AHA Scientific Sessions 2026 Abstract · Nov 2, 2026
Invisible Burden: Severe Premature Coronary Atherosclerosis Unmasked by Female-Specific and Inflammatory Risk Enhancers in an Asymptomatic South Asian Woman
By Mobin Z, Kulinski JP
Introduction: Current cardiovascular risk models underperform in younger women when female-specific,inflammatory, and ethnicity-related risk-enhancing factors accumulate. The compounded risk burdenremains difficult to quantify, contributing to delayed diagnosis and missed prevention windows. Case Presentation: A 44-year-old asymptomatic South Asian woman was referred following markedly elevated coronaryartery calcium (CAC) scoring on executive health screening. She exercised regularly, maintained a normalBMI, followed a plant-forward diet, and had no history of hypertension, diabetes, or tobacco use — aprofile conventionally prompting lifestyle counseling rather than aggressive intervention. Careful reviewrevealed a convergence of risk-enhancing factors: lipoprotein(a) [Lp(a)] 140.9 mg/dL, high-sensitivity C-reactive protein (hs-CRP) 8.26 mg/L, history of preeclampsia, estrogen-containing oral contraceptive use(~12 years), plaque psoriasis, South Asian ancestry, and multigenerational premature CAD from thepaternal fourth decade. Standard lipids were misleadingly unremarkable: LDL-C 101 mg/dL, triglycerides170 mg/dL, HbA1c 4.9%. CAC revealed severe multi-vessel atherosclerosis: Agatston score 576 (99thpercentile), across LAD (129), LCx (187), and RCA (260). Stress echocardiography demonstratedexceptional functional capacity (13.4 METs) but revealed apical hypokinesis and lateral ST-segmentdepressions, consistent with hemodynamically significant clinically silent ischemia. Rosuvastatin 5 mgnightly was initiated; evolocumab 140 mg every two weeks was added for markedly elevated Lp(a),targeting LDL-C <55 mg/dL. Colchicine 0.5 mg daily addressed inflammatory risk. Estrogen-containingcontraception was discontinued per CDC Medical Eligibility Criteria and replaced with progestin-onlyformulation. Follow-up showed substantial risk marker reduction: LDL-C 101 to 21 mg/dL, non-HDL-C130 to 35 mg/dL, triglycerides 170 to 61 mg/dL, apolipoprotein B 71 to 37 mg/dL, and hs-CRP 8.26 to1.37 mg/L. Hs-CRP reduction within weeks may reflect modifiable inflammatory exposures, thoughisolating contributions remains difficult. Lp(a) remained stable (~144 mg/dL), consistent with resistanceto conventional therapy. Colchicine was discontinued due to rising transaminases; hs-CRP remainedbelow baseline, suggesting oral contraceptives as a contributor. The patient remained asymptomaticthroughout. Conclusion: No single risk factor explained this patient's 99th-percentile CAC at age 44 — it was the convergence ofmultiple risk-enhancing factors. Comprehensive risk assessment including Lp(a), hs-CRP, and CAC scoringenabled timely guideline-directed preventive therapy before clinical ASCVD emerged. Recognition ofsex-specific and ethnicity-related risk factors may improve cardiovascular risk assessment in youngerwomen.