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Markedly elevated Lp(a) unmasks vulnerable plaque missed by a zero calcium score, case report in sarcoidosis (J Clin Lipidol 2026)
Original title: Low-attenuation plaque-mediated NSTEMI in a patient with sarcoidosis and high Lp(a)
Case report of a 54-year-old man with newly diagnosed hyperlipidaemia (LDL-C 136 mg/dL) and controlled sarcoidosis who presented with syncope and exertional dyspnoea. Despite a coronary artery calcium score of 0 and low estimated risk by the PREVENT equation (3.0%), coronary CT angiography revealed extensive noncalcified plaque and severe (>75%) left anterior descending stenosis, confirmed physiologically significant by CT-based fractional flow reserve (0.72, normal >0.8); quantitative plaque analysis found 100% noncalcified plaque and 30% low-attenuation plaque, the highest reported to the authors' knowledge. Lp(a) was markedly elevated at 191 nmol/L (normal <75) while apolipoprotein B (72 mg/dL) and polygenic risk (6%) were unremarkable. The patient went on to have an NSTEMI while awaiting catheterisation. The authors propose that elevated Lp(a) plus a chronic inflammatory condition like sarcoidosis may warrant CT angiography despite a reassuring calcium score.
Original abstract
Background: Current coronary artery disease (CAD) risk assessment with risk calculators, including the Predicting Risk of cardiovascular disease EVENTs (PREVENT) equation, lipoprotein(a) [Lp(a)] screening, and coronary artery calcium (CAC) scoring, can miss individuals with vulnerable plaque. Low-attenuation plaque (LAP) is a high-risk imaging feature associated with higher myocardial infarction (MI) risk.
Objective: To describe a patient with a CAC score of 0 and low estimated CAD risk by conventional tools who nonetheless harbored extensive high-risk, low-attenuation plaque, and to define an imaging and biomarker phenotype in whom coronary CT angiography may add value despite reassuring standard risk metrics.
Methods: A 54-year-old man with recently diagnosed hyperlipidemia (low-density lipoprotein-cholesterol [LDL-C] of 136 mg/dL) and controlled sarcoidosis presented with syncope and exertional dyspnea. He was evaluated with coronary computed tomography angiography (CCTA), CT-based fractional flow reserve (FFR), artificial intelligence-enabled quantitative plaque analysis, and comprehensive risk assessment including the PREVENT equation, Lp(a), apolipoprotein B, polygenic risk scoring, and coronary inflammation by fat attenuation indexing.
Results: Despite a CAC score of 0, CCTA revealed extensive noncalcified plaque and severe left anterior descending stenosis (>75%). CT-based FFR confirmed physiologically significant stenosis, with FFR of 0.72 (normal >0.8). Artificial intelligence-enabled quantitative plaque analysis revealed 100% noncalcified plaque and 30% LAP, the highest LAP reported to our knowledge. CAD risk was 3.0% by the PREVENT equation, Lp(a) was 191 nmol/L (normal <75 nmol/L), apolipoprotein B was 72 mg/dL (normal <90 mg/dL), polygenic risk was 6%, and coronary inflammation by fat attenuation indexing was low risk. The patient experienced a non-ST-segment elevation MI while awaiting outpatient catheterization and underwent revascularization.
Conclusion: This case suggests that markedly elevated Lp(a), in the setting of above-optimal LDL-C, can promote vulnerable, lipid-rich plaque even at relatively low cumulative LDL-C exposure. It also defines a patient phenotype that may warrant further risk stratification with CCTA despite a CAC score of 0: those with elevated Lp(a) and at least 1 additional risk enhancer, such as a chronic inflammatory disease like sarcoidosis.
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Summary written by lp-a.org from the published abstract; figures as published. Page updated 17 August 2026. Methods.