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: Patients undergoing carotid revascularization may show distinct patterns of bilateral carotid vulnerability and clinical risk. This study used latent class analysis (LCA) to identify high-resolution magnetic resonance imaging (HR-MRI)-based clinical–radiological phenotypes and evaluate their association with long-term major adverse cardiovascular events (MACE). Methods: This retrospective cohort included 289 patients who underwent carotid endarterectomy (CEA) or carotid artery stenting (CAS) between April 2017 and April 2024 and had preoperative carotid HR-MRI within 90 days. Ipsilateral and contralateral plaque features were assessed on multi-contrast vessel-wall HR-MRI. LCA included five indicators: ipsilateral intraplaque hemorrhage, ipsilateral lipid-rich necrotic core, contralateral intraplaque hemorrhage, cardiovascular disease history, and symptomatic status. MACE comprised cardiovascular death, nonfatal myocardial infarction, coronary revascularization, or stroke. Outcomes were assessed using Kaplan–Meier analysis and multivariable Cox regression. Results: Among 289 patients undergoing carotid revascularization, the mean age was 65.12 ± 9.46 years, and 237 (82.0%) patients were men. LCA identified three phenotypes: Systemic High-Risk (n = 128), Silent High-Risk (n = 37), and Stable/Moderate (n = 124). The Systemic High-Risk phenotype showed high probabilities of symptomatic presentation, cardiovascular disease history, and bilateral carotid vulnerability, whereas the Silent High-Risk phenotype showed marked ipsilateral plaque vulnerability despite lower clinical risk. During a median follow-up of 4.4 years, MACE-free survival differed significantly across phenotypes (log-rank p = 0.043). Compared with the Stable/Moderate phenotype, the Systemic High-Risk and Silent High-Risk phenotypes were both associated with increased MACE risk (HR 1.65, 95% CI 1.15–2.37, p = 0.039; HR 1.43, 95% CI 1.12–2.15, p = 0.034). Conclusions: HR-MRI-based LCA identified clinically meaningful carotid vulnerability phenotypes associated with long-term MACE after carotid revascularization. These findings support integrated assessment of bilateral plaque vulnerability and clinical risk for postoperative cardiovascular risk stratification.