Background: Left ventricular hemodynamic forces (LV HDFs) are altered in myocardial dysfunction. While infarct location and size influence post-ST-segment elevation myocardial infarction (STEMI) remodeling, their specific effects on HDFs remain unclear. This study investigated how infarct location and size impact left ventricular HDFs and assessed HDFs’ prognostic value for predicting subsequent heart failure (HF) in STEMI patients. Methods: In this retrospective study, 275 STEMI patients underwent cardiac magnetic resonance (CMR) 3–7 days after primary percutaneous coronary intervention. HDFs were derived from routine CMR cine images. Patients were stratified by infarct location (anterior vs. non-anterior) and median infarct size (IS). Key parameters—apical–basal (A-B) and lateral-septal (L-S) forces, their ratio, force direction angle (φ), and force reversal during systolic–diastolic transition—were compared. The primary endpoint was new-onset congestive HF during follow-up. Results: Compared to non-anterior STEMI, anterior STEMI showed significantly impaired A-B and L-S HDFs throughout the cardiac cycle (all p < 0.05) and was independently associated with force reversal (OR 2.31, 95% CI: 1.05–5.07). Larger IS correlated with reduced A-B HDFs and altered force distribution (increased L-S/A-B ratio, decreased φ). Force reversal predicted HF (HR: 2.10, 95% CI: 1.22–3.62) and provided incremental prognostic value beyond left ventricular ejection fraction (LVEF) alone (C-statistic: LVEF 0.680 vs. LVEF + force reversal 0.770, p = 0.034). Conclusions: Anterior infarction causes global HDF impairment and force reversal, while larger IS primarily reduces longitudinal forces and disrupts force distribution. Force reversal predicts subsequent HF and enhances prognostic value beyond LVEF.

Background: Pentraxin 3 (PTX3) is a well-established inflammatory biomarker with significant implications in the pathogenesis and prognostic assessment of cardiovascular diseases. This study aimed to investigate the potential value of serum PTX3 as a circulating biomarker when combined with the high-resolution magnetic resonance vessel wall imaging (HR-VWI) for identifying carotid vulnerable plaque (CVP) and its specific vulnerable features. Methods: This prospective cross-sectional study enrolled 86 patients with carotid atherosclerosis who underwent HR-VWI. Patients were classified into CVP and non-carotid vulnerable plaque (NCVP) groups, and CVP was divided into unilateral carotid vulnerable plaque (UCVP) and bilateral carotid vulnerable plaque (BCVP). CVP was defined as meeting ≥ 1 major criteria: lipid-rich necrotic core (LRNC) maximum area percentage > 40% combined with thin fibrous cap (FC), intraplaque hemorrhage (IPH), FC discontinuity, and focal inflammation. Multivariate logistic regression analysis identified factors influencing CVP and the formation of specific vulnerable features. Results: Serum PTX3 levels progressively increased across the NCVP, UCVP, and BCVP groups (median 638.23, 858.52, 1113.62 pg/mL; p < 0.001). PTX3 independently predicted the presence of CVP (OR = 2.88; 95% CI: 1.16–8.91; p = 0.039) and specific vulnerable features, including FC discontinuity (OR = 2.47; 95% CI: 1.32–4.63; p = 0.005) and focal inflammation (OR = 2.25; 95% CI: 1.18–4.32; p = 0.014) with high diagnostic performance for these conditions. PTX3 levels exhibited a moderate positive correlation with the number of vulnerable features (r = 0.610, p < 0.01). Conclusions: Elevated serum PTX3 levels were significantly associated with HR-VWI-defined carotid plaque vulnerability and its severity, serving as a reliable circulating biomarker for identifying FC discontinuity and focal inflammation.

Background/Objectives: This study aimed to investigate the associations between preoperative carotid high-resolution magnetic resonance imaging (HR-MRI) plaque features and coronary atherosclerotic burden, and to compare the cross-vascular association patterns of plaque burden-related measures and individual vulnerable plaque features. Methods: This retrospective study included consecutive patients who underwent carotid revascularization and had both preoperative carotid HR-MRI and coronary computed tomography angiography (CTA) between April 2017 and December 2024. Carotid plaque characteristics included calcification, lipid-rich necrotic core (LRNC), intraplaque hemorrhage (IPH), loose matrix (LM), ulceration, maximum wall thickness (MWT), maximum wall area (MWA), and normalized wall index (NWI). Coronary atherosclerotic burden was characterized using coronary artery calcium score (CACS), maximum luminal stenosis, and the number of diseased coronary arteries; the number of coronary arteries with ≥50% stenosis was additionally recorded. Associations between carotid plaque characteristics and coronary atherosclerotic burden were evaluated using correlation analyses and multivariable logistic regression. Results: A total of 162 patients were included (mean age, 66.11 ± 7.54 years; 138 [85.2%] men). CACS ≥ 400 was present in 76 patients (46.9%), obstructive coronary disease (≥50% stenosis in at least one coronary artery) in 96 patients (59.3%), and involvement of ≥3 diseased coronary arteries in 128 patients (79.0%). Greater coronary atherosclerotic burden was consistently associated with higher carotid calcification volume and MWT and NWI (all p < 0.05). After adjustment for clinical risk factors and correction for multiple testing, calcification volume, MWT and NWI remained associated with CACS ≥ 400, obstructive coronary disease, and involvement of ≥3 diseased coronary arteries. In contrast, individual vulnerable plaque features, including LRNC, IPH, LM, and ulceration, showed weaker and less consistent associations. Conclusions: In patients undergoing carotid revascularization, preoperative carotid HR-MRI-derived plaque burden-related features showed more consistent associations with coronary atherosclerotic burden than individual vulnerable plaque features. These findings suggest that plaque burden-related and vulnerable plaque features may reflect different aspects of atherosclerosis, with plaque burden-related measures more closely reflecting cumulative systemic atherosclerotic involvement and vulnerable plaque features primarily characterizing local plaque composition and instability.