This study aimed to explore the relationship between familial hypercholesterolemia and premature coronary artery disease, particularly in the context of acute coronary syndrome, by reviewing current evidence and highlighting the need for improved screening and aggressive lipid-lowering strategies in high-risk populations.

Dyslipidaemia and familial hypercholesterolemia (FH) are a common disorder that causes premature coronary artery disease.

The lifelong burden of elevated low-density lipoprotein cholesterol (LDL-C) in FH accelerates endothelial dysfunction and plaque formation, often culminating in acute coronary syndrome (ACS) at a young age. ACS in patients with undiagnosed FH may be their first clinical manifestation, underscoring the importance of early identification and intervention.

Inclusion Criteria:

• Age ≥18 years at the time of presentation.
• Both sexes.
• Confirmed diagnosis of coronary artery disease (CAD), established by clinical presentation, electrocardiographic findings, elevated cardiac biomarkers, and/or angiographic evidence of ≥50% luminal stenosis in at least one major coronary artery.
• Hospital admission to the participating cardiology department between [insert study period, e.g., January 2020 and December 2024] for acute coronary syndrome (ACS), including unstable angina, non-ST-elevation myocardial infarction (NSTEMI), or ST-elevation myocardial infarction (STEMI).
• Availability of complete clinical, laboratory, and echocardiographic data necessary for classification and analysis.

Exclusion Criteria:

• Incomplete medical records or missing essential laboratory, imaging, or demographic data.
• Secondary causes of dyslipidemia, including uncontrolled hypothyroidism, nephrotic syndrome, chronic liver disease, or use of lipid-altering medications (other than statins) before presentation.
• Previous congenital or structural heart disease, cardiomyopathy, or significant valvular heart disease unrelated to CAD.
• Severe chronic kidney disease (estimated glomerular filtration rate <30 mL/min/1.73 m²) or patients on dialysis.
• Autoimmune, inflammatory, or systemic diseases known to influence vascular inflammation or lipid metabolism.
• Malignancy or life expectancy <6 months due to non-cardiac causes.
• Pregnant or lactating women.
• Non-Saudi patients (focusing on Saudi population in southern region).

This was a prospective, cross-sectional, observational study conducted at the Department of Cardiology, Prince Khaled Ben Sultan, between December 2021 and March 2025. A total of 2,000 consecutive adult patients admitted with a confirmed diagnosis of coronary artery disease (CAD) were included.

The data will be available upon a reasonable request from the corresponding author after the end of study for one year.

After the end of study for one year.

The data will be available upon a reasonable request from the corresponding author.