Elevated lipoprotein(a) and its association with early-onset myocardial infarction and coronary burden.

Objectives: Cardiovascular diseases (CVDs) remain a leading cause of morbidity and mortality worldwide, with myocardial infarction (MI) representing one of the most severe manifestations. Lipoprotein(a) [Lp(a)], a genetically influenced lipoprotein subclass, has gained attention for its role in atherogenesis and thrombogenesis. This study investigates clinical and demographic differences in early MI patients with varying Lp(a) levels, dividing them into two groups: Lp(a) < 50 mg/dL and Lp(a) ≥ 50 mg/dL. A retrospective analysis assessed demographic and clinical features, lipid profiles, and comorbidities.

Methods: A retrospective cohort analysis was conducted on 189 patients aged 18-55 years with early-onset MI. Patients were grouped by Lp(a) levels (< 50 mg/dL, n = 109; ≥ 50 mg/dL, n = 80). Clinical parameters analyzed included age at MI onset, number of affected coronary vessels, comorbidities (diabetes mellitus, arterial hypertension, smoking status), statin therapy, and lipid profiles (total cholesterol, triglycerides, HDL, non-HDL, and LDL). Statistical comparisons and correlation analyses were performed to evaluate associations between Lp(a) levels and clinical features.

Results: Elevated Lp(a) levels (≥ 50 mg/dL) were associated with younger MI onset, greater vascular burden, and less frequent statin use. Patients with higher Lp(a) had higher BMI and lower HDL levels. Significant differences were observed in age at MI onset (p = 0.0026), number of affected vessels (p = 0.0001), smoking prevalence (p = 0.002), statin use (p < 0.0001), BMI (p = 0.0061), triglycerides (p = 0.0121), and HDL levels (p < 0.0001). A positive correlation between Lp(a) levels and the number of affected vessels (r = 0.303) was identified.

Conclusion: Elevated Lp(a) levels are strongly associated with younger age at MI onset, increased coronary involvement, and a pro-atherogenic lipid profile. These findings underscore the importance of Lp(a) as a biomarker for risk stratification in MI patients and highlight the need for targeted therapeutic approaches for individuals with high Lp(a) levels.