Association of the abdominal aortic calcification with all-cause and cardiovascular disease-specific mortality: Prospective cohort study

Abstract

Background

Abdominal aortic calcification (AAC) is a prevalent form of vascular calcification associated with adverse cardiovascular outcomes. While previous studies on AAC and cardiovascular risk exist, many have limitations such as small sample sizes and limited clinical significance outcomes. This study aims to prospectively investigate the association between AAC and all-cause and cardiovascular disease (CVD)-specific mortality rates in a nationally representative sample of adults in the United States, using data from the National Health and Nutrition Examination Survey (NHANES).

Methods

The study, conducted on NHANES participants aged 40 years or older during the 2013–2014 cycle, assessed AAC using the Kauppila scoring system. Demographic characteristics, mortality data, and comorbid factors such as age, gender, diabetes, and hypertension were considered. Statistical analyses, including weighted percentages, Kaplan-Meier survival curves, and multivariable Cox proportional hazards regression models, were employed to evaluate the associations between AAC and mortality risks.

Results

After analyzing a final sample of 2717 participants, the study found a significant association between severe AAC (SAAC) and higher all-cause mortality risk (HR 1.70, 95% CI 1.17–2.48). The dose-response relationship indicated an increased risk with higher AAC scores. However, no independent association was observed between AAC and cardiovascular mortality. Stratified analysis revealed variations in the AAC-all-cause mortality association based on gender and hypertension.

Conclusion

This population-based study provides valuable insights into the prospective association between AAC and all-cause mortality, emphasizing the potential role of AAC assessment in identifying individuals at higher risk.

Introduction

Abdominal aortic calcification (AAC), a prevalent form of vascular calcification [1], is commonly observed in the general population, and its incidence and severity increase with advancing age [2]. Numerous epidemiological studies have established an association between AAC and adverse cardiovascular outcomes, including stroke [3], coronary heart disease [4], and myocardial infarction [5]. The escalation in the severity of aortic calcification has been recognized as a predictor of specific cardiovascular events and overall mortality [6–10]. Some reports suggest that the visible amount of AAC in imaging tests determines the risk of cardiovascular events, fatal cardiovascular events, and all-cause mortality, with the highest risk observed in patients with advanced calcification [11–13].

Despite the recognized importance of AAC, existing studies suffer from limitations such as relatively small sample sizes, limited reporting of clinically significant outcomes, and a need to establish the relevance of AAC in various patient subgroups. The National Health and Nutrition Examination Survey (NHANES) is a periodic, cross-sectional health survey program that utilizes a stratified, multistage, and probability-cluster design to obtain a nationally representative sample of non-institutionalized individuals in the United States. Combining interviews and medical examinations, NHANES collects a wide range of demographic, socioeconomic, dietary, physiological, and laboratory information, providing a robust platform to investigate the prognostic implications of AAC.

To contribute to the existing evidence, our study prospectively explores the relationship between AAC and all-cause, as well as cardiovascular mortality rates among adult individuals in the United States. Furthermore, we also aim to determine the strength of this association and assess whether it varies among populations with different comorbid factors such as gender, age, hypertension, and diabetes.

Methods

Study design and participants

Administered by the National Center for Health Statistics (NCHS), NHANES is conducted with approval from the institutional ethics review board of NCHS, and written informed consent is obtained from all participants. The research data were obtained on February 9, 2024, ensuring that individual participants remained anonymous throughout the study. Our study specifically focused on NHANES participants aged 40 years or older during the 2013–2014 cycle. Inclusion criteria encompassed individuals with complete survival information, AAC measurements, and relevant demographic variables. At the outset, our initial study cohort consisted of 10175 participants. Subsequently, we refined the sample by excluding individuals below the age of 40 years (n = 6360), those with incomplete AAC data (n = 675), insufficient survival data (n = 9), and participants with missing covariate information (n = 690). A comparison of all-cause mortality between the 690 participants with missing covariate data and those with complete data revealed no significant difference. Consequently, we derived a final analytical sample comprising 2717 participants.

The analyzed cohort exhibited common characteristics of younger age, higher PIR, cohabitation status, and lower educational levels. Moreover, the study cohort predominantly consisted of non-Hispanic white participants (S1 Table). It should be noted that the differences between the included and excluded subsets highlight the need for cautious extrapolation of the study results to a broader population.

Study variables

Demographic characteristics.

Demographic Characteristics: Information obtained through questionnaires during in-home interviews, categorized age into two groups (40–59 years or ≥ 60 years). Race included non-Hispanic White, non-Hispanic Asian, Mexican American, Other Hispanic, non-Hispanic Black, and Other Race. The PIR evaluated income in relation to federal poverty thresholds and was divided into three categories: < 1.38 (indicating low income), 1.38–3.99 (representing middle income), and ≥ 4.00 (reflecting high income) [14]. Marital status was characterized as either married/living with a partner or single [15]. Educational levels were categorized into college graduate or above, some college or associate’s degree, and high school degree/equivalency or less [15].

Definition of mortality.

Mortality Definition: Baseline information from NHANES 2013–2014 was linked with mortality records sourced from the National Death Index death certificates, extending through December 31, 2019. The linkage employed a probabilistic matching algorithm to ascertain mortality status. The study’s outcomes encompassed both all-cause mortality and mortality specific to cardiovascular disease (CVD) (coded I00–I09, I11, I13, I20–I51, and I60–I69), utilizing the International Classification of Diseases, Tenth Revision.

Measurements and definition of AAC.

AAC Measurements and Definition: The degree of AAC was evaluated using the Kauppila scoring system [16], ranging from 0 to 3 for each of the eight segments, with a total score of 24. A widely accepted threshold designating severe abdominal aortic calcification (SAAC) was applied when the AAC score exceeded 6. In contrast, mild–moderate AAC (MAAC) was defined as a score ranging from 1 to 6 points [15, 17].

Statistical methods

Considering the complex sampling design of NHANES, all analyses were conducted by incorporating sample weights, clustering, and stratification to ensure nationally representative estimates. Weighted percentages presented categorical variables, and weighted means were used for continuous variables.

The decision to categorize AAC was motivated by the evident skewness in the data, with around thirty percent of participants reporting AAC. Kaplan-Meier survival curves were employed to compute cumulative mortality, utilizing three score categories of AAC metrics (no, mild–moderate, severe). Survey-weighted multivariable Cox proportional hazards regression models were then utilized to derive hazard ratios (HRs) and corresponding 95% confidence intervals (CIs) to assess the associations of AAC with the risks of all-cause and CVD-specific mortality. Model 1 did not incorporate adjustments for any covariates; Model 2 was adjusted for gender, age (as a continuous variable), race, education levels, marital status, and poverty ratio (as a continuous variable); Model 3 expanded on Model 2 by incorporating hypertension and diabetes. Schoenfeld residuals were used to test the proportional hazards assumption, and no violation was observed. To visualize the dose-response association of AAC levels with all-cause and CVD-specific mortality, we employed the restricted cubic spline (RCS) model without weights. This choice was made due to the unavailability of an RCS model specifically designed for complex, multistage sampling survey data.

To probe demographic-related disparities within susceptible subpopulations, we conducted stratified analyses based on age strata, sex, poverty ratio, hypertension, and diabetes. The significance of interactions was assessed by determining the P values for the product terms between AAC and the stratified factors. All statistical analyses were performed using R software (version 4.2.1), considering a two-sided P value of less than 0.05 as statistically significant.

Results

Participants characteristics

Following the application of weights, the study encompassed a total of 111799277 participants. Table 1 provides a summary of the baseline characteristics of the study population, organized by AAC level. The weighted mean age of the study participants was 57.42±11.53 years, with the weighted proportion of females being 51.34%. Statistically significant differences (all P values < 0.05) were observed in age, poverty status, education level, marital status, smoking, albuminuria, chronic kidney disease, hypertension, diabetes, CVD, albumin, and across different AAC levels (Table 1). Specifically, participants with SAAC were more likely to be older, economically disadvantaged, single, and smokers. They were also more likely to have concomitant renal insufficiency, diabetes, and cardiovascular diseases, as well as lower educational levels.

[Figure omitted. See PDF.]

Over a median follow-up period of 72 months (up to 85 months), there were 235 all-cause deaths, including 78 attributed to CVD. The weighted all-cause mortality rates were 5.3%, 12.2%, and 26.6% for the no, mild–moderate, and severe AAC groups, respectively. Similarly, the weighted CVD-specific mortality rates were 1.3%, 4.3%, and 10.4% for the respective AAC groups., respectively. Participants with a higher AAC score exhibited a significantly elevated cumulative incidence rate of both all-cause and CVD-specific mortality (P < 0.001 for all log-rank tests, Fig 1).

[Figure omitted. See PDF.]

Abbreviations: CVD = cardiovascular disease, AAC = abdominal aortic calcification, SAAC = severe AAC, MAAC = mild–moderate AAC.

Survival analysis

In the fully adjusted model (multivariable model 3), individuals with SAAC exhibited a higher risk of all-cause mortality in comparison to participants with no AAC (hazard ratio [HR] 1.70, 95% confidence interval [CI] 1.17–2.48). The multivariate-adjusted HR for each one-point increase in AAC score associated with all-cause mortality was 1.04 (95% CI 1.02–1.07; refer to Table 2). Notably, there were linear dose–response associations of AAC score with all-cause mortality (P for non-linearity >0.05; see Fig 2), suggesting that the risk of all-cause mortality increased linearly as the AAC score increased.

[Figure omitted. See PDF.]

The red line and shaded area represent the HR and 95% CI, respectively. The histogram illustrates the score distribution within the population. The HR (95% CI) was adjusted using Model 3, considering sex, age, race, marital status, education, poverty level, hypertension, and diabetes. Abbreviation: AAC = abdominal aortic calcification, HR = hazard ratio, CI = confidence interval.

[Figure omitted. See PDF.]

After adjusting for potential confounders, neither MAAC (HR 1.50, 95% CI 0.88–2.56) nor SAAC (HR 1.58, 95% CI 0.81–3.09) was independently associated with CVD-specific mortality risk. Additionally, with each incremental point increase in AAC score, there was no significant rise in the risk of CVD mortality (HR 1.04, 95% CI 1.00–1.08).

Stratified analysis

To enhance the applicability of the study outcomes, this analysis segment divides AAC into two groups: the AAC group (AAC score ≥ 1 point) and the non-AAC group. The results of subgroup analyses are summarized in Fig 3. We observed that the AAC group had higher all-cause mortality than the non-AAC group. In most subgroups, there was a positive correlation between AAC and all-cause mortality. However, we noted that the relationship between AAC and all-cause mortality was influenced by the interactions of gender and hypertension (gender: P Value<0.001 for interaction; hypertension: P Value = 0.004 for interaction).

[Figure omitted. See PDF.]

The HR (95% CI) was adjusted using Model 3, considering sex, age, race, marital status, education, poverty level, hypertension, and diabetes except the corresponding stratification variable. Abbreviation: HR = hazard ratio, CI = confidence interval.

The direct association between AAC and all-cause mortality was not evident in males, participants younger than 60 years, and participants without hypertension. Conversely, the direct association between AAC and all-cause mortality was observed in females, participants aged 60 years or older, and those with hypertension. These findings underscore the importance of considering demographic and clinical factors in assessing the impact of AAC on all-cause mortality.

Discussion

Utilizing a substantial representative sample of U.S. adults, our study demonstrates that individuals with elevated AAC levels face a heightened risk of all-cause mortality. Specifically, compared to patients without AAC, those with SAAC experience a 70% higher risk of all-cause mortality. Furthermore, for each additional point increase in AAC score, participants experience a 4% higher risk of all-cause mortality. However, the association with CVD-specific mortality was not as pronounced after adjusting for confounding factors. There is an approximately linear dose-response relationship between increases in AAC score and the elevated risk of all-cause mortality. Subgroup analyses revealed that the correlation between AAC and all-cause mortality remains significant in females, older individuals, and those with hypertension. Age and hypertension status were identified as important factors modifying the relationship between AAC and the risk of all-cause mortality. These results provide new evidence for the prognostic value of AAC, proving to be practical in predicting future rates of all-cause mortality. Incidentally discovered AAC in patients without known cardiovascular risk factors may necessitate further cardiovascular diagnostic testing.

Previous studies have primarily focused on specific populations such as dialysis patients and those with chronic kidney disease [18–20]. Our study targets the general population, expanding the breadth of knowledge in this area. There exists evidence supporting the promotive role of AAC in diabetes, cardiovascular diseases, and late-life mortality [2, 7, 9, 19]. A comprehensive systematic review and meta-analysis uncovered that individuals with advanced abdominal aortic calcification (AAC) face an elevated risk of cardiovascular events (risk ratio [RR] 1.83, 95% CI 1.40–2.39), all-cause mortality (RR 1.98, 95% CI 1.55–2.53), and fatal cardiovascular events (RR 1.85, 95% CI 1.44–2.39) [8]. Nevertheless, it is crucial to acknowledge that the encompassed studies were restricted to patients with chronic kidney disease and the elderly population, possibly amplifying the association between AAC and the risk of mortality. There are also conflicting study results, such as the research conducted by Ohya et al., which recruited 137 patients [21]. They reported that AAC is not a significant prognostic factor for all-cause mortality (HR 1.02, 95% CI 0.99–1.04). Of course, due to the limited sample size, the strength of evidence is insufficient. In alignment with earlier investigations, this study affirms that affordable and widely accessible imaging modalities can be employed to identify populations characterized by a notably heightened risk of mortality [9]. Our study’s linear dose-response findings suggest that any improvement is significant, particularly for patients with lower AAC scores, which is a novel result compared to previous research [8].

Notably, our study contributes to the literature by using NHANES, offering a larger and more diverse sample, thus enhancing the generalizability of the results. The stratified analysis revealed gender and hypertension as modifiers of the association between AAC and all-cause mortality. Hypertension is significantly associated with an elevated risk of CVD-specific and all-cause mortality [22]. Hypertension also mediates the relationship between aortic calcification and arterial stiffness, left ventricular hypertrophy, and diastolic dysfunction [23]. This emphasizes the importance of considering demographic factors in understanding the nuanced impact of AAC on mortality outcomes. Future research should explore the mechanisms underlying these variations and tailor preventive strategies accordingly. The prospective design enhances the credibility of the observed associations. However, limitations include the observational nature of the study, potential for residual confounding, and the exclusion of certain population segments, highlighting the need for cautious interpretation. Additionally, it must be acknowledged that, during the analysis, due to detected collinearity among covariates, our study did not account for numerous covariates, potentially introducing some degree of error into the results. However, on the flip side, it is worth noting that this study may be less susceptible to confounding factors.

It is now evident that SAAC can effectively identify individuals with an elevated risk of all-cause mortality. The potential utility of this information extends to aiding in treatment decisions, fostering patients’ awareness of disease risks and symptoms, serving as a motivational tool for lifestyle decisions and changes, enhancing individual risk prediction, and presenting new targets for innovative treatments. Furthermore, future research should delve into whether knowledge about AAC has enhanced primary prevention and clinical management strategies. Given its potential to complement the assessment of coronary artery calcification, it holds promise for contributing to the early detection and primary prevention strategies of prevalent clinical cardiovascular diseases.

Conclusions

In conclusion, our study, based on a nationally representative sample, establishes a significant association between AAC and an increased risk of all-cause mortality. The findings underscore the importance of considering AAC as a predictive marker for adverse health outcomes in the general population of the U.S. Further research and clinical attention to AAC could enhance risk prediction and inform preventive strategies.

Supporting information

S1 Table. Baseline characteristics of the included and excluded populations.

https://doi.org/10.1371/journal.pone.0314776.s001

(DOCX)

Acknowledgments

We extend our gratitude to the dedicated NCHS staff for their meticulous design, data collection, and administration of NHANES, making the valuable data accessible to the public. Our sincere thanks also go to all study participants for their invaluable cooperation.

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Citation: Sheng C, Cai Z, Yang P (2025) Association of the abdominal aortic calcification with all-cause and cardiovascular disease-specific mortality: Prospective cohort study. PLoS ONE 20(1): e0314776. https://doi.org/10.1371/journal.pone.0314776

About the Authors:

Chang Sheng

Roles: Formal analysis, Investigation, Methodology, Visualization, Writing – original draft

Affiliation: Department of Vascular Surgery, Xiangya Hospital, Central South University, Changsha, Hunan, China

Zhou Cai

Contributed equally to this work with: Zhou Cai, Pu Yang

Roles: Supervision, Writing – review & editing

E-mail: [email protected] (PY); [email protected] (ZC)

Affiliation: Department of Vascular Surgery, Xiangya Hospital, Central South University, Changsha, Hunan, China

Pu Yang

Contributed equally to this work with: Zhou Cai, Pu Yang

Roles: Funding acquisition, Supervision, Writing – review & editing

E-mail: [email protected] (PY); [email protected] (ZC)

Affiliations: Department of Vascular Surgery, Xiangya Hospital, Central South University, Changsha, Hunan, China, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, Hunan, China

ORICD: https://orcid.org/0000-0003-1370-9847

References

1. Reaven PD, Sacks J: Reduced coronary artery and abdominal aortic calcification in Hispanics with type 2 diabetes. Diabetes Care 2004, 27(5):1115–1120. pmid:15111530

2. Bartstra JW, Mali W, Spiering W, de Jong PA: Abdominal aortic calcification: from ancient friend to modern foe. Eur J Prev Cardiol 2021, 28(12):1386–1391. pmid:34647579

3. Levitzky YS, Cupples LA, Murabito JM, Kannel WB, Kiel DP, Wilson PW, et al: Prediction of intermittent claudication, ischemic stroke, and other cardiovascular disease by detection of abdominal aortic calcific deposits by plain lumbar radiographs. Am J Cardiol 2008, 101(3):326–331.

4. Chen HC, Wang WT, Hsi CN, Chou CY, Lin HJ, Huang CC, et al: Abdominal aortic calcification score can predict future coronary artery disease in hemodialysis patients: a 5-year prospective cohort study. BMC Nephrol 2018, 19(1):313. pmid:30409161

5. van der Meer IM, Bots ML, Hofman A, del Sol AI, van der Kuip DA, Witteman JC: Predictive value of noninvasive measures of atherosclerosis for incident myocardial infarction: the Rotterdam Study. Circulation 2004, 109(9):1089–1094. pmid:14993130

6. Harbaugh CM, Terjimanian MN, Lee JS, Alawieh AZ, Kowalsky DB, Tishberg LM, et al: Abdominal aortic calcification and surgical outcomes in patients with no known cardiovascular risk factors. Ann Surg 2013, 257(4):774–781. pmid:23001086

7. Echouffo-Tcheugui JB, Allison M, Kalyani RR, Sims M, Bertoni AG, Golden SH: Abdominal Aortic Calcification Among Individuals With and Without Diabetes: The Jackson Heart Study. Diabetes Care 2017, 40(8):e106–e107. pmid:28626009

8. Lewis JR, Schousboe JT, Lim WH, Wong G, Wilson KE, Zhu K, et al: Long-Term Atherosclerotic Vascular Disease Risk and Prognosis in Elderly Women With Abdominal Aortic Calcification on Lateral Spine Images Captured During Bone Density Testing: A Prospective Study. J Bone Miner Res 2018, 33(6):1001–1010. pmid:29443425

9. Leow K, Szulc P, Schousboe JT, Kiel DP, Teixeira-Pinto A, Shaikh H, et al: Prognostic Value of Abdominal Aortic Calcification: A Systematic Review and Meta-Analysis of Observational Studies. J Am Heart Assoc 2021, 10(2):e017205. pmid:33439672

10. Ishii D, Sakamoto S, Okazaki T, Kuwabara M, Hosogai M, Horie N: Abdominal Aortic Calcification Volume Is Associated with Wall Enhancement of Unruptured Intracranial Aneurysm. World Neurosurg 2022, 167:e122–e126. pmid:35948212

11. Criqui MH, Denenberg JO, McClelland RL, Allison MA, Ix JH, Guerci A, et al: Abdominal aortic calcium, coronary artery calcium, and cardiovascular morbidity and mortality in the Multi-Ethnic Study of Atherosclerosis. Arterioscler Thromb Vasc Biol 2014, 34(7):1574–1579. pmid:24812323

12. Miwa Y, Tsushima M, Arima H, Kawano Y, Sasaguri T: Pulse pressure is an independent predictor for the progression of aortic wall calcification in patients with controlled hyperlipidemia. Hypertension 2004, 43(3):536–540. pmid:14757775

13. Schousboe JT, Taylor BC, Kiel DP, Ensrud KE, Wilson KE, McCloskey EV: Abdominal aortic calcification detected on lateral spine images from a bone densitometer predicts incident myocardial infarction or stroke in older women. J Bone Miner Res 2008, 23(3):409–416. pmid:17956153

14. Almohamad M, Krall Kaye E, Mofleh D, Spartano NL: The association of sedentary behaviour and physical activity with periodontal disease in NHANES 2011–2012. J Clin Periodontol 2022, 49(8):758–767. pmid:35634657

15. Fan H, Xiong Y, Huang Y, Li W, Xu C, Feng X, et al: Coffee consumption and abdominal aortic calcification among adults with and without hypertension, diabetes, and cardiovascular diseases. Nutr Metab Cardiovasc Dis 2023.

16. Pepe J, Diacinti D, Fratini E, Nofroni I, D’Angelo A, Pilotto R, et al: High prevalence of abdominal aortic calcification in patients with primary hyperparathyroidism as evaluated by Kauppila score. Eur J Endocrinol 2016, 175(2):95–100. pmid:27165861

17. Chen W, Eisenberg R, Mowrey WB, Wylie-Rosett J, Abramowitz MK, Bushinsky DA, et al: Association between dietary zinc intake and abdominal aortic calcification in US adults. Nephrol Dial Transplant 2020, 35(7):1171–1178. pmid:31298287

18. Tsai CH, Lin LY, Lin YH, Tsai IJ, Huang JW: Abdominal aorta calcification predicts cardiovascular but not non-cardiovascular outcome in patients receiving peritoneal dialysis: A prospective cohort study. Medicine (Baltimore) 2020, 99(37):e21730. pmid:32925715

19. Niu Q, Hong Y, Lee CH, Men C, Zhao H, Zuo L: Abdominal aortic calcification can predict all-cause mortality and CV events in dialysis patients: A systematic review and meta-analysis. PLoS One 2018, 13(9):e0204526. pmid:30240443

20. Tatami Y, Yasuda Y, Suzuki S, Ishii H, Sawai A, Shibata Y, Ota T, Shibata K, Niwa M, Morimoto R et al: Impact of abdominal aortic calcification on long-term cardiovascular outcomes in patients with chronic kidney disease. Atherosclerosis 2015, 243(2):349–355. pmid:26519631

21. Ohya M, Otani H, Kimura K, Saika Y, Fujii R, Yukawa S, et al: Vascular calcification estimated by aortic calcification area index is a significant predictive parameter of cardiovascular mortality in hemodialysis patients. Clin Exp Nephrol 2011, 15(6):877–883. pmid:21850576

22. Wang C, Yuan Y, Zheng M, Pan A, Wang M, Zhao M, et al: Association of Age of Onset of Hypertension With Cardiovascular Diseases and Mortality. J Am Coll Cardiol 2020, 75(23):2921–2930.

23. Cho IJ, Chang HJ, Park HB, Heo R, Shin S, Shim CY, et al: Aortic calcification is associated with arterial stiffening, left ventricular hypertrophy, and diastolic dysfunction in elderly male patients with hypertension. J Hypertens 2015, 33(8):1633–1641. pmid:26002844