosed HCL, the EDOU started 3.2% (2/62) on lipid lowering therapy while 66.1% (41/62) were on therapy within 1-year of EDOU discharge. Overall, 54.0% (229/424, 95% CI 49.1-58.8%) of patients with known or newly diagnosed HCL were on treatment within 1-year. Fig. 2 describes the missed opportunity for initiating treatment among patients with known or newly diagnosed HCL.

At 1-year, 36.7% (238/649, 95% CI 33.0-40.5%) of all patients were

tested with a lipid panel, including 5.9% (38/649) in the EDOU and 31.7% (206/649) in the outpatient setting. Among these, 0.9% (6/649) were tested in both care settings. Fig. 1C demonstrates the missed test- ing opportunity among all patients. Testing rates at 1-year were similar for white vs. non-white patients (36.2% [132/365] vs. 37.3% [106/284]; OR 0.95, 95% CI 0.69-1.31; p = 0.81) and men vs. women (32.7% [86/

263] vs. 39.4% [152/386]; OR 0.75, 95% CI 0.54-1.04; p = 0.10). In the

adjusted model, testing rates remained similar among white vs. non- white patients (aOR 0.91, 95% CI 0.65-1.27) and men vs. women (aOR 0.79, 95% CI 0.57-1.11). Rates of HCL therapy at 1-year among patients with known or newly diagnosed HCL were similar among white vs. non-white (50.6% [123/243] vs. 58.6% [106/181]; OR 0.73, 95% CI

0.49-1.07; p = 0.12) and male vs. female (55.7% [93/167] vs. 52.9%

[136/257]; OR 1.12, 95% CI 0.76-1.65; p = 0.62) patients. After

adjusting, therapy rates at 1-year remained similar among white vs.

non-white (aOR 0.74, 95% CI 0.53-1.03) and male vs. female (aOR 1.08, 95% CI 0.77-1.51) patients.

Among the 36.7% (238/649) of patients with lipid panel testing in the ED/EDOU or within 1-year of follow-up, full lipid panel results were available for 83.6% (199/238). Lipid panel results are summarized in Table 2. Patients on lipid lowering therapy during the ED/EDOU en- counter or within 1-year of the encounter had lower LDL-C measure- ments compared to patients not on therapy (106.6 +- 42.8 mg/dL vs. 122.0 +- 40.3 mg/dL; p = 0.02). Fig. 3 shows the overall lipid measure- ment distributions.

  1. Discussion

Current ED and EDOU care practices among patients with acute chest pain miss a large opportunity to reduce ASCVD risk by failing to evaluate for HCL or initiate lipid lowering therapy. Among patients without known HCL, >70% had not been evaluated for HCL at any point during the 1-year outpatient follow-up period. Similarly, among patients with known HCL, nearly 50% were not on any form of lipid low- ering therapy in the 1-year follow-up window. These findings suggest that the EDOU chest pain patient population is at high risk for undiag- nosed and unmanaged HCL, a key contributor to ASCVD risk.

Addressing HCL is a leading priority for the US Department of Health and Human Services’ (DHHS) in its “Healthy People 2030” initiative [30]. An ED- or EDOU-based preventive care model for HCL directly ad- dresses two key Healthy People 2030 objectives: “Increase cholesterol treatment in adults” and “Reduce cholesterol in adults.” Furthermore, the Society for Academic Emergency Medicine (SAEM) and the American College of Emergency Physicians (ACEP) have adopted policy statements encouraging emergency providers to initiate preventive car- diovascular care [16-19]. However, neither SAEM nor ACEP specifically address HCL testing or management. However, an ED- or EDOU-based HCL testing and treatment program meets these high-priority DHHS ob- jectives, aligns with national emergency medicine organization preven- tive care policies, and may have the ability to drastically reduce ASCVD risk among patients with undiagnosed or unmanaged HCL.

Multiple lipid lowering drugs exist, which the ED or EDOU could use to treat HCL. Statins are by far the most commonly prescribed lipid low- ering medication [31]. A large meta-analysis found that statins are effec- tive in lowering LDL-C and that for every 38.7 mg/dL reduction in LDL-C, five-year ASCVD risk is reduced by 24% and cardiac death by 20% [32]. Furthermore, the US Preventive Services Task Force found that statins are safe, well-tolerated, and associated with decreased all-cause mortal- ity (RR 0.86), stroke (RR 0.71), and myocardial infarction (RR 0.64) [33]. Additionally, statins are largely affordable and available for less than $20 for a 30-day supply [34]. Given the unmet need for HCL therapy and the safety, effectiveness, minimal side effects, and affordability of statin medications, the ED and EDOU are likely in a prime position to initiate statin therapy for patients with HCL.

An ED- or EDOU-based approach to HCL diagnosis and manage- ment may help reduce cardiovascular care disparities. Black, female, and Uninsured patients are less likely to have a source for primary care [23]. These subgroups are also traditionally thought to be less likely to be prescribed HCL therapy [24,35,36]. National Health and Nutrition Examination Survey literature suggests that black pa- tients are up to 40% less likely to be prescribed a statin than white patients [36,37]. Given the barriers associated with accessing out- patient primary care, no required co-pays in the ED or EDOU, and 24/7/365 ED availability, economically and socially disadvantaged patients may use the ED or EDOU for primary care instead of a tradi- tional outpatient care team [38]. However, within our cohort, the rates of testing for HCL at 1-year were similarly low among men vs. women and white vs. non-white patients. However, 8% more non-white patients received HCL therapy at 1-year than white pa- tients. Although this finding was not statistically significant, it sug- gests that. Among this select patient population, a race-based

Image of Fig. 1

Fig. 1. Missed opportunity for EDOU HCL testing among patients with A) no known HCL, B) known HCL, and C) all patients. HCL – Hypercholesterolemia, EDOU – Emergency Department Observation Unit.

disparity in HCL therapy may not exist. However, this inference is limited by sample size.

Historically, LDL-C levels have been used to guide the initiation of lipid lowering therapy. However, current preventive cardiovascular care guidelines generally recommend assessing 10-year ASCVD risk rather than just LDL-C levels before initiating therapy for primary

prevention [39-41]. As anticipated, we found that patients on lipid low- ering therapy during the 1-year follow-up period had lower levels of LDL-C compared to patients not on lipid lowering therapy. However, non-HDL-C, total cholesterol, HDL\\C, and triglyceride levels were sim- ilar among groups. It is likely that this analysis was underpowered to de- tect a difference in these measures. Multiple previous high-quality

Image of Fig. 2Fig. 2. Missed opportunity EDOU-initiated lipid lowering therapy among patients with known or newly diagnosed HCL.

HCL – Hypercholesterolemia, EDOU – Emergency Department Observation Unit.

Fig. 3. Lipid measurement distributions.

LDL-C – low-density lipoprotein cholesterol, Non-HDL-C – non-high-density lipoprotein cholesterol, HDL-C – high-density lipoprotein cholesterol.

randomized controls trials have demonstrated that statins lower non- HDL-C, total cholesterol, and triglyceride levels while raising HDL-C [42,43].

  1. Limitations

This study has limitations. The generalizability of this study may be limited because it was conducted at a single academic site and among a select group of patients being evaluated for possible acute coronary syndrome in the EDOU. Data were retrospectively collected using the EHR of a single healthcare system. It is possible that patients received HCL testing or therapy in an outside healthcare system. However, previous studies have demonstrated high health system brand loyalty among our patients, making this source of misclassification bias less likely [44]. HCL was defined by self-report or clinician diagnosis in the EHR, possibly contributing

to misclassification bias. Furthermore, lifestyle interventions for HCL were not recorded. Finally, precision and power to detect dif- ferences were limited by the sample size.

  1. Conclusion

Among ED patients with acute chest pain who were evaluated in the EDOU, we found a large missed opportunity to reduce ASCVD risk by failing to assess for HCL and initiate lipid lowering therapy. The lack of outpatient preventive cardiovascular care for HCL following the initial EDOU visit suggests that the ED or EDOU setting may be the only pre- ventive cardiovascular care option accessible for many patients. These findings suggest that it may be reasonable for ED and EDOU providers to routinely screen patients with chest pain for HCL with a lipid panel and initiate safe and effective pharmacotherapy when indicated. Future research should test ED- and EDOU-based HCL diagnosis and treatment strategies.

Table 2

Lipid measurements among patients with a lipid profile within 1-year after the EDOU encounter.

Measure

Any Therapy (n = 92)

No Therapy (n = 107)

Overall (n = 199)

Absolute Difference (95% CI)

p-value+

LDL-C (mg/dL)

106.6 +- 42.8

122.0 +- 40.3

113.0 +- 42.3

15.4 (2.1-28.6)

0.02

(mean +- SD)

Non-HDL-C (mg/dL)

172.4 +- 51.8

174.9 +- 58.9

173.5 +- 55.1

2.5 (-13.0-18.0)

0.75

(mean +- SD)

Total Cholesterol (mg/dL)

178.5 +- 49.6

187.8 +- 49.2

182.8 +- 49.5

9.3 (-4.6-23.1)

0.19

(mean +- SD)

HDL-C (mg/dL)

48.4 +- 14.0

50.4 +- 14.8

49.3 +- 14.3

1.9 (-2.1-6.0)

0.34

(mean +- SD)

Triglycerides (mg/dL)

123.0 (92.0-176.0)

139.5 (101.0-181.5)

127.5 (94.0-178.0)

9.0 (-9.0-26.0)?

0.33

(median, IQR)

LDL-C – low-density lipoprotein cholesterol, Non-HDL-C – non-high-density lipoprotein cholesterol, HDL-C – high-density lipoprotein cholesterol.

+Comparisons between groups made with the two-sample t-test, except for triglycerides, which were compared using the Wilcoxon Rank Sum Test.

* Difference calculated using the Hodges-Lehmann estimator.

Funding

None.

CRediT authorship contribution statement Nicklaus P. Ashburn: Writing – review & editing, Writing – original

draft, Supervision, Project administration, Methodology, Investigation, Formal analysis, Data curation, Conceptualization. Anna C. Snavely: Writing – review & editing, Software, Methodology, Investigation, Formal analysis, Data curation, Conceptualization. Rishi Rikhi: Writing

  • review & editing, Methodology, Conceptualization. Michael D. Shapiro: Writing – review & editing, Methodology, Investigation, Data curation. Michael A. Chado: Conceptualization, Investigation, Writing
  • review & editing. Alexander P. Ambrosini: Writing – review & editing, Investigation, Data curation. Amir A. Biglari: Writing – review & editing, Investigation, Data curation. Spencer T. Kitchen: Writing – review & editing, Investigation, Data curation. Marissa J. Millard: Writ- ing – review & editing, Methodology, Data curation. Jason P. Stopyra: Writing – review & editing, Supervision, Methodology, Investigation, Data curation, Conceptualization. Simon A. Mahler: Writing – review & editing, Supervision, Project administration, Methodology, Investiga- tion, Data curation, Conceptualization.

Declaration of Competing Interest

Dr. Ashburn receives funding from NHLBI (T32HL076132).

Dr. Snavely receives funding from Abbott and HRSA (1H2ARH399760100).

Dr. Rikhi receives funding from NHLBI (T32HL076132).

Dr. Shapiro has participated in scientific advisory boards with Amgen, Novartis, Ionis, Precision BioSciences and has served as a con- sultant for Regeneron, Ionis, Novartis, and EmendoBio.

Dr. Stopyra receives research funding from NCATS/NIH (KL2TR001421), HRSA (H2ARH39976-01-00), Roche Diagnostics, Ab-

bott Laboratories, Pathfast, Genetesis, Cytovale, Forest Devices, Vifor Pharma, and Chiesi Farmaceutici.

Dr. Mahler receives funding/support from Roche Diagnostics, Abbott Laboratories, QuidelOrtho, Siemens, Grifols, Pathfast, Genetesis, Cytovale, and HRSA (1H2ARH399760100). He is a consultant for Roche, Abbott, Beckman Coulter, Siemens, Genetesis, Inflammatix, Radiometer, and Amgen and is the Chief medical officer for Impathiq Inc.

The other authors report no conflicts.

Acknowledgements

We would like to thank Gregory Noe, Ian Kinney, Ryan Morgan, Weston Colbaugh, Ravenna Chhabria, Benjamin Brendamour, James Black, Harris Cannon, and Philip Kayser for their assistance with data collection.

Appendix A. Supplementary data

Supplementary data to this article can be found online at https://doi. org/10.1016/j.ajem.2023.06.009.

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