Jun-Xia Huang

Objective: To identify risk factors for major adverse cardiovascular events (MACE) in patients with multiple myeloma (MM) and to evaluate the performance of an external risk-score–based stratification.Methods: We retrospectively analyzed 162 newly diagnosed MM patients treated at Qingdao University Affiliated Hospital (2017–2023). Baseline demographics, comorbidities, laboratory and echocardiographic indices, and treatment exposures were collected. MACE (heart failure, acute coronary syndrome, malignant arrhythmias, cardiogenic shock, or cardiac sudden death) were adjudicated during therapy. Multivariable logistic regression identified independent risk factors. Progression-free survival (PFS) was compared by Kaplan–Meier analysis. An externally derived 0–4 point cardiovascular risk score was applied and patients were grouped as low (0–1), intermediate (2), or high (3–4) risk.Results: MACE occurred in 31/162 patients (19.14%). Independent risk factors included age at diagnosis (OR = 1.059 per year), cigarette smoking (OR = 3.652), anthracycline exposure (OR = 5.850), and ISS stage III (OR = 2.593; 95% CI: 1.108–6.067; all P < 0.05). Using the external risk score, 79, 54, and 29 patients were classified as low, intermediate, and high risk, respectively, with a stepwise rise in MACE incidence from ≈15% (low) to ≈18% (intermediate) and ≈31% (high). Discrimination of the score for MACE was modest (ROC AUC = 0.594). Patients experiencing MACE had significantly shorter PFS.Conclusion: Age, smoking, anthracycline use, and ISS stage III independently predict MACE in MM. External risk-score stratification demonstrates a clear gradient of risk but only modest discrimination, underscoring the need for prospective validation and optimization (e.g., integrating disease stage and treatment exposures). These findings support proactive cardio-oncology assessment and tailored therapy—particularly in older, smoking, ISS III, and anthracycline-treated patients.

Pulmonary hypertension (PH) is a progressive, pulmonary vascular disease with high morbidity and mortality. Unfortunately, the pathogenesis of PH is complex and remains unclear. Existing studies have suggested that inflammatory factors are key factors in PH. Interleukin-6 (IL-6) is a multifunctional cytokine that plays a crucial role in the regulation of the immune system. Current studies reveal that IL-6 is elevated in the serum of patients with PH and it is negatively correlated with lung function in those patients. Since IL-6 is one of the most important mediators in the pathogenesis of inflammation in PH, signaling mechanisms targeting IL-6 may become therapeutic targets for this disease. In this review, we detailed the potential role of IL-6 in accelerating PH process and the specific mechanisms and signaling pathways. We also summarized the current drugs targeting these inflammatory pathways to treat PH. We hope that this study will provide a more theoretical basis for targeted treatment in patients with PH in the future.

The association between blood eosinophil (EOS) counts and arterial/venous thrombosis is unclear. We aim to explore whether EOS count is a risk factor for thrombosis. We searched several databases and preprint platforms using core terms ‘eosinophil’, ‘myocardial infarction’, ‘ischemic stroke’, and ‘venous thromboembolism’ (VTE), among others. Studies comparing the odds ratios (ORs) or risk ratios (RRs) of EOSs with the abovementioned diseases were eligible. Overall, 22 studies were included. A high EOS count was associated with acute coronary artery thrombosis events (OR: 1.23, 95% CI: 1.15–1.32), short‐term cerebral infarction and mortality (RR: 2.87, 95% CI: 1.49–5.51). The short‐term risk of VTE was more common in patients with EOS‐related diseases (RR: 6.52, 95% CI: 2.42–17.54). For coronary artery disease, a high EOS count was a protective factor against 6‐month to 1‐year mortality (RR: 0.56, 95% CI: 0.45–0.69) but was associated with long‐term mortality (RR: 1.64, 95% CI: 1.25–2.14). Therefore, we conclude that for coronary artery thrombosis, EOS count is not associated with AMI events in general population. It may be associated with NSTEMI and STEMI in CAD patients, but more studies are needed to confirm this. In addition, EOS count is associated with an increased risk of both short‐ and long‐term mortality but is not predictive of the composite endpoints. For cerebral artery thrombosis, EOS count may be associated with cerebral infarction and could lead to an increased risk of poor short‐term prognosis. For VTEs, EOS count was a risk factor for some patients, especially those with acute‐phase EOS‐related diseases.