Associations between Life’s Essential 8 and abdominal aortic calcification among US Adults: a cross-sectional study

Abdominal aortic calcification (AAC) refers to the accumulation of calcium deposits in the abdominal aorta, the largest artery in the abdominal cavity [1]. This buildup within the arterial wall can render the aorta rigid and potentially narrow its passageway. Furthermore, these deposits contribute to the formation of atherosclerotic plaques, where lipid plaques accumulate and calcify along blood vessel walls, ultimately triggering cardiovascular disease (CVD) [2, 3]. Numerous prospective studies have affirmed the link between the severity of AAC and the incidence of CVD, including coronary artery disease, myocardial infarction, stroke, and increased mortality rates [4‐6]. Managing and preventing AAC is critical and desirable in reducing the prevalence and occurrence of cardiovascular disease.

In 2010, the American Heart Association (AHA) introduced Life’s Simple 7 (LS7), a set of cardiovascular health (CVH) metrics encompassing seven key behavioral and health factors: healthy diet, physical activity, normal body mass index (BMI), no smoking, normal blood pressure, normal fasting glucose, and normal total cholesterol [7]. Subsequent extensive research has shed light on the strengths and limitations of this initial approach in defining and quantifying cardiovascular health. Consequently, the AHA has recently updated its CVH assessment tool to Life’s Essential 8 (LE8), a scoring system more attuned to individual variations, emphasizing the significance of social factors and mental health in determining CVH [8]. Higher CVH scores, as assessed by LS7/LE8, have been correlated with a reduced risk of CVD and related mortality [9‐11].

Given the established correlation between LE8 and AAC with cardiovascular disease and cardiovascular death, we hypothesize that ideal CVH is associated with lower severity of AAC. Several lifestyle and clinical measures, such as a heart-healthy diet, physical activity, smoking status, sleep pattern, blood glucose, blood lipid, and blood pressure, have been associated with AAC risk [12‐16]. However, there remains unexplored territory concerning the relationship between CVH metrics evaluated through the LE8 score and AAC.

To explore the association of novel CVH metrics, and its components, with AAC, we first conducted an observational study utilizing data from the National Health and Nutrition Examination Survey (NHANES) cohort of 2013–2014.

This study, conducted among US NHANES participants (2013–2014), affirmed our hypothesis that adults with higher levels of CVH metrics assessed by LE8 have a reduced risk of ACC. We observed a linear dose–response association between increased LE8 score and decreased ACC risk, with each 10-point rise in LE8 score associated with a 13% reduction in mild-to-moderate ACC and a 23% reduction in severe ACC.

Several previous studies have explored the connection between CVH and artery calcification. For instance, a cohort study of 65,494 adults found a correlation between higher cardiovascular health scores assessed by LF7 and a lower prevalence of coronary artery calcification [24]. Similarly, The Coronary Artery Risk Development in Young Adults (CARDIA) Study, after a 20-year follow-up, identified a link between positive CVH changes during young adulthood and a reduced risk of coronary artery calcification risk in middle age [25]. Our findings align with these studies and expand on them by utilizing new CVH metrics based on the updated LE8 assessment. The LE8 scoring system, an enhancement of the LS7 metrics proposed by the AHA in 2010, provides a more refined evaluation of cardiovascular health, considering individual behaviors and indicators with increased sensitivity [8]. Our study demonstrated that higher total CVH metrics scores were associated with a notably reduced risk of mild-to-moderate and severe ACC in a dose–response manner. Spline plots illustrated that improvements at any level of CVH scores were associated with decreased ACC risks, underscoring the significance of even marginal improvements, particularly within individuals holding CVH scores of 61.25 or higher. Additionally, the subgroup analysis revealed a more robust inverse association between the novel CVH metrics and mild-moderate ACC in participants without CKD. The negative correlation between the CVH metrics and severe ACC was more pronounced among participants without CKD, without a history of CVD, and never married/widowed/divorced/separated. Notably, the novel CVH metrics in CKD/CVD patients is susceptible to more confounding factors, such as the presence of various illnesses, accompanying poor nutritional status, and altered lifestyle [26, 27]. Consequently, the novel CVH metrics may not accurately reflect the degree of ACC in CKD/CVD patients compared to general population. Furthermore, previous studies indicate that individuals who are never married, widowed, divorced, or separated represent potentially vulnerable subgroups due to diminished social support, higher psychological burdens and an increased risk of cardiovascular diseases [28, 29]. Therefore, special attention is warranted to prevent adverse health outcomes and mitigate additional burdens on healthcare systems in the future for this specific population.

The prevalence of a high CVH score based on LE8 among US adults was found to be low, and this total CVH score is inversely correlated with all-cause and CVD-specific mortality [30, 31]. AAC, as a marker of subclinical atherosclerotic disease and an independent predictor of subsequent vascular morbidity and mortality, could be utilized to identify individuals benefiting from more aggressive cardiovascular primary prevention strategies. While our study confirms the correlation between CVH and ACC, further prospective research is necessary to determine the causal relationship between cardiovascular health evaluated based on the LE8 score and arterial calcification.

In our correlation analysis between LE8 components and AAC, nicotine exposure score, blood glucose score, and blood pressure scores emerged as primary contributors to arterial calcification. Smoking, extensively studied for its association with arterial calcification, was examined here through nicotine exposure assessed by LE8, encompassing both active smoking and secondhand smoke exposure [32‐34], providing a more comprehensive and reasonable evaluation of smoking status. Elevated glucose levels have been linked to vascular smooth muscle cell calcification, contributing to diabetes-related vascular calcification [35, 36]. Our findings support a reduced risk of vascular calcification associated with optimal blood glucose levels, encompassing biochemical glucose levels, diabetic history, and medication status. Elevated blood pressure has been an independent and robust predictive factor for cardiovascular diseases, with significant correlations between systolic pressure and vascular calcification across all vessels [37]. Our detailed blood pressure assessment considered medication usage, revealing a negative correlation between blood pressure scores and calcification. Moreover, prior research has suggested obesity as a contributing factor to cardiovascular disease. However, our investigation evaluated participants’ weight status using BMI and found a positive correlation between BMI scores of LE8 and ACC risk. It’s worth noting that the association between BMI and arterial calcification has been inconsistent in previous studies [38, 39]. BMI, being an imperfect measure, does not precisely capture body fat and is unsuitable for multi-species studies [40]. Comparing our finding with previous research on this topic is rather difficult due to variations in study objectives, analytical approaches, and the diverse ethnic composition of the study populations.

Our study noted that physical activity levels and blood lipid scores were only associated with mild-to-moderate calcification and not with severe calcification. While previous studies have explored the link between physical activity and arterial calcification, our findings did not show consistent results [41, 42]. The latest research utilizing the NHANES database discovered a negative correlation between physical activity during working hours and the ACC score, while leisure-time physical activity exhibited no such association [13]. Given the inclusion of all moderate-to-vigorous physical activities, encompassing both work and leisure, consistent outcomes weren’t attained. Similarly, the relationship between blood lipid scores and severe calcification did not exhibit significant differences due to the limited number of participants with severe ACC.

Inconsistent with prior data, our study did not find an association between diet scores assessed by HEI-2015 and AAC, potentially due to scoring method variations [43]. Additionally, sleep health scores assessed by LE8 criteria did not correlate with ACC, differing from findings in previous cohort studies. Previous studies found longer sleep durations were significantly associated with decreased artery calcification, while severe obstructive sleep apnea was associated with a greater extent of AAC [12, 44]. However, the LE8 scoring system does not consider extended sleep beneficial; instead, an excessively extended sleep duration receives lower scores. These outcomes suggest that the AHA may consider reconsidering the ideal dietary or sleep health levels concerning ACC in future updates.

There are several strengths in this study. Our study was the first to explore the association of novel CVH metrics using LE8 and its components with AAC. Meanwhile, all the data we used were obtained from NHANES, which has a standardized data collection process to ensure data accuracy. Additionally, we explored the dose–response relationship between CVH and ACC, determining the minimum threshold for beneficial associations. However, we need to consider several potential limitations in our study. Firstly, although we controlled for several potential confounding factors, the cross-sectional design of our study limits establishing a causal relationship between CVH and AAC. Meanwhile, our findings distinctly indicate a correlation between better CVH and reduced ACC risk, laying the groundwork for further prospective research. Secondly, our analysis involved participants from a single nation, potentially limiting the generalizability of this study’s conclusions to many countries worldwide. Lastly, many indicators of CVH in our study relied on self-reported questionnaires, possibly introducing measurement errors and recall biases.

The findings of this study underscore the importance of public education and health campaigns emphasizing CVH concepts to promote overall health and prevent cardiovascular diseases. Enhancing public awareness of CVH concepts can elevate health consciousness and encourage proactive measures. Further research will deepen our understanding of the mechanisms and associations between cardiovascular health and arterial calcification, offering strategies for future prevention and treatment.

This cross-sectional study demonstrated that the novel CVH metrics, evaluated using LE8, had an inverse association with the risk of AAC. Among the LE8 components, nicotine exposure, blood glucose, and blood pressure emerged as significant factors linked to ACC risk. These findings suggest a promising role for LE8 as a viable method to promote cardiovascular health. Additionally, these findings may support further large-scale prospective studies to clarify the precise causality of this relationship for preventing vascular calcification and CVD.