Background: Myocardial infarction (MI) in young adults, once a rarity, is increasingly recognized as a distinct clinical entity. Unlike traditional MI patients, younger individuals often present without established risk factors or advanced atherosclerosis, prompting a reevaluation of pathophysiologic paradigms and risk assessment strategies. Objective: This review synthesizes current evidence on the epidemiology, pathophysiology, and diagnostic challenges of MI in adults under 55 years, with emphasis on risk factor profiles. We distinguish between traditional cardiovascular risk factors—smoking, dyslipidemia, hypertension, diabetes, obesity, and family history—and emerging contributors, including elevated lipoprotein(a), recreational drug use (cocaine, cannabis, amphetamines), autoimmune and inflammatory conditions, psychosocial stress, sleep disorders, genetic predisposition, and non-atherosclerotic mechanisms such as myocardical infarction with non-obstructive coronary arteries, spontaneous coronary artery dissection, SCAD and Takotsubo syndrome. Methods: A narrative literature review was conducted, focusing on studies from the last five years addressing MI in young adults, including data from large registries, cohort studies, and recent experimental findings.

Introduction: Cardiovascular diseases are the leading cause of mortality worldwide, with a significant impact on socioeconomic aspects. Various biomarkers have been studied in relation to the diagnosis, progression, and prognosis of atherosclerotic disease, with lipoprotein (a) [Lp (a)] standing out as an important predictor of cardiovascular risk. This observational study aimed to clarify the association between Lp (a) levels and the severity of significant multivessel coronary lesions in acute myocardial infarction (AMI) patients. Materials and Methods: Conducted at the Clinical Emergency County Hospital of Craiova, Romania, the study involved 256 young patients divided into two groups based on Lp (a) levels: Group A (Lp (a) < 30 mg/dL) and Group B (Lp (a) ≥ 30 mg/dL). Patients included young adults up to 55 years for males and 60 years for females, excluding those with familial hypercholesterolemia. Results: The study revealed a significant association between elevated Lp (a) levels and the presence of multivessel coronary lesions. Patients with Lp (a) concentrations ≥ 30 mg/dL exhibited a higher prevalence of multivessel disease compared to those with lower levels. Discussion: The findings suggest that elevated Lp (a) levels are a crucial biomarker for the risk of coronary artery disease, particularly in young patients with AMI. The study emphasizes the need for aggressive lipid management strategies and personalized treatment approaches, considering the significant role of Lp (a) in atherosclerosis and AMI. Conclusions: Lipoprotein A levels above 30 mg/dL are associated with a higher prevalence of multivessel coronary lesions. Multivariate analysis revealed that higher Lp (a) levels and lower HDL levels are linked to an increased risk of multivessel coronary lesions.

Background and Objectives: This observational study investigates the relationship between Lipoprotein (a) (Lp(a)) levels and the risk of acute myocardial infarction (AMI). This study aims to highlight the association of elevated Lipoprotein (a) levels with an increased atherogenic profile and the potential risk of AMI. Materials and Methods: We conducted a case–control study involving 106 individuals, including 64 AMI patients (both STEMI and NSTEMI) and 42 healthy controls. Comprehensive clinical and biochemical assessments, including Lp(a) measurements, were conducted. Results: Patients with Lp(a) levels ≥ 30 mg/dL had a threefold increased risk of AMI compared to those with lower levels, independent of traditional risk factors such as cholesterol, smoking, and body weight. Elevated Lp(a) was observed in 50% of AMI patients compared to 28.57% in controls (p = 0.028). Notably, a multivariate analysis identified high Lp(a) levels, low HDL-C levels, and obesity as significant independent predictors of AMI, indicating these factors may contribute to AMI risk more prominently than other conventional risk factors in patients with elevated Lp(a). Moreover, the association between Lp(a) and AMI risk was consistent across various patient subgroups, with low HDL-C further compounding the risk. Conclusions: Lp(a) is a significant independent risk factor for acute myocardial infarction; therefore, screening for Lp(a) levels can help identify high-risk individuals beyond traditional markers. Therapeutic approaches targeting Lp(a) may reduce AMI incidence. Future research should explore how Lp(a) promotes atherosclerosis and assess Lp(a)-lowering therapies to improve patient outcomes.

Background: The incidence of acute myocardial infarction (AMI) in young adults has been steadily rising, emphasizing the need for new biomarkers to improve risk stratification. Lipoprotein(a) (Lp(a)), a genetically determined lipoprotein with pro-atherogenic and pro-thrombotic properties, has gained increasing attention in this context. Methods: We evaluated serum Lp(a) levels in young patients with AMI and compared them with healthy controls. Associations between elevated Lp(a) levels (≥30 mg/dL) and coronary artery disease patterns were analyzed separately for STEMI and NSTEMI presentations. Results: Elevated Lp(a) levels were significantly more common in young patients with AMI compared with healthy controls. Importantly, Lp(a) ≥ 30 mg/dL was strongly associated with multivessel coronary artery disease in NSTEMI, conferring more than a fourfold increased risk. In STEMI, the effect was weaker and largely influenced by concomitant factors such as diabetes and elevated LDL cholesterol. Conclusions: These findings highlight key pathophysiological differences between infarct phenotypes and position Lp(a) as a particularly relevant biomarker in young NSTEMI patients. The systematic assessment of Lp(a) may enhance coronary risk stratification and support more tailored secondary prevention strategies.

Background: Myocardial infarction (MI) in young adults, once a rarity, is increasingly recognized as a distinct clinical entity. Unlike traditional MI patients, younger individ-uals often present without established risk factors or advanced atherosclerosis, prompt-ing a reevaluation of pathophysiologic paradigms and risk assessment strategies. Objective: This review aims to synthesize recent evidence on the epidemiology, tradi-tional and emerging risk factors, pathophysiological mechanisms, and diagnostic chal-lenges of MI in individuals under 55, with emphasis on the unique features of this population. Methods: A narrative literature review was conducted, focusing on studies from the last five years addressing MI in young adults, including data from large registries, cohort studies, and recent experimental findings.

Background and Objectives: Although acute myocardial infarction (AMI) is traditionally regarded as a disease of older age, its rising incidence in younger patients challenges age-based assumptions regarding in-hospital management and prognosis. Length of hospital stay is a critical marker of disease complexity and healthcare burden, yet its determinants across age groups remain insufficiently characterized. Materials and Methods: We retrospectively analyzed 200 consecutive patients admitted with ST-segment eleva-tion myocardial infarction (STEMI), stratified by age (< 45 vs. >45 years). Clinical, bio-logical, echocardiographic, and angiographic parameters were assessed. Prolonged hospitalization was defined as a hospital stay exceeding 7 days. Independent predictors were identified using multivariable logistic regression. Results: Despite marked differences in risk profiles and coronary anatomy between age groups, chronological age was not an independent determinant of hospitalization duration. Di-abetes mellitus and left anterior descending artery involvement were independently associated with prolonged hospital stay, whereas percutaneous coronary intervention significantly reduced hospitalization duration. Conclusions: In STEMI, hospitalization burden is shaped by comorbidity burden and revascularization strategy rather than age itself. These findings challenge age-centered clinical paradigms and support an individualized, mechanism-driven approach to in-hospital management aimed at reducing hospitalization duration and resource utilization.