Abstract
Background
The “warranty period” of a zero coronary artery calcium (CAC) score—the time until conversion to a detectable score—remains undefined for the Japanese population. This study determined the time to CAC incidence in a cohort of asymptomatic Japanese individuals with a CAC score of 0.
Materials and methods
This retrospective study analyzed 1,395 asymptomatic Japanese adults (median age 57 years [range 40–90]; 56% men) with a baseline CAC score of 0 who underwent repeated CAC scanning (median follow-up, 4.1 years). The time to conversion to detectable CAC (> 0) was estimated using Kaplan-Meier analysis and Cox proportional hazards models. Warranty periods were defined as the estimated time to reach cumulative incidence thresholds of 10% and 15%. Continuous relationships between baseline characteristics and warranty periods were visualized using spline curves.
Results
The progression from a zero to a positive CAC score was significantly associated with sex, age, and baseline risk. The estimated time to reach a 10% cumulative incidence was shorter for men (2.5 years; 95% CI, 2.1–3.0) than for women (4.0 years; 95% CI, 3.0–4.6). Interactions were observed between sex and age (p = 0.006) and sex and atherosclerotic cardiovascular disease (ASCVD) risk (p = 0.001). In men, the warranty period (10% threshold) shortened rapidly with age, decreasing from 3.5 years at age 42 to < 2.0 years at age 68. Conversely, women maintained a period > 3.0 years even at age 68. Higher baseline ASCVD risk scores were associated with shorter warranty periods; for the 10% threshold, the period dropped from 4.1 years at 1% risk to approximately 1.6 years for those with > 20% risk.
Conclusions
The warranty period for a zero CAC score in Japanese individuals varies substantially by age, sex, and cardiovascular risk. Older men and high-risk individuals exhibit rapid conversion (< 2 years), suggesting the need for more frequent surveillance.
Supplementary Information
The online version contains supplementary material available at 10.1007/s11604-026-01980-0.
Keywords: Coronary artery calcium, Atherosclerosis, Computed tomography, Prevention
Introduction
Atherosclerotic cardiovascular disease (ASCVD) remains a leading cause of morbidity and mortality worldwide [1, 2]. Approximately 50% of ASCVD-related deaths occur in asymptomatic individuals, underscoring the critical need for accurate risk stratification and timely preventive interventions in this population [3]. As the progression of atherosclerosis is largely driven by modifiable risk factors [4], the early identification of subclinical coronary atherosclerosis is essential to initiate interventions that can slow the progression to overt coronary heart disease, such as myocardial infarction.
Coronary artery calcium (CAC), quantified by non-contrast cardiac computed tomography (CT), is a robust marker of subclinical atherosclerosis strongly associated with ASCVD risk [5, 6]. The absence of coronary calcification (i.e., CAC = 0) serves as a powerful negative risk predictor, associated with a very low risk of future coronary events [7–12]. Consequently, the 2019 AHA/ACC guidelines suggest that individuals with intermediate 10-year ASCVD risk can avoid statin therapy if their CAC score is 0 [13].
The prevalence and severity of CAC vary substantially by age, sex, and ethnicity [14, 15]. A significant proportion of Japanese individuals in the target age group for ASCVD risk assessment fall into the intermediate-risk category yet have a CAC score of 0 [15]. For these individuals, determining the appropriate re-assessment interval is crucial for long-term risk management. Defining the time course for CAC development specifically in the Japanese population would help establish evidence-based re-screening guidelines and provide insights into ethnic differences in atherosclerotic progression. Therefore, this study aimed to determine the time to CAC incidence in a large cohort of asymptomatic Japanese individuals with a baseline CAC score of 0.
Materials and methods
Study design and cohort
This single-center retrospective observational study was approved by the Ethics Committee of Tohoku University (identifier: 2023-1-855). The requirement for written informed consent was waived due to the retrospective nature of the study.
Figure 1 illustrates the study eligibility flow. We included asymptomatic individuals who underwent comprehensive health check-ups at Yamanakako Clinic (Yamanashi, Japan) between 2016 and 2023. CAC scanning was an optional, self-paid component of this program. Repeat CAC scanning was not performed according to a pre-specified study protocol; rather, follow-up data were available only for participants who voluntarily elected to undergo subsequent health check-ups. We excluded individuals who did not undergo CAC scanning (representing those who opted out), those with detectable CAC (score > 0) at baseline, those with only a single CAC scan (no follow-up), and those with a history of percutaneous coronary intervention, myocardial infarction, stroke, transient ischemic attack, or heart failure at baseline.
Fig. 1.
Flowchart of study participant selection. Out of 6,843 individuals screened, 1,395 asymptomatic participants with a baseline CAC score of 0 and at least one follow-up scan were included in the final analysis. Major exclusions were detectable baseline CAC >0, lack of repeat scanning, and history of cardiovascular disease. CAC = coronary artery calcium; TIA = transient ischemic attack
Clinical data collection and laboratory measurements
Data on age, sex, medical history, medication use, and smoking status were obtained via a standardized questionnaire and verified against electronic medical records. Obesity was defined as a body mass index ≥ 25 kg/m². Hypertension was defined as systolic blood pressure ≥ 140 mmHg, diastolic blood pressure ≥ 90 mmHg, or current use of antihypertensive medication. Hypercholesterolemia was defined as a total cholesterol level ≥ 220 mg/dL. These definitions align with those used in the Hisayama Study [16]. The 10-year atherosclerotic cardiovascular disease (ASCVD) risk was calculated using a validated prediction model derived from the Hisayama Study [17]. Risk categories were classified as low (< 5.0%), intermediate (5.0% to 19.9%), and high (≥ 20%), consistent with American guidelines [13].
Coronary artery calcium scanning and measurements
Baseline and follow-up CAC scans were performed using a standardized protocol on a 32-slice CT scanner (Biograph mCT Flow, Siemens Healthineers, Erlangen, Germany) without iodine contrast and with electrocardiography gating. Scan parameters included a tube voltage of 120 kVp, tube current regulated by automatic exposure control (CARE Dose 4D), and a slice thickness and increment of 3.0 mm. CAC was quantified by experienced technicians using semi-automated software (AZE Virtual Place; AZE, Inc, Tokyo, Japan) according to the Agatston method [18].
Statistical analyses
Continuous variables are presented as medians with interquartile ranges (Q1–Q3), and categorical variables as numbers and percentages. To describe the overall progression of coronary calcification, we estimated the cumulative incidence of conversion from a baseline CAC score of 0 to scores > 0, >10, and > 100 using the Kaplan-Meier method. For individuals with multiple follow-up scans, the time-to-event for each specific threshold was defined as the time to the first scan demonstrating that the respective threshold (> 0, > 10, or > 100) was reached. Subsequent scans after reaching a specific threshold were not included in the analysis for that endpoint. Participants who did not reach the respective threshold during the study period were censored at the time of their last available scan. To assess the impact of demographics and risk profiles, we stratified the cumulative incidence of detectable CAC (score > 0) by age group (< 55, 55–65, > 65 years) and 10-year ASCVD risk category (Low < 5%, Intermediate 5–19.9%, High ≥ 20%), assessing differences with the log-rank test.
To determine the “warranty period” for a zero CAC score, we estimated the time required for the cumulative incidence of detectable CAC to reach clinically relevant thresholds of 10% (number needed to scan [NNS] = 10), 15% (NNS = 6), and 20% (NNS = 5). Before estimation, we confirmed the validity of the Cox proportional hazards models used for these projections by testing the proportional hazards assumption using Schoenfeld residuals. We then constructed Cox proportional hazards models with age and sex, or the 10-year ASCVD risk score, as covariates. Based on these models, we generated predicted survival curves for a continuous sequence of baseline ages and 10-year ASCVD risk scores. From each predicted curve, the time point at which the cumulative incidence reached the specified threshold was extracted as the point estimate. Corresponding 95% confidence intervals (CIs) were derived from the intersection of the threshold with the upper and lower 95% confidence bounds of the predicted survival curves. To visualize the continuous relationship between baseline characteristics and the warranty period, we applied locally weighted scatterplot smoothing (LOWESS) regression with a span of 0.7 to smooth both the point estimates and their 95% CIs.
As a sensitivity analysis, we performed the same warranty period estimation using a Weibull parametric survival model to confirm the robustness of our findings [19–21]. To evaluate potential selection bias due to loss to follow-up, we compared the baseline characteristics of included participants (those with repeat CAC scanning) versus those excluded due to a lack of follow-up scans. Differences between groups were assessed using the Wilcoxon rank-sum test for continuous variables and the Chi-square test for categorical variables. A two-sided p-value < 0.05 was considered statistically significant. All analyses were performed using R version 4.4.0 [22].
Results
Participant characteristics
Of 6,843 individuals screened, 1,395 asymptomatic participants with a baseline CAC score of 0 were included in the final analysis (Fig. 1). Primary exclusions were the absence of CAC testing, detectable baseline CAC (> 0), lack of repeat scanning, or history of cardiovascular disease. Table 1 summarizes baseline characteristics. The median age was 57 years (IQR 50–64), and 56% were men. Hypertension (35%) and hypercholesteremia (50%) were common, while diabetes mellitus was rare (4.7%). Most participants fell into the low (34%) or intermediate (61%) 10-year ASCVD risk categories. The risk factor profiles differed notably between sexes; men had a higher prevalence of hypertension, hypercholesteremia, and smoking, as well as higher 10-year ASCVD risk scores compared to women. The median follow-up duration was 4.1 years (IQR 2.0–6.0). Regarding potential selection bias, participants excluded due to a lack of follow-up scans (n = 1,713) were significantly younger and had lower antihypertensive medication use but higher smoking rates compared to the study cohort (Supplemental Table 1). However, the median 10-year ASCVD risk score was identical (5.6%) between the groups, suggesting a broadly comparable cardiovascular risk profile.
Table 1.
Characteristics of the study population
| Variables | Overall N = 1,395 |
Men N = 784 |
Women N = 611 |
|---|---|---|---|
| Age, yr. | 57 (50–64) | 53 (47–61) | 59 (55–66) |
| Age categories, n (%) | |||
| <55 years | 590 (42%) | 443 (57%) | 147 (24%) |
| 55–65 years | 510 (37%) | 223 (28%) | 287 (47%) |
| >65 years | 295 (21%) | 118 (15%) | 177 (29%) |
| Body mass index, kg/m2 | 23.6 (21.4–25.7) | 24.6 (22.8–26.8) | 21.7 (19.8–24.1) |
| Waist circumference, cm | 89 (83–96) | 91 (86–97) | 85 (79–93) |
| Obesity, n (%) | 455 (33%) | 351 (45%) | 104 (17%) |
| Hypertension, n (%) | 487 (35%) | 306 (39%) | 181 (30%) |
| Hypercholesteremia, n (%) | 696 (50%) | 353 (45%) | 343 (56%) |
| Diabetes mellitus, n (%) | 66 (4.7%) | 52 (6.7%) | 14 (2.3%) |
| Systolic blood pressure, mmHg | 125 (113–135) | 126 (115–135) | 124 (112–135) |
| Diastolic blood pressure, mmHg | 78 (70–86) | 80 (73–88) | 75 (67–82) |
| Serum total cholesterol, mg/dL | 220 (197–244) | 215 (190–240) | 226 (204–250) |
| Serum LDL cholesterol, mg/dL | 130 (108–150) | 128 (107–149) | 131 (110–152) |
| Serum HDL cholesterol, mg/dL | 64 (53–77) | 57 (48–68) | 73 (62–87) |
| Serum triglycerides, mg/dL | 96 (70–143) | 116 (81–173) | 81 (61–106) |
| Hemoglobin A1c, % | 5.1 (4.9–5.4) | 5.1 (4.9–5.4) | 5.1 (5.0–5.3) |
| Current or past smoker, n (%) | 692 (50%) | 550 (60%) | 142 (23%) |
| Antihypertensive agents, n (%) | 261 (19%) | 162 (21%) | 99 (16%) |
| Statin, n (%) | 144 (10%) | 72 (9.2%) | 72 (12%) |
| 10-year ASCVD risk, % | 5.6 (4.2–9.8) | 7.4 (4.2–12.8) | 5.6 (4.2–7.4) |
| Risk categories, n (%) | |||
| Low (< 5%) | 479 (34%) | 206 (26%) | 273 (45%) |
| Intermediate (5%–19.9%) | 849 (61%) | 520 (66%) | 329 (54%) |
| High (≥ 20%) | 67 (4.8%) | 58 (7.4%) | 9 (1.5%) |
Continuous variables are summarized as median and interquartile ranges (25–75%) in parentheses, and categorical variables are summarized raw number and percentages in parentheses
LDL = low-density lipoprotein; HDL = high-density lipoprotein; ASCVD = atherosclerotic cardiovascular disease
Cumulative incidence of coronary artery calcium
The number of rescreened participants decreased over time, from 997 (71%) at 0–2 years to 279 (20%) after 6 years (Table 2). The crude incidence of detectable CAC (score > 0) increased from 7.2% at 0–2 years to 11.5% at 4–6 years. Figure 2 illustrates incidence stratified by severity. While the cumulative incidence of detectable CAC increased steadily, progression to moderate CAC (> 100) remained negligible (< 1%) during the first 4 years. Stratified analyses showed significant differences in CAC incidence by sex, age, and ASCVD risk (all Log-rank p < 0.001) (Supplemental Fig. 1). As shown in Fig. 3, incidence rates increased with advancing age and higher risk categories in both sexes. Notably, men in the high-risk group (≥ 20%) exhibited a rapid rise, exceeding 50% cumulative incidence by year 6.
Table 2.
Number of participants scanned
| Time from index CAC Scan | Number of participants rescanned with baseline CAC = 0 | Number of participants with incident CAC N (% of those rescanned) |
|---|---|---|
| 0–2 yrs. | 997 (71%) | 72 (7.2%) |
| 2–4 yrs. | 864 (61%) | 71 (8.2%) |
| 4–6 yrs. | 620 (44%) | 71 (11.5%) |
| > 6 yrs. | 279 (20%) | 28 (10.0%) |
Participants with multiple follow-up scans are counted in each applicable time interval
Fig. 2.
Cumulative incidence of coronary artery calcium progression. The curves illustrate the cumulative incidence of developing detectable CAC (score >0), mild or more CAC (score >10), and moderate or more CAC (score >100) among asymptomatic Japanese with a baseline CAC score of 0. Shaded areas indicate 95% confidence intervals. CAC = coronary artery calcium
Fig. 3.
Cumulative incidence of detectable coronary artery calcium according to age and ASCVD risk. Kaplan-Meier curves show the cumulative incidence of developing detectable CAC (score > 0). Panel (a) and (b) display stratification by age groups (< 55, 55–65, and > 65 years) for men and women, respectively. Panels (c) and (d) display stratification by 10-year ASCVD risk categories (Low < 5%, Intermediate 5–19.9%, and High ≥ 20%). Shaded regions indicate 95% confidence intervals. ASCVD = atherosclerotic cardiovascular disease; CAC = coronary artery calcium
Estimated time to onset of coronary artery calcium (warranty period)
The proportional hazards assumption was satisfied for all models (global p > 0.05 for all). Table 3; Fig. 4 present the estimated time to reach 10% and 15% CAC incidence. Overall, the time to 10% incidence was significantly shorter for men (2.5 years; 95% CI, 2.1–3.0) than for women (4.0 years; 95% CI, 3.0–4.6). Similarly, for the 15% threshold, men required 3.8 years compared to 5.0 years for women. Significant interactions were observed between sex and age (p = 0.006) and between sex and ASCVD risk (p = 0.001). Spline curves in Fig. 4 visualize these continuous relationships. In men, the estimated time to 10% incidence decreased from approximately 4.2 years at age 42 to 1.9 years at age 68. Women maintained longer intervals, decreasing from approximately 6.2 years to 2.9 years over the same age range. Regarding ASCVD risk, the warranty period shortened non-linearly as risk scores increased; for the 10% threshold, the time dropped from 4.9 years at 1% risk to approximately 1.8 years at > 20% risk (Fig. 4c). A similar pattern was observed for the 15% threshold (Fig. 4d), where the warranty period decreased from 6 years in the lowest risk range to approximately 2 years in the highest risk range.
Table 3.
Time to incidence of CAC by cox proportional hazard model
| 10% (NNS = 10) Men |
10% (NNS = 10) Women |
15% (NNS = 6) Men |
15% (NNS = 6) Women |
20% (NNS = 5) Men |
20% (NNS = 5) Women |
|
|---|---|---|---|---|---|---|
| All | 2.5 (2.1–3.0) | 4.0 (3.0–4.6) | 3.8 (3.0–4.3) | 5.0 (4.4–5.8) | 4.6 (4.1–5.0) | 6.0 (5.1–6.8) |
| Age category | ||||||
| <55 years | 3.0 (2.5–4.0) | 4.9 (4.1–6.2) | 4.3 (3.8–5.0) | 6.2 (5.1–7.5) | 5.0 (4.6–6.1) | 7.1 (6.3–NR) |
| 55–65 years | 2.8 (2.2–3.7) | 4.6 (3.9–5.3) | 4.0 (3.0–4.8) | 5.8 (5.0–7.0) | 4.8 (4.1–5.7) | 6.8 (6.0–NR) |
| >65 years | 1.9 (1.6–2.1) | 2.5 (2.1–3.4) | 2.1 (2.0–2.9) | 3.8 (3.0–4.6) | 2.9 (2.2–3.8) | 4.7 (4.0–5.4) |
| Risk category | ||||||
| Low | 4.7 (4.0–6.0) | 5.3 (4.6–7.0) | 5.9 (5.0–7.3) | 6.8 (5.9–NR) | 7.0 (6.0–NR) | 7.4 (7.0–NR) |
| Intermediate | 2.4 (2.1–3.0) | 3.0 (2.4–4.0) | 3.7 (3.0–4.2) | 4.3 (3.8–5.0) | 4.4 (4.0–5.0) | 5.0 (4.6–6.0) |
| High | 1.6 (1.0–2.0) | 1.9 (1.4–2.5) | 2.0 (1.7–2.6) | 2.2 (1.9–3.8) | 2.2 (2.0–3.4) | 2.9 (2.1–4.6) |
NNS = number need to scan; NR = not reached
Fig. 4.
Estimated Time to onset of detectable coronary artery calcium according to age and ASCVD risk by cox proportional hazard model. The spline curves illustrate the estimated years until the incidence of detectable CAC (score > 0) reaches 10% (NNS = 10; a, c) and 15% (NNS = 6; b, d). Panels (a) and (b) display estimates stratified by baseline age and sex. Panels (c) and (d) display estimates according to the baseline 10-year ASCVD risk score. Shaded regions indicate 95% confidence intervals. ASCVD = atherosclerotic cardiovascular disease; CAC = coronary artery calcium; NNS = number need to scan
Sensitivity analyses
Estimates derived from the Weibull parametric survival model were consistent with the primary Cox proportional hazards analysis (Supplemental Table 2). For instance, the time to 10% incidence in men was estimated at 2.8 years (95% CI, 2.5–3.1) using the Weibull model, compared to 2.5 years in the primary analysis. The trajectories of the age- and risk-dependent curves were also similar between models (Supplemental Fig. 2), confirming the robustness of the findings.
Discussion
In this large-scale longitudinal study of asymptomatic Japanese individuals with a baseline CAC score of 0, we determined the “warranty period” (time to CAC incidence) stratified by age, sex, and ASCVD risk. Our main findings are threefold. First, the warranty period shortened significantly with advancing age, with men developing calcification markedly earlier than women across all age groups. Second, a higher baseline 10-year ASCVD risk score was strongly associated with a shorter warranty period in a dose-response manner. Third, we established specific time intervals required for the cumulative incidence of detectable CAC to reach clinically relevant thresholds of 10% (NNS = 10) and 15% (NNS = 6). These estimates provide the first population-specific reference tool to guide personalized re-screening intervals for the Japanese population. Additionally, we observed a substantial lag time between the onset of detectable CAC and the progression to more advanced calcification (CAC > 100), suggesting a window of opportunity for early intervention.
The observed sex-dependent disparity in the time to CAC incidence aligns with established biological mechanisms and is strongly corroborated by our recent cross-sectional analysis of the same cohort [15]. In that study, the prevalence of detectable CAC in men surged rapidly between the ages of 40 and 60, whereas in women, a comparable increase was delayed until after the age of 60. The present longitudinal study extends these observations by quantifying the “speed” of this progression. The rapid shortening of the warranty period in middle-aged men directly corresponds to the steep rise in prevalence seen in the cross-sectional data, reflecting an accelerated atherosclerotic process during this life stage. Conversely, the sustained warranty period in pre- and peri-menopausal women mirrors the delayed onset of calcification prevalence, likely attributable to the vasoprotective effects of estrogen [23]. Together, these complementary datasets provide a comprehensive picture of CAC dynamics in the Japanese population: men experience an earlier “calcification phase” starting in their 40s, while women benefit from a prolonged “latent phase” that extends well into their 60s.
Our warranty period estimates also highlight important ethnic differences when compared to the MESA study [20]. In our Japanese cohort, the estimated times to 15% (NNS = 6) and 20% (NNS = 5) CAC incidence for men were 3.8 and 4.6 years, respectively. These intervals are longer than those reported for White and Black men in MESA but shorter than those for Chinese American men. Conversely, for Japanese women, the warranty periods were 5.0 and 6.0 years, respectively, which are longer even than those of Chinese American women in MESA. These variations likely stem from a combination of factors, including differences in ethnicity, lifestyle-related risk profiles at baseline (Supplemental Table 3), and potentially the high follow-up rate in the early phase of our study. Specifically, the markedly longer warranty period in Japanese women suggests a lower atherosclerotic burden in this subgroup, reinforcing the need for population-specific screening guidelines rather than applying Western or even generalized Asian data.
The robust inverse association between baseline 10-year ASCVD risk scores and the warranty period provide compelling radiographic evidence that a higher burden of cardiovascular risk factors accelerates subclinical vascular damage. Our data demonstrate a clear dose-response relationship: as the ASCVD risk score increases, the time to developing calcification shortens progressively. This non-linear decay is particularly steep in the transition from low to intermediate risk, highlighting that even moderate elevations in risk profile can significantly precipitate the onset of calcification. These findings are consistent with observations from the MESA study, which also reported a graded shortening of the warranty period with increasing risk factor burden and demonstrated the varying contributions of individual risk factors such as diabetes and smoking to CAC incidence [24]. Importantly, our results extend this concept to the Japanese population, showing that despite a generally lower atherosclerotic baseline, the fundamental biological impact of aggregated risk factors on arterial calcification remains consistent. This underscores the potential of using the ASCVD risk score not only for estimating event risk but also for tailoring the timing of initial and repeat CAC screening; individuals with intermediate-to-high risk scores warrant earlier and more frequent surveillance to detect the transition from a “zero” to a “positive” score. While the emergence of mild calcification (CAC > 0) does not imply an immediate high risk of cardiovascular events, it signifies the loss of the unique “very low risk” status (“power of zero”) that justifies withholding statin therapy. According to the 2019 AHA/ACC guidelines [13], for adults with intermediate (10-year ASCVD risk 7.5% to 20%) or borderline (5% to 7.5%) risk, initiating statin therapy is reasonable if the CAC score is 1 to 99 (particularly for those ≥ 55 years of age) or ≥ 100 (or ≥ 75th percentile). Although these specific US-based criteria may not be directly applicable to Japanese clinical practice in their entirety, they reinforce the concept that the transition to a positive CAC score marks a critical clinical inflection point. This transition signals the need to re-evaluate preventive strategies—such as considering statin initiation or intensifying lifestyle modifications—based on the individual’s comprehensive ASCVD risk profile.
This study has several limitations. First, this was a single-center, retrospective observational study of voluntary health check-up participants at a facility requiring a membership fee. This design introduces potential selection bias, as participants may have higher socioeconomic status and health awareness compared to the general population. Additionally, our analysis comparing included participants with those excluded due to a lack of follow-up (Supplemental Table 1) showed that the excluded group was significantly younger. These factors suggest that our warranty period estimates may more closely represent a slightly older, health-conscious population with higher socioeconomic status and might not be fully generalizable to the general public or younger individuals who do not undergo regular health check-ups. Second, we defined the warranty period based on CAC conversion, not hard cardiovascular events. Since we did not evaluate the occurrence of outcomes such as myocardial infarction or cardiovascular death, the warranty period defined here represents the duration of maintaining a zero CAC score and cannot be directly equated to a period free from clinical cardiovascular events. Future prospective studies are needed to confirm the prognostic validity of these intervals in the Japanese population. Third, non-contrast CT cannot detect non-calcified plaque; thus, a zero score does not rule out all atherosclerosis. Fourth, due to the relatively short follow-up (median 4.1 years), we could not fully estimate warranty periods for advanced calcification endpoints or higher incidence thresholds (e.g., 20%) in low-risk subgroups. Fifth, because health check-ups were performed at discrete intervals rather than continuously, the data are subject to interval censoring, meaning the precise moment of CAC onset could not be determined. Finally, the number of participants in certain subgroups (e.g., high-risk young women) was small, limiting estimation precision.
In conclusion, we determined the time to the incidence of CAC in asymptomatic Japanese individuals with a baseline CAC score of 0, stratified by age, sex, and ASCVD risk. Our findings provide compelling radiographic evidence of the cumulative vascular damage associated with aging, male sex, and elevated cardiovascular risk factors. Clinically, these population-specific warranty periods provide a practical framework for determining re-screening intervals when follow-up testing is considered appropriate, facilitating more personalized risk assessment strategies tailored to the specific profile of each patient.
Supplementary Information
Below is the link to the electronic supplementary material.
Acknowledgements
None.
Abbreviations
- ASCVD
Atherosclerotic cardiovascular disease
- CAC
Coronary artery calcium
- CI
Confidence interval
- CT
Computed tomography
- NNS
Number need to scan
Funding
This work was supported by research funding from the Department of Early Imaging Diagnosis (a joint research course); and by a Grant-in-Aid for Young Scientists from the Japan Society for the Promotion of Science (JSPS KAKENHI Grant Number 23K15150).
Data availability
The data that support the findings of this study are not publicly available due to ethical restrictions protecting patient privacy. De-identified data underlying the results presented in this article (including tables, figures, and supplemental materials) may be made available from the corresponding author upon reasonable request. Any request will require a formal data use agreement and approval from the Institutional Review Board of Tohoku University before data can be shared.
Declarations
Competing interests
All authors have no competing interest.
Ethical approval
This study was approved by the Ethics Committee of Tohoku University (identifier: 2023-1-855). The requirement for written informed consent was waived due to the retrospective nature of the study.
Footnotes
Publisher’s note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Data Availability Statement
The data that support the findings of this study are not publicly available due to ethical restrictions protecting patient privacy. De-identified data underlying the results presented in this article (including tables, figures, and supplemental materials) may be made available from the corresponding author upon reasonable request. Any request will require a formal data use agreement and approval from the Institutional Review Board of Tohoku University before data can be shared.