Apolipoprotein B and reverse remodeling in ischemic heart failure
I P Rodean, I S B Benedek, V B Halatiu, T BenedekAbstract
Background
Apolipoprotein B (ApoB) integrates the total burden of atherogenic lipoproteins and has been associated with adverse cardiovascular outcomes, but its relationship with left ventricular (LV) reverse remodeling in ischemic heart failure (HF) is unclear. Identifying lipid-related predictors of remodeling could refine risk stratification beyond conventional HF markers.
Purpose
To evaluate whether baseline ApoB is associated with LV reverse remodeling and clinical outcomes in patients with ischemic HFrEF treated with guideline-directed medical therapy.
Methods
We conducted a single-center prospective cohort study including 112 patients with ischemic HFrEF (LVEF ≤40%) enrolled between 2022 and 2025. Baseline ApoB and non-HDLcholesterol were measured at enrolment; patients were classified into low (<80 mg/dL) and high (≥80 mg/dL) ApoB groups. Transthoracic echocardiography was performed at baseline and 12 months. LV reverse remodeling was defined as ΔLVEF ≥10 percentage points and/or absolute LVEF ≥40% at follow-up. The secondary endpoint was a composite of HF hospitalization or all-cause death at 12 months. Multivariable logistic regression and Cox models adjusted for age, sex, baseline LVEF, NT-proBNP, etiology, systolic blood pressure, body mass index, and use of statins or other lipid-lowering therapy were used to evaluate associations between ApoB and outcomes.
Results
The cohort had a mean age of 59±12 years; 36% were women, and median baseline LVEF was 30% (IQR 25–35). High ApoB (≥80 mg/dL) was present in 89 patients (42.0%). At 12 months, LV reverse remodeling occurred in 111 patients (52.4%): 71/123 (57.7%) in the low-ApoB group versus 40/89 (44.9%) in the high-ApoB group (p=0.04). Patients with high ApoB showed smaller mean LVEF improvement (ΔLVEF 8.1±9.7% vs 11.5±10.2%; p=0.01) and less LV end-systolic volume reduction. In adjusted analysis, high ApoB was independently associated with a lower likelihood of reverse remodeling (adjusted OR 0.56, 95% CI 0.33–0.95; p=0.03), whereas non-HDL-cholesterol was not (p=0.21). The 12-month composite endpoint occurred in 29/123 (23.6%) low-ApoB patients and 30/89 (33.7%) high-ApoB patients (p=0.11). In Cox models, high ApoB was associated with a higher risk of HF hospitalization or death (adjusted HR 1.68, 95% CI 1.01–2.80; p=0.046), and the addition of ApoB to a clinical model modestly improved discrimination for the composite endpoint (C-statistic from 0.73 to 0.77; p=0.08).
Conclusion(s)
In ischemic HFrEF, higher baseline ApoB was associated with less LV reverse remodeling and a greater risk of HF hospitalization or death at 12 months. ApoB may reflect lipid-related residual risk beyond traditional HF markers and help identify patients who could benefit from intensified lipid-lowering therapy and closer follow-up.