Premature CAD occurred in 31.9% of ACS patients and was strongly associated with smoking (OR 4.71), family history of dyslipidemia (OR 6.73), high cholesterol (OR 2.26), high LDL (OR 2.10), and high triglycerides (OR 1.77).
Cross-Sectional (n=2,000)
No
What are the clinical and laboratory predictors of premature coronary artery disease in patients presenting with acute coronary syndrome?
Premature CAD in patients presenting with ACS is strongly driven by smoking and familial dyslipidemia rather than traditional metabolic comorbidities like diabetes and hypertension.
Effect estimate: OR 4.71 for smoking, OR 6.73 for family history of dyslipidemia, OR 2.26 for cholesterol ≥200 mg/dL, OR 2.10 for LDL ≥100 mg/dL, OR 1.77 for triglycerides ≥150 mg/dL (95% CI Smoking 3.68-6.03; family history 4.78-9.48; cholesterol 1.80-2.83; LDL 1.74-2.54; triglycerides 1.45-2.17)
Absolute Event Rate: 31.9% vs 68.1%
p-value: p=<0.0001 for significant predictors
Background: Premature coronary artery disease (CAD) in patients presenting with acute coronary syndrome (ACS) is an increasing clinical concern driven by genetic predisposition and lifestyle factors. This study compared clinical and laboratory characteristics of premature versus non-premature CAD and identified predictors of early-onset disease. Methods: This was a cross-sectional observational study of 2,000 patients admitted with confirmed ACS. Premature CAD was defined as males <55 years and females <65 years. Clinical, laboratory, and cardiological variables were compared between groups. Results: From December 2021 to March 2025, 2,000 patients were enrolled. Premature CAD occurred in 637 patients (31.9%), who were younger (median age 49 years) and predominantly male (68.4%). Smoking (32.8% vs. 9.4%), family history of dyslipidemia (20.4% vs. 3.7%), higher total cholesterol (174.0 vs. 145.0 mg/dL, p<.001), higher low-density lipoprotein (LDL) cholesterol (108.3 vs. 85.1 mg/dL, p<.001), and higher corrected LDL (155.8 vs. 147.3 mg/dL, p<.001) were more common in premature CAD, whereas diabetes and hypertension were less frequent. Independent predictors included smoking (OR 4.71, 95% CI 3.68 6.03), family history of dyslipidemia (OR 6.73, 95% CI 4.78 9.48), cholesterol ≥200 mg/dL (OR 2.26, 95% CI 1.80 2.83), LDL ≥100 mg/dL (OR 2.10, 95% CI 1.74 2.54), and hypertriglyceridemia (OR 1.77, 95% CI 1.45 2.17). Conclusions: Premature CAD in patients presenting with ACS demonstrates a risk profile dominated by smoking and familial dyslipidemia rather than metabolic comorbidities. Early lipid screening and aggressive modification of lifestyle risk factors are essential to reduce early atherosclerotic disease burden.
Saad et al. (Fri,) conducted a cross-sectional in Acute coronary syndrome with premature coronary artery disease (n=2,000). Premature coronary artery disease (defined as males <55 years, females <65 years) vs non-premature CAD vs. Non-premature CAD was evaluated on Presence of premature CAD among ACS patients and associated risk factors (OR 4.71 for smoking, OR 6.73 for family history of dyslipidemia, OR 2.26 for cholesterol ≥200 mg/dL, OR 2.10 for LDL ≥100 mg/dL, OR 1.77 for triglycerides ≥150 mg/dL, 95% CI Smoking 3.68-6.03; family history 4.78-9.48; cholesterol 1.80-2.83; LDL 1.74-2.54; triglycerides 1.45-2.17, p=<0.0001 for significant predictors). Premature CAD occurred in 31.9% of ACS patients and was strongly associated with smoking (OR 4.71), family history of dyslipidemia (OR 6.73), high cholesterol (OR 2.26), high LDL (OR 2.10), and high triglycerides (OR 1.77).