Early-onset atherosclerotic cardiovascular disease in young adults: Lifestyle, environmental, and psychosocial risk factors

Abstract

Early-onset atherosclerotic cardiovascular disease (ASCVD) must be distinguished from cardiovascular risk factors and subclinical vascular abnormalities that may arise at younger ages. This narrative review critically examines lifestyle, environmental, metabolic, psychosocial, and inherited determinants among adolescents (10-19 years), young adults (20-39 years), and selected adults aged 40-54 years who remain within commonly used thresholds for premature events. The 40-54-year band is included selectively to bridge younger-adult prevention with guideline-based adult risk assessment and is not intended to redefine the upper age limit of premature ASCVD. Epidemiological evidence demonstrates a substantial burden of cardiovascular disease (CVD) among people aged 15-39 years; however, evidence of increasing clinically manifest ASCVD is less consistent than evidence of rising obesity, hypertension, dyslipidemia, diabetes, nicotine exposure, and subclinical vascular injury. Established causal drivers, including cumulative exposure to apolipoprotein B-containing lipoproteins and cigarette smoking, are distinguished from predominantly associative evidence concerning sleep disruption, psychosocial stress, e-cigarette use, and air pollution. Prevention should combine population-level health promotion with age-appropriate clinical risk assessment, including lipid screening and measurement of lipoprotein(a) at least once in adulthood, with additional targeted evaluation for familial hypercholesterolemia, a family history of premature ASCVD, obesity, hypertension, diabetes, chronic kidney disease, and smoking or vaping. Coronary artery calcium scoring and carotid imaging are not recommended as universal screening tests for asymptomatic young people, although they may refine clinical decisions in carefully selected adults. Digital tools may support engagement but should complement, rather than replace, validated clinical care and public-health measures.

Graphical abstract

Highlights

• •Premature ASCVD is defined separately from risk factors and subclinical vascular abnormalities.
• •Inherited susceptibility interacts with modifiable lifestyle, environmental, and psychosocial exposures.
• •Evidence is strongest for cumulative atherogenic-lipoprotein exposure, smoking, hypertension, and diabetes.
• •Prevention requires population measures plus age-appropriate, targeted risk assessment rather than universal imaging.

1. Introduction

CVD remains a leading cause of morbidity and mortality worldwide [1,2]. In this review, clinically manifest ASCVD refers to coronary heart disease, ischemic stroke, or peripheral arterial disease attributable to atherosclerosis. Although some epidemiological studies apply thresholds of <40 or <50 years, premature or early-onset ASCVD is commonly defined as a first clinical event before 55 years of age in men or 65 years of age in women. We use the term adolescents for individuals aged 10-19 years and young adults for those aged 20-39 years; younger adults is used only when a cited source encompasses a broader age range. The review focuses primarily on adolescents and young adults. Adults aged 40-54 years are included selectively because this age band provides a clinically relevant bridge to guideline-based 10-year/lifetime risk estimation and selective imaging, and because men in this band remain within the commonly used <55-year threshold for premature ASCVD. This organizational age band does not imply that premature ASCVD ends at age 54; women aged 55-64 years may still meet the conventional <65-year definition but are outside the principal population focus of this review. Risk factors, such as hypertension and dyslipidemia, and subclinical abnormalities, such as endothelial dysfunction, increased arterial stiffness, or coronary artery calcium (CAC), are not classified as clinical ASCVD.

Although clinical events are uncommon during adolescence, atherosclerosis may begin in childhood. Unfavorable lifestyle patterns, including physical inactivity, an unhealthy diet, nicotine exposure, insufficient sleep, and chronic stress, are associated with adverse adiposity, blood pressure, glycemia, lipid profiles, and vascular function [[3], [4], [5], [6]]. These pathways interact with inherited susceptibility and cumulative exposure across the life course; observational associations should not be interpreted as evidence that each exposure independently causes ASCVD.

Endothelial dysfunction, lipid deposition, low-grade inflammation, and arterial stiffening may occur decades before symptoms develop [4,5,7]. Their presence indicates vascular vulnerability but does not necessarily constitute clinically established disease.

The increasing prevalence of obesity, metabolic syndrome, dyslipidemia, hypertension, and insulin resistance among younger populations is therefore concerning because it may increase the future burden of premature ASCVD, even when temporal trends in clinical events remain uncertain [1,2,6].

Premature cardiovascular risk is also shaped by environmental and psychosocial conditions. Rapid urbanization, limited access to nutritious food and safe opportunities for physical activity, socioeconomic inequality, academic pressure, chronic stress, and social isolation may increase the vulnerability of younger populations [2,[7], [8], [9]]. These conditions may influence cardiovascular health through biological pathways, including inflammation and oxidative stress, and indirectly by encouraging unhealthy behaviors such as poor diet, smoking, physical inactivity, and insufficient sleep [4,[7], [8], [9], [10], [11]].

This narrative review critically appraises the epidemiology, modifiable and inherited determinants, biological mechanisms, risk assessment, and prevention of premature ASCVD. It distinguishes clinical events from risk-factor prevalence and subclinical vascular abnormalities, grades conclusions according to the underlying evidence, and considers the feasibility and implementation of age-specific approaches for adolescents and young adults.

Fig. 1 presents a life-course framework illustrating how inherited susceptibility, modifiable exposures, and environmental and psychosocial conditions relate to cardiovascular risk factors, subclinical vascular abnormalities, and clinically manifest premature ASCVD.

Fig. 1.

Life-course pathway to premature atherosclerotic cardiovascular disease.

Inherited susceptibility interacts with modifiable exposures and environmental and psychosocial conditions to influence conventional cardiovascular risk factors and subclinical vascular abnormalities. Although these states may increase the lifetime probability of clinically manifest premature ASCVD, they should not themselves be classified as clinical ASCVD. Solid arrows represent comparatively well-established relationships, whereas dashed arrows indicate relationships supported mainly by observational or surrogate-outcome evidence. Targeted, age-appropriate prevention may operate at multiple stages across the life course.

2. Methods

A structured search was conducted in PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar to identify English-language articles published between 1 January 2010 and 20 August 2026. Older landmark studies were retained when they were directly relevant to the narrative. The searches were last updated on 20 August 2026.

Search concepts were combined using Boolean operators and included (“premature” OR “early-onset” OR “young adult” OR adolescent) AND (“atherosclerotic cardiovascular disease” OR coronary disease OR stroke OR atherosclerosis), together with terms related to epidemiology, obesity, physical activity, diet, smoking, e-cigarettes, sleep, stress, air pollution, familial hypercholesterolemia, lipoprotein(a), dyslipidemia, family history, CAC, carotid ultrasound, digital health, telemedicine, sex, ethnicity, and prevention. The reference lists of key reviews and current ACC/AHA and ESC guidelines were also searched manually. A focused check of current ACC/AHA and ESC/EAS guidance was repeated through 18 September 2026 to verify recommendations on lipid assessment, lipoprotein(a), coronary artery calcium, and carotid imaging.

Eligible sources included clinical guidelines, systematic reviews, meta-analyses, cohort and case-control studies, randomized trials, and major mechanistic studies addressing adolescents, young adults, or premature ASCVD. Studies confined to older populations were included only when they informed a relevant mechanism, assessment method, or intervention and were explicitly identified as indirect evidence. Titles and abstracts were screened for relevance, followed by full-text assessment. Duplicate, non-English, non-peer-reviewed, and clinically unrelated reports were excluded. Because this was a narrative review, study selection was purposive rather than PRISMA-based, and no pooled effect estimate was calculated (see Table 1).

Table 1.

Age- and risk-stratified assessment of premature ASCVD.

Population	Baseline approach	When to intensify assessment	Imaging context
Adolescents (10-19 years)	Routine pediatric preventive care, including blood pressure, growth/adiposity, and exposure history; under 2026 ACC/AHA guidance, obtain a lipid profile at ages 9-11 years if not previously tested	Earlier/cascade lipid testing is appropriate from age ≥2 years when first- or second-degree relatives have premature ASCVD, severe hypercholesterolemia, or FH; also assess glycemia and other risk factors when clinically indicated	CAC and carotid imaging are not routine screening tests
Young adults (20-39 years)	Review conventional risk factors and lifetime risk; screen with a lipid profile from age 19 years and at least every 5 years under 2026 ACC/AHA guidance; measure Lp(a) at least once in adulthood [12,13]	Intensify evaluation for severe LDL-C elevation or FH, family history, elevated Lp(a), blood pressure, diabetes, CKD, inflammatory disease, nicotine exposure, and adverse social context	Consider CAC only in exceptional cases of persistent decision uncertainty; evidence below 40 years of age is limited
Selected adults (40-54 years)	Continue periodic lipid/risk-factor assessment; estimate 10-year and longer-term risk using guideline-recommended tools (e.g., PREVENT-ASCVD in ACC/AHA guidance) and ensure Lp(a) has been measured at least once [12,13]	Incorporate risk enhancers, family history, subclinical disease, and treatment preferences; this 40-54-year band is an organizational focus and does not redefine the upper age limit of premature ASCVD	CAC may refine lipid-lowering decisions when uncertainty persists (ACC/AHA: men ≥40 years, women ≥45 years with borderline/intermediate risk); ESC guidance also recognizes increased CAC/subclinical atherosclerosis as a risk modifier, while carotid/femoral plaque may be considered in selected settings [[12], [13], [14]]
Known risk factor or subclinical disease	Clinical management rather than population screening	Treat the identified condition and reassess adherence and response	Use imaging only if it changes diagnosis or management

Evidence was appraised qualitatively according to its hierarchy, consistency, directness to younger populations, sample size, duration, outcome ascertainment, and susceptibility to residual confounding. Guideline recommendations and randomized or genetically informed evidence were weighted more heavily than cross-sectional associations or surrogate outcomes. Because no formal risk-of-bias instrument was applied, the synthesis should be interpreted as a critical narrative overview rather than a systematic review or meta-analysis. For Table 2, evidence-strength labels were assigned using an explicit narrative framework: “strong” indicated convergent support from guideline recommendations plus randomized, genetic/causal, and/or consistent prospective clinical-outcome evidence with low concern for residual confounding; “moderate-to-strong” indicated consistent prospective or interventional evidence for risk-factor improvement with some causal or outcome support but fewer event-based data in younger populations; “moderate” indicated generally consistent observational and mechanistic or surrogate-outcome evidence with limited direct event-based or randomized evidence and plausible residual confounding; and “predominantly observational” indicated that associations were supported mainly by observational or surrogate-outcome studies, with important concerns about confounding, reverse causation, or indirectness. These categories are descriptive rather than formal GRADE ratings and were assigned by considering the hierarchy, consistency, directness, sample size, duration, outcome ascertainment, and confounding domains stated above.

Table 2.

Modifiable determinants, mechanisms, evidence strength, and preventive responses.

Determinant	Proposed pathway	Evidence appraisal	Prevention
Atherogenic lipoproteins/unhealthy diet	Cumulative retention of apoB-containing particles and foam-cell formation; diet also influences adiposity and glycemia	Strong evidence for LDL-C causality; moderate evidence for specific dietary patterns and premature events	Identify severe dyslipidemia or FH; promote a heart-healthy dietary pattern; provide guideline-directed lipid-lowering therapy
Physical inactivity/obesity	Adiposity, insulin resistance, BP, inflammation and endothelial function	Moderate-to-strong evidence for risk-factor improvement; fewer event-based trials in younger populations	Promote physical activity and less sedentary time through weight-sensitive, stigma-aware support
Combustible smoking	Endothelial injury, oxidative stress, thrombosis and inflammation	Strong, causal	Prevent initiation; cessation support; policy and smoke-free environments
E-cigarettes	Acute hemodynamic, oxidative and endothelial effects	Moderate evidence for acute surrogate outcomes; limited evidence for long-term clinical events	Prevent uptake among young people; support complete nicotine cessation; avoid implying proven long-term equivalence with smoking
Sleep disruption/psychosocial stress	Neuroendocrine, autonomic and behavioral pathways	Predominantly observational evidence; residual confounding and reverse causation remain concerns	Promote adequate sleep and mental-health and social support; address coexisting health behaviors
Air pollution/social environment	Inflammation, oxidative stress, autonomic effects; constrained health choices and care access	Moderate observational evidence; limited evidence for events specifically among younger populations	Support clean-air and healthy urban policies and equitable access to nutritious food, physical activity, and preventive care

3. Epidemiology of early-onset cardiovascular disease

The global burden of CVD among people aged 15-39 years is well documented, with substantial geographic and sex-based differences [1,2]. However, these broad estimates include multiple forms of CVD and do not establish a uniform increase in clinical atherosclerotic events among adolescents and young adults. The clearest and most consistent contemporary signal is the rising prevalence of obesity, hypertension, dyslipidemia, diabetes, nicotine exposure, and subclinical vascular abnormalities in younger populations, whereas clinical myocardial infarction and ischemic stroke remain uncommon at the youngest ages [15,16].

Accordingly, trends in cardiovascular risk factors should not be presented as trends in clinical events. Some registries report stagnation or less favorable declines in coronary outcomes among younger adults, but differences in age definitions, coding practices, geography, and outcome ascertainment limit causal interpretation. Because of the long interval between exposure and clinical events, lifetime and 30-year risk may be particularly informative even when 10-year absolute risk is low.

The burden of premature cardiovascular risk may be particularly pronounced in low- and middle-income countries, where rapid urbanization, air pollution, limited access to preventive healthcare, low health literacy, and unhealthy food environments can increase the vulnerability of younger populations [2,7,8]. In these settings, hypertension, obesity, dyslipidemia, and prediabetes may remain undetected until more advanced disease develops [1,2,17,18].

Premature clinical ASCVD has disproportionate consequences for employment, family responsibilities, productivity, quality of life, and lifetime healthcare use [1,2,15]. Prevention should therefore address cumulative risk early without medicalizing all young people or conflating risk markers with clinical disease.

4. Lifestyle risk factors

Lifestyle-related factors are central to the development of cardiovascular risk among young adults [6,15,17]. Because many of these factors are modifiable, early prevention and sustained behavioral change may reduce future risk [3,6]. Key contributors include physical inactivity, unhealthy dietary patterns, nicotine exposure, inadequate sleep, and chronic stress [3,6,9,10,15,17].

4.1. Physical inactivity

Physical inactivity is an important contributor to early cardiovascular risk. Sedentary behavior, prolonged screen time, and insufficient daily activity may contribute to weight gain, insulin resistance, dyslipidemia, and elevated blood pressure [3,17]. These changes may impair vascular function and promote inflammatory activity within the arterial wall [4,19].

Regular physical activity benefits cardiovascular health by improving blood pressure control, lipid metabolism, insulin sensitivity, weight management, and endothelial function [3,6]. Reducing sedentary time and promoting physical activity are therefore important strategies for preventing adverse cardiovascular risk trajectories in younger populations [3,6,15].

4.2. Unhealthy diet

Unhealthy dietary patterns are associated with premature cardiovascular risk. Frequent consumption of fast food and other energy-dense, nutrient-poor foods is associated with obesity, hypertension, dyslipidemia, insulin resistance, and metabolic syndrome [6,17].

Sugar-sweetened beverages, ultra-processed foods, and energy-dense products are associated with adverse adiposity, blood pressure, glycemia, triglycerides, and low-density lipoprotein cholesterol (LDL-C) [3,6]. Randomized dietary studies demonstrate improvements in several intermediate risk factors, but direct evidence linking specific dietary patterns to premature clinical events in young adults remains limited.

4.3. Nicotine exposure

Combustible cigarette smoking is an established causal cardiovascular risk factor. Nicotine acutely increases heart rate and blood pressure, while constituents of tobacco smoke promote oxidative stress, endothelial dysfunction, inflammation, and thrombosis [17,19]. E-cigarette exposure is associated with acute adverse vascular and hemodynamic effects; however, its independent long-term contribution to ASCVD remains uncertain because of device heterogeneity, dual use, short follow-up, and reliance on surrogate outcomes [8,17,19].

These effects may contribute to arterial stiffness, endothelial dysfunction, and early atherosclerotic changes [15,19,20]. Because nicotine use often begins during adolescence or early adulthood, exposure may persist for decades. Preventing cigarette and e-cigarette use among young people therefore remains essential to reducing premature cardiovascular risk [6,21].

4.4. Poor sleep

Short or irregular sleep is associated with obesity, hypertension, insulin resistance, and adverse health behaviors [20,21]. Plausible pathways include sympathetic activation, neuroendocrine disruption, and inflammation; however, much of the evidence is observational and remains susceptible to confounding and reverse causation.

These changes may favor vascular inflammation, endothelial dysfunction, and metabolic dysregulation [10,22]. Adequate, regular sleep is therefore an important component of cardiovascular prevention, particularly for students and young adults whose sleep patterns may be disrupted by academic, social, occupational, or digital demands [6,10].

4.5. Chronic stress

Chronic psychosocial stress is associated with adverse cardiovascular outcomes and may influence sympathetic nervous system and hypothalamic-pituitary-adrenal axis activity [10]. Because its direct effects are difficult to separate from socioeconomic conditions, depression, sleep, and health behaviors, stress is best characterized as a probable risk contributor rather than a uniformly established independent cause in younger populations.

Stress may also increase cardiovascular risk indirectly through coping behaviors such as overeating, smoking, alcohol use, inadequate sleep, and physical inactivity [6,9]. It may therefore influence cardiovascular health through both biological and behavioral pathways [9,23].

Lifestyle-related risks are closely interconnected. Sedentary behavior, unhealthy diet, nicotine exposure, inadequate sleep, and chronic stress frequently coexist and may reinforce one another [6,15,17]. Early interventions that address these modifiable factors collectively may help reduce the future burden of premature ASCVD [3,6,15].

5. Metabolic and biological mechanisms

Several interrelated metabolic and biological processes contribute to the development of atherosclerosis before clinical manifestations appear [4,5,19]. These processes include endothelial dysfunction, oxidative stress, chronic inflammation, abnormal lipid metabolism, insulin resistance, metabolic syndrome, and arterial stiffness [4,5,15,19]. Together, they create conditions that favor early plaque formation and increase future cardiovascular risk [4,15,19].

5.1. Endothelial dysfunction

Endothelial dysfunction is an early feature of atherogenesis [4,7]. Smoking, obesity, dyslipidemia, hyperglycemia, and hypertension are supported by strong mechanistic and clinical evidence, whereas associations with psychosocial stress and air pollution are less directly established in younger populations.

Endothelial dysfunction facilitates the entry of LDL-C into the arterial wall and promotes the recruitment of inflammatory cells [4,5,19]. Over time, these processes contribute to fatty-streak formation and atherosclerotic plaque development. Endothelial dysfunction therefore represents an important mechanism linking established lifestyle and metabolic risks to premature cardiovascular disease [4,19].

5.2. Oxidative stress

Oxidative stress occurs when the production of reactive oxygen species exceeds antioxidant defense capacity [4,5]. It can damage endothelial cells, lipids, proteins, and DNA and promote LDL oxidation, an important step in foam-cell formation [4,5].

Macrophage uptake of oxidized LDL contributes to foam-cell formation [4,5]. Diet, nicotine exposure, air pollution, sleep disruption, and stress have each been associated with oxidative biomarkers; however, heterogeneous assays and predominantly observational designs limit conclusions about their independent causal contributions to premature clinical ASCVD.

5.3. Chronic inflammation

Chronic low-grade inflammation contributes to early atherogenesis [4,19]. Obesity, smoking, unhealthy diet, insulin resistance, and physical inactivity may increase systemic inflammation [6,15,17]. Inflammatory cytokines and immune cells contribute to endothelial injury and plaque development.

Inflammation and oxidative stress interact in a self-reinforcing cycle of vascular injury [4,5]. This interaction contributes to the progression of early fatty streaks toward more advanced atherosclerotic lesions [4,19]. Addressing modifiable inflammatory drivers may therefore support the prevention of premature cardiovascular disease [6,15,17].

5.4. Lipid metabolism disorders

Abnormal lipid metabolism is central to atherogenesis [4,5,15]. Elevated LDL-C and triglyceride levels, together with low high-density lipoprotein cholesterol, are associated with lipid deposition in the arterial wall [5,15]. LDL particles retained within the arterial wall may become oxidized and subsequently taken up by macrophages, leading to foam-cell formation [5,24,25]. Foam cells contribute to fatty streaks, an early visible manifestation of atherosclerosis [4,5]. In young people, dyslipidemia may reflect unhealthy diet, obesity, physical inactivity, inherited susceptibility, or a combination of these factors [15,17]. Severe or persistent lipid abnormalities therefore warrant timely evaluation and management [6,15].

5.5. Insulin resistance and metabolic syndrome

Insulin resistance and metabolic syndrome are increasingly prevalent among adolescents and young adults, particularly in association with obesity and sedentary behavior [1,15,17]. Insulin resistance contributes to hyperglycemia, dyslipidemia, hypertension, and chronic inflammation [15,17].

These abnormalities adversely affect vascular function and may promote atherosclerotic change [4,15,19]. Metabolic syndrome in younger individuals is therefore an important marker of future cardiovascular risk [15,17]. Weight management, physical activity, and a healthy dietary pattern can improve insulin sensitivity and related risk factors [3,6,17].

5.6. Arterial stiffness

Arterial stiffness is an important marker of premature vascular aging [15,19]. Reduced arterial elasticity increases cardiac workload and may contribute to elevated blood pressure [15,19]. Obesity, high sodium intake, physical inactivity, smoking, chronic inflammation, and insulin resistance are associated with greater arterial stiffness, including among younger populations [6,15,17,19].

Arterial stiffening may progress silently and remain undetected for years. Greater stiffness is associated with hypertension, impaired hemodynamics, and future cardiovascular complications; it should therefore be interpreted as a marker of vascular aging rather than clinically manifest ASCVD [15,19].

Premature ASCVD arises from interacting biological, inherited, behavioral, and environmental influences rather than from a single determinant [4,15,19]. Lifestyle and environmental exposures are associated with endothelial dysfunction, oxidative stress, inflammation, abnormal lipid metabolism, insulin resistance, and arterial stiffness [4,5,7,15,19]. Understanding these pathways reinforces the value of prevention before irreversible vascular injury develops [6,15,17].

5.7. Inherited predisposition and interaction with modifiable risk

Inherited susceptibility is central to premature ASCVD. Familial hypercholesterolemia (FH) causes lifelong elevation of LDL-C and substantially increases the risk of early coronary events if left untreated. Persistent LDL-C levels of at least 190 mg/dL in adults, or severe age-specific elevations in children and adolescents, should prompt evaluation for FH, secondary causes, family history, characteristic physical findings, and cascade testing of relatives [15,26]. Early identification is important because cumulative lifetime LDL-C exposure, rather than a single measurement, influences risk.

Lipoprotein(a) [Lp(a)] concentration is largely genetically determined and is independently associated with ASCVD and aortic-valve disease. The 2026 ACC/AHA dyslipidemia guideline recommends measurement of Lp(a) at least once in all adults for ASCVD risk assessment, and the 2025 ESC/EAS focused update similarly advises considering Lp(a) measurement at least once in every adult's lifetime, ideally with the first or next lipid profile. Targeted/cascade assessment remains especially relevant for premature ASCVD, FH, severe hypercholesterolemia, or a family history of premature events or elevated Lp(a) [12,13,27]. Other inherited dyslipidemias and polygenic susceptibility may also contribute, although routine polygenic risk scoring is not established for population screening.

Inherited and modifiable risks are interactive rather than mutually exclusive. Smoking, hypertension, diabetes, obesity, and prolonged exposure to atherogenic lipoproteins can amplify absolute risk in genetically susceptible young people. Conversely, favorable cardiovascular health may delay events but does not eliminate the need to identify and treat severe inherited dyslipidemia. Young age or low 10-year risk should therefore not provide false reassurance when a family history of premature ASCVD or severe lipid abnormality is present.

6. Environmental and psychosocial factors

Environmental and psychosocial conditions also contribute to premature cardiovascular risk [2,[7], [8], [9]]. Individual behaviors are shaped by the settings in which young people live, study, and work. Air pollution, urbanization, socioeconomic inequality, chronic stress, social isolation, and limited access to preventive healthcare may compound cardiovascular risk [2,[7], [8], [9]].

Long-term exposure to particulate air pollution is associated with CVD and is biologically linked to systemic inflammation, oxidative stress, autonomic imbalance, and endothelial dysfunction [9,22]. Because exposure is not randomized and covaries with socioeconomic and neighborhood characteristics, estimates may be affected by residual confounding. Evidence specific to premature clinical events remains limited.

Urbanization may also influence cardiovascular risk by changing daily behavior [2,7,8]. Young people may spend prolonged periods sitting in schools, universities, workplaces, or in front of digital devices. Limited access to safe walking routes, parks, sports facilities, and green spaces can further restrict physical activity [3,7,8]. At the same time, fast food, sugar-sweetened beverages, and ultra-processed foods are widely available and heavily marketed to adolescents and young adults [6,17].

Socioeconomic inequality also influences cardiovascular health [2,8]. Young people with limited financial resources may have less access to nutritious food, safe places to exercise, routine healthcare, and health education [2,8]. Consequently, hypertension, obesity, dyslipidemia, and abnormal glycemia may remain undetected until more advanced cardiovascular injury develops [2,8,17].

Psychosocial adversity, including financial insecurity, social isolation, discrimination, anxiety, and depression, is associated with unfavorable cardiovascular risk profiles [10,28]. These associations may operate through neuroendocrine pathways and through smoking, sleep, diet, medication adherence, and access to care; however, attributing causality to any single pathway remains difficult.

Mental health conditions may also influence cardiovascular risk indirectly by increasing the likelihood of smoking, overeating, inadequate sleep, alcohol use, and physical inactivity [6,9]. Mental health support should therefore form an integral component of cardiovascular prevention [6,9,29].

Environmental and psychosocial conditions can allow cardiovascular risk to develop early and progress silently [2,[7], [8], [9]]. Measures to reduce air pollution, improve urban planning, expand access to nutritious food and opportunities for physical activity, strengthen health education, and support mental health may help reduce the future burden of premature ASCVD [[6], [7], [8],15].

Sex-specific and ethnic considerations also influence risk interpretation. Conventional thresholds for premature ASCVD differ between men and women; pregnancy-related conditions may identify women at increased later risk; and autoimmune or inflammatory disorders may modify risk. Observed ethnic differences reflect complex interactions among ancestry, migration, structural disadvantage, environmental exposure, healthcare access, and measurement practices. Ethnicity should therefore not be treated as a simple biological proxy without attention to these contexts [14,30].

7. Prevention strategies

Prevention should combine population-wide health promotion with individualized, age-appropriate clinical risk assessment. Routine health maintenance and policy interventions must be distinguished from universal testing for subclinical atherosclerosis. Current ACC/AHA and ESC/EAS guidance emphasizes cumulative lifetime exposure, risk-enhancing factors, shared decision-making, and treatment of major risk factors rather than indiscriminate imaging of asymptomatic young people [[12], [13], [14],30].

Health education is an important preventive strategy. Young people should be informed about the long-term cardiovascular consequences of unhealthy diet, physical inactivity, smoking, inadequate sleep, chronic stress, and obesity [3,6,9,10,15,17]. Schools, universities, families, and healthcare professionals can promote awareness and support the adoption of healthier behaviors [3,6].

Physical activity is a cornerstone of cardiovascular prevention. Young adults should be encouraged to reduce sedentary behavior and engage regularly in moderate-intensity physical activity [3]. Exercise benefits blood pressure, lipid profiles, insulin sensitivity, weight management, endothelial function, and psychological well-being [3,6].

Improving dietary quality is another important strategy. A healthy dietary pattern emphasizes fruits, vegetables, whole grains, legumes, lean proteins, and unsaturated fats while limiting trans fats, excess saturated fat, sodium, added sugars, and ultra-processed foods [6,17]. Reducing fast food, sugar-sweetened beverages, and energy-dense snacks may help prevent obesity, dyslipidemia, hypertension, and insulin resistance [6,17].

For adults, the 2026 ACC/AHA dyslipidemia guideline recommends lipid-profile screening beginning at age 19 years and at least every 5 years thereafter, with more frequent assessment when additional risk factors are present; it also recommends Lp(a) measurement at least once in all adults. The 2025 ESC/EAS focused update similarly advises considering Lp(a) measurement at least once in every adult's lifetime [12,13]. Beyond this baseline assessment, targeted evaluation is appropriate when clinical history or routine care identifies a family history of premature ASCVD, suspected FH or another inherited dyslipidemia, elevated Lp(a), obesity, hypertension, diabetes, chronic kidney disease, inflammatory disease, smoking or vaping, or adverse social determinants. Depending on age and clinical context, assessment may include repeated blood-pressure measurement, body-mass index and waist circumference, fasting or nonfasting lipids, glycemic testing, renal function, and a detailed tobacco and nicotine history [[12], [13], [14],26,27,30]. Symptoms such as chest discomfort or dyspnea require diagnostic evaluation and should not be described as screening. Population-wide CAC or carotid-ultrasound screening is not recommended for adolescents or most asymptomatic young adults. Under 2026 ACC/AHA guidance, CAC may be used selectively to refine risk and lipid-lowering decisions in men aged at least 40 years and women aged at least 45 years with borderline or intermediate estimated risk when uncertainty remains after conventional assessment; evidence for routine use below these ages is limited [12]. In ESC guidance, increased CAC or imaging-detected subclinical atherosclerosis can act as a risk modifier around treatment thresholds, and carotid/femoral plaque burden may be considered as a risk modifier in selected low- or moderate-risk adults; carotid intima-media thickness alone is not recommended for routine risk prediction [13,14]. Imaging should follow guideline-based clinical assessment and shared decision-making rather than serve as a general screening test.

Preventing tobacco and nicotine use should remain a major public-health priority [6,20,21]. Programs for adolescents and young adults should address cigarettes, e-cigarettes, and other nicotine products and communicate their potential vascular effects, including vasoconstriction, endothelial dysfunction, oxidative stress, thrombosis, and elevated blood pressure [20,21].

Stress management and sleep hygiene should be incorporated into cardiovascular prevention [6,9,10]. Counseling, social support, regular sleep schedules, reduced problematic digital use, and appropriate stress-reduction techniques may benefit both psychological and cardiovascular health [6,9,10]. Because chronic stress and inadequate sleep are associated with hypertension, inflammation, obesity, and insulin resistance, addressing them may help reduce premature cardiovascular risk [9,10,22].

Public policy has an important role in enabling individual behavior change [[6], [7], [8]]. Governments and local authorities can promote cardiovascular health by expanding access to safe parks, walking routes, sports facilities, nutritious food, and preventive healthcare services [3,6,8]. Policies that reduce air pollution, regulate the marketing of unhealthy foods, limit trans fats and excess sodium, and support healthier urban planning can reduce risk at the population level [[6], [7], [8]].

Preventing premature ASCVD requires coordinated involvement from individuals, families, schools, healthcare systems, communities, and policymakers [6,15,17]. Education, lifestyle support, targeted risk assessment, mental healthcare, and environmental improvements may collectively reduce the future burden of premature cardiovascular disease [3,6,15,17].

7.1. Digital and scalable prevention for younger populations

Mobile-health applications, telemedicine, wearable devices, step-count feedback, and remote coaching may make preventive support easier to integrate into education, work, and daily life. Trials involving high-risk adults and meta-analytic evidence following acute coronary syndrome suggest benefits for selected digital-management outcomes [[31], [32], [33], [34], [35], [36]]. These findings are encouraging but may not generalize to healthy adolescents or young adults, whose baseline risk, motivations, and relevant outcomes differ.

Effective digital programs should be individualized, behaviorally grounded, interoperable with clinical care, and evaluated for sustained engagement and clinically meaningful outcomes rather than app-based metrics alone. Digital prevention should complement, not replace, face-to-face assessment, family- and school-based support, regulation of unhealthy-food marketing, or environmental policy. Equitable implementation requires attention to device and internet access, language, disability, digital literacy, privacy, cybersecurity, algorithmic bias, informed consent, and transparent data governance.

8. Discussion

The available literature supports a life-course model in which atherosclerotic processes may begin early, whereas clinically manifest ASCVD generally emerges later. Global burden studies demonstrate substantial CVD morbidity among people aged 15-39 years, but these findings do not justify classifying every adolescent risk factor or subclinical marker as clinical ASCVD [1,2]. The most defensible interpretation is that unfavorable risk-factor trajectories and cumulative exposure create a preventable reservoir of future premature events.

The strength of evidence varies across determinants. Cumulative LDL-C exposure, FH, smoking, hypertension, and diabetes are supported by convergent genetic, mechanistic, longitudinal, and interventional evidence. By contrast, evidence concerning sleep disruption, psychosocial stress, and air pollution is biologically plausible and often consistent but depends more heavily on observational designs, surrogate outcomes, and studies of older populations. Prevention messages should reflect this hierarchy rather than imply that all relationships are equally causal.

Cardiovascular risk among young people is also shaped by social and environmental conditions [2,[7], [8], [9]]. Air pollution, limited access to green space, widespread availability of fast food, socioeconomic disadvantage, low health literacy, and restricted access to preventive healthcare may increase exposure to harmful risk factors [2,7,8].

Even when young people understand cardiovascular risk, environmental and socioeconomic barriers may constrain their ability to adopt healthier behaviors. Premature cardiovascular disease should therefore be viewed not only as a clinical concern but also as a broader public-health and social challenge [2,6,8].

The intensity of clinical intervention should be proportionate to risk. Population-level measures can improve diet, physical activity, nicotine avoidance, sleep opportunity, air quality, and access to preventive services without labelling individuals as diseased. Clinical services should identify severe or clustered risk, inherited dyslipidemia, and relevant symptoms; communicate long-term risk clearly; and offer treatments with demonstrated benefit. Digital tools may extend reach and engagement, but they require validation in younger populations and appropriate safeguards for equity and data governance [[31], [32], [33], [34], [35], [36]].

Key uncertainties include inconsistent age thresholds, limited event-based evidence below 40 years of age, underrepresentation of women and diverse populations, few randomized prevention trials involving young people, and uncertainty regarding the clinical utility of imaging or emerging biomarkers in very young asymptomatic individuals. Future studies should harmonize definitions; distinguish risk factors, subclinical disease, and clinical events; report outcomes by sex and ethnicity; evaluate acceptability and cost-effectiveness; and determine whether early, sustained interventions improve clinical outcomes without causing unnecessary testing or overdiagnosis.

9. Conclusion

Premature ASCVD is clinically manifest atherosclerotic disease occurring earlier than expected—commonly before 55 years of age in men or 65 years of age in women—and should not be conflated with cardiovascular risk factors or subclinical vascular abnormalities. Adolescents and young adults increasingly carry obesity, hypertension, dyslipidemia, diabetes, and nicotine exposure; however, evidence of a uniform increase in clinical ASCVD events remains less certain.

The most robust prevention strategy combines equitable population-level measures with routine adult lipid assessment, Lp(a) measurement at least once in adulthood, and targeted clinical assessment of severe or clustered risk, FH, elevated Lp(a), and a family history of premature ASCVD. Imaging should be reserved for carefully selected adults when clinical decisions remain uncertain rather than used for universal screening. Digital approaches may improve reach and engagement but should complement validated clinical care and public-health interventions. Research priorities include harmonized definitions, younger and more diverse cohorts, event-based outcomes, and trials that establish effectiveness, feasibility, acceptability, and cost-effectiveness while minimizing overdiagnosis.

CRediT authorship contribution statement

Tukhtaeva Nigora Khasanovna: Writing – review & editing, Writing – original draft, Visualization, Validation, Supervision, Software, Resources, Project administration, Methodology, Investigation, Funding acquisition, Formal analysis, Data curation, Conceptualization. Babajanov Xudoybergan Egamberdi son: Writing – original draft, Methodology, Investigation, Formal analysis, Data curation, Conceptualization.