Highlights
Key takeaways
– Adolescents with higher systolic blood pressure (SBP) had a dose-dependent higher prevalence of coronary atherosclerosis by coronary computed tomography angiography (CCTA) four decades later.
– Stage 2 hypertension in adolescence was associated with nearly doubled odds of severe coronary stenosis (≥50%) in middle age (OR 1.84; 95% CI, 1.40–2.42), with adjusted prevalence of 10.1% versus 6.9% for normal BP.
– Even adolescents meeting the newer ‘‘elevated’’ BP ranges (2025 ACC/AHA 120–129/<80 mm Hg and 2024 ESC 120–139/70–89 mm Hg) showed excess risk for severe coronary atherosclerosis.
Background and clinical importance
Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality globally. Atherosclerosis begins early in life, and traditional risk factors in youth — notably elevated blood pressure (BP) — have been linked to adverse cardiovascular structure and function in adulthood. Prior studies have used surrogate markers (carotid intima‑media thickness, coronary artery calcium) to infer long-term risk, but these markers capture limited aspects of the coronary atherosclerotic spectrum. Coronary computed tomography angiography (CCTA) offers a more granular, high‑resolution assessment, identifying luminal stenosis and plaque characteristics that more directly reflect clinically relevant coronary artery disease.
Understanding whether adolescent BP predicts later-life coronary atherosclerosis as defined by CCTA has major implications: it may inform early screening strategies, lifetime risk communication, and policy around BP thresholds and preventive interventions in youth.
Study design and population
This population‑based cohort linked adolescent BP measured at Swedish Military Conscription (1972–1987) to coronary atherosclerosis assessed by CCTA within the Swedish Cardiopulmonary Bioimage Study (SCAPIS; 2013–2018). The analytic sample comprised 10,222 men with mean age 18.3 (SD 0.5) years at baseline and median age 57.8 years at follow-up. Median follow‑up was 39.5 years. Adolescent BP was categorized using the 2025 American College of Cardiology/American Heart Association (ACC/AHA) and 2024 European Society of Cardiology (ESC) guideline cut points, allowing evaluation of contemporary threshold definitions.
Primary outcome
The primary outcome was coronary atherosclerosis assessed by CCTA, groupable by maximal stenosis severity (no stenosis, 1–49% stenosis, and ≥50% stenosis). Analyses included multinomial logistic regression, adjusted marginal prevalences, and restricted cubic spline modeling to explore dose‑response relationships.
Key findings
Study population and event rates
– N = 10,222 men; baseline mean (SD) SBP 127.6 (10.7) mm Hg; DBP 68.3 (9.5) mm Hg.
– After ~40 years, 4,159 (45.7%) had 1%–49% coronary stenosis and 784 (8.6%) had ≥50% stenosis on CCTA.
Association between adolescent BP and coronary atherosclerosis
– There was a graded, dose‑dependent association between higher adolescent BP and later coronary stenosis. Both categorical and spline analyses supported a monotonic relationship.
– Adolescents with stage 2 hypertension (per the study’s guideline categorization) had higher odds of severe coronary stenosis (≥50%) in middle age: OR 1.84 (95% CI, 1.40–2.42) compared with those with normal BP.
– Adjusted prevalence of severe stenosis for stage 2 hypertension in adolescence was 10.1% (95% CI, 8.6%–11.5%), compared with 6.9% (95% CI, 5.7%–8.1%) for those with normal adolescent BP.
– Notably, adolescents in the ‘‘elevated’’ BP categories used by the 2025 ACC/AHA (120–129/<80 mm Hg) and the 2024 ESC (120–139/70–89 mm Hg) also demonstrated higher prevalence of severe coronary atherosclerosis in middle age, indicating excess risk even below conventional hypertensive thresholds.
– The associations were stronger for systolic BP than diastolic BP, consistent with SBP’s increasing importance as a predictor of atherosclerotic outcomes over the life course.
Clinical and statistical significance
The observed effect sizes (ORs near 1.8 for stage 2 hypertension) and absolute differences in adjusted prevalence are clinically meaningful when applied across populations: even modest relative increases in severe atherosclerosis translate to substantive population burden when adolescent elevations are common.
Interpretation and biological plausibility
These results reinforce the thesis that BP exposure beginning in adolescence contributes to the pathogenesis and progression of coronary atherosclerosis over decades. Mechanistically, early elevated SBP may exert chronic hemodynamic stress on the arterial wall, promoting endothelial dysfunction, intimal thickening, arterial remodeling, and pro‑atherogenic inflammatory signaling. Pulse pressure and systolic load are closely linked to shear stress abnormalities that accelerate plaque formation and progression, which aligns with the stronger association observed for SBP.
That risk is evident at BP levels traditionally considered ‘‘elevated but not hypertensive’’ suggests a continuum of vascular injury beginning earlier than thresholds used for adult treatment decisions. These data underscore the importance of lifetime cumulative exposure to elevated BP rather than cross‑sectional adult measurements alone.
Clinical and public health implications
Screening and surveillance
– Routine BP measurement in adolescents is affirmed as an important preventive activity. The findings support earlier and sustained monitoring of BP beginning in adolescence.
Risk communication and prevention
– Clinicians should view adolescent SBP elevations as meaningful signals for long‑term cardiovascular risk. Behavioral interventions (dietary modification, physical activity promotion, weight management, sleep hygiene, and tobacco avoidance) are first‑line, scalable strategies appropriate for adolescents with elevated BP.
Treatment considerations
– The study stops short of prescribing pharmacotherapy thresholds in adolescents. Current pediatric and adolescent hypertension guidelines generally reserve antihypertensive medication for persistent, higher‑grade hypertension, end‑organ effects, or secondary causes. However, population‑level results like these may prompt re‑evaluation of thresholds for intensified prevention and closer follow‑up.
Policy and systems-level actions
– Schools, primary care, and public health programs should incorporate accessible BP screening, counseling, and programs targeting upstream determinants (obesity prevention, healthy food access, physical activity infrastructure).
Strengths
– Large, population‑based sample with long follow‑up (~40 years), reducing short‑term biases and allowing assessment of midlife coronary disease.
– Use of CCTA provides a detailed, clinically relevant measure of coronary atherosclerosis across the stenosis spectrum, beyond traditional surrogate markers.
– Evaluation against contemporary guideline BP categories highlights the translational relevance of the findings for current clinical thresholds.
Limitations
– The cohort comprised men conscripted for military service; results may not generalize to women or to populations with different sociodemographic characteristics.
– Adolescent BP was measured at conscription; if measurements were single occasions, this could introduce misclassification (regression dilution) and attenuate associations.
– The observational design cannot prove causality and is susceptible to residual confounding (e.g., childhood socioeconomic status, family history, dietary patterns) despite adjustment.
– The study did not present lifelong BP trajectories or account for BP changes and treatment across adulthood; cumulative exposure to BP and adult management likely modulate risk.
Expert commentary and guideline context
These findings add weight to growing evidence that early BP elevations carry long‑term vascular consequences. While adult guidelines (e.g., the 2017 ACC/AHA guideline) have emphasized lower BP thresholds for risk classification in adults, the optimal approach for adolescents remains debated. The study’s observation that ‘‘elevated’’ adolescent BP portends more severe later disease argues for intensified lifestyle interventions and systematic follow‑up.
Experts would caution that population‑level policies should balance potential benefits of earlier intervention against risks of medicalization and the lack of randomized trial evidence for pharmacologic prevention in adolescents without clear indications. Nevertheless, the data make a strong case for integrating adolescent BP into lifetime cardiovascular risk assessment and prevention frameworks.
Conclusions
In this large, long‑term cohort of Swedish men, higher SBP in adolescence was associated with a dose‑dependent increase in coronary atherosclerosis by CCTA in middle age, with excess risk evident even in BP ranges labeled ‘‘elevated’’ by contemporary guideline definitions. The findings reinforce the concept of blood pressure as a life‑course exposure and support intensified surveillance and primary prevention beginning in youth. Future work should include women and diverse populations, clarify the role of BP trajectories and adult treatment, and evaluate interventions (behavioral or pharmacologic) that alter lifetime BP exposure and downstream atherosclerotic risk.
Funding and clinicaltrials.gov
Funding and specific trial registration details are reported in the original publication: Herraiz‑Adillo Á, Eriksson H, Ahlqvist VH, et al. Blood Pressure in Adolescence and Atherosclerosis in Middle Age. JAMA Cardiol. 2025. Readers should consult the primary article for full funding declarations and registration information.
References
– Herraiz‑Adillo Á, Eriksson H, Ahlqvist VH, Ballin M, Wennberg P, Daka B, Lenander C, Berglind D, Östgren CJ, Lundgren O, Rådholm K, Henriksson P. Blood Pressure in Adolescence and Atherosclerosis in Middle Age. JAMA Cardiol. 2025 Nov 19:e254271. doi:10.1001/jamacardio.2025.4271. Epub ahead of print. PMID: 41259058; PMCID: PMC12631567.
– Whelton PK, Carey RM, Aronow WS, et al. 2017 Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Hypertension. 2018;71(6):e13–e115. doi:10.1161/HYP.0000000000000065