Elevated Lp(a) and its association with cardiac fibrosis in group II pulmonary hypertension patients
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Updated: May 29, 2025
Left Atrial Stenosis Induced Pulmonary Venous Arterialization and Group 2 Pulmonary Hypertension in Rat
Published on: November 18, 2018
Arif Albulushi1,2, Shabib Al-Asmi2,3, Moosa Al-Abri4
1Advanced Heart Failure & Transplant Cardiology, National Heart Center, The Royal Hospital, Muscat, Oman.
Background:
Group II Pulmonary Hypertension (PH) secondary to Heart Failure with preserved Ejection Fraction (HFpEF) is associated with significant morbidity and mortality. Lipoprotein(a) [Lp(a)] is a novel biomarker implicated in cardiovascular pathology, yet its role in myocardial fibrosis within this population remains underexplored. This study investigates the association between elevated Lp(a) levels and cardiac fibrosis to improve understanding of its prognostic and diagnostic utility.
Methods:
This retrospective cohort study included 100 patients with Group II PH secondary to HFpEF. Serum Lp(a) levels were quantified using enzymatic assays, and myocardial fibrosis was assessed using Cardiac Magnetic Resonance Imaging (CMR) techniques, including T1 mapping and late gadolinium enhancement (LGE). Statistical models adjusted for confounding factors.
Results:
Elevated Lp(a) levels were significantly associated with increased myocardial extracellular volume (31% vs. 27%, p < 0.01), prolonged native T1 times, and increased odds of myocardial scar formation. Structural cardiac changes correlated with Lp(a) concentrations.
Conclusion:
Elevated Lp(a) is a key marker of myocardial fibrosis and structural remodeling in Group II PH secondary to HFpEF. Routine Lp(a) measurement may enhance risk stratification and inform therapeutic strategies.
