Myocardial infarction (MI) is one of the leading causes of death in the world. Early myocardial reperfusion improves acute MI survival. Bioflavonoid quercetin is known to have antioxidant, anti-inflammatory, and anti-proliferative properties. The presented pilot study aims to investigate the cardioprotective effect of quercetin on infarct size limiting in ST-segment elevation myocardial infarction (STEMI) patients. Patients (n=143) with the first anterior STEMI within 6 hours from symptoms onset were included in the open-label multicenter pilot study. Patients were randomized either to quercetin group (n=70) in addition to standard treatment or recommended therapy alone (control group, n=73). Quercetin infusions were initiated before reperfusion and repeated during the next 5 days. The infarct size assessed by CK-MB AUC was the primary study outcome. The study arms matched well regarding demographics, time to admission, and main clinical data. The median early CK-MB AUC was significantly lower in quercetin group than in controls (8036±7594 vs 11219±8146 U×1h/L, p=0.015). Intravenous quercetin was associated with less reperfusion-induced intramyocardial hemorrhage by Cardiac Magnetic Resonance on Day 3 (11.1% of patients in quercetin group vs 53.3% of patients in control group, p<0.024). There were no significant differences in left ventricle ejection fraction (LVEF) and LV remodeling indicators. Our pilot study is the first to demonstrate novel insight into ischemia/reperfusion damage in STEMI patients. The addition of quercetin to standard STEMI therapy limits infarct size and prevents intramyocardial hemorrhage after the first anterior STEMI. Further research will be necessary to both validate and expand upon these findings.

Background: We investigated the role of a high-sensitive cardiac troponin T (hsTnT) increase below the upper limit of normal (ULN) in patients with breast cancer (BC). hsTnT assays accurately quantify very low plasma troponin concentrations and enable the early detection of cardiomyocyte injury before a drop in the left ventricular ejection fraction (LVEF). The increase in hsTnT below the ULN in response to chemotherapy has not previously been studied. Method: This was an open-label pilot study. Female patients with newly diagnosed BC scheduled to receive systemic cancer treatment were recruited. Blood sampling and echocardiography were performed at baseline, at 3 and 6 months of cancer treatment. hsTnT concentrations were measured using the Elecsys TnT hs assay (Roche Diagnostics). The limit of blank and 99th percentile cutoff values for the hsTnT assay were 3 and 14 ng/L. We calculated the rise in hsTnT (ΔhsTnT) by the difference (%) between its baseline level and during follow-up (FU) in each patient. Results: Among eligible subjects, we excluded 4 patients before the start of treatment and 17 patients during the follow-up with values for the hsTnT >14 ng/L. Finally, 60 women with a median age of 48.6 ± 1.3 years were included in the study. The median baseline hsTnT concentration was 5.5 ± 1.4 ng/L. During 6 months of cancer treatment, hsTnT increased in all patients by up to 10–305% from baseline, with an average of 94.2%. LV EF was normal at baseline and decreased significantly compared to the value before cancer treatment (61.9 ± 3.3% vs. 56.3 ± 7.0%; p < 0.045). We correlated the hsTnT rise with a drop in LV EF ≥ 10% from its baseline level. Logistic regression analysis showed that Δ hsTnT has a good predictive value for LV dysfunction, 0.78 (p = 0.05), 95% CI (0.67–0.90). The increase in hsTnT > 81% was determined as the optimal threshold value for detecting early biochemical cardiotoxicity. Conclusion: It was investigated that hsTnT rise within the cutoff < 14 ng/L can be used as a marker of early biochemical cardiotoxicity and is valuable for predicting LV drop in 6 months of FU. We conclude that BC patients with increased hsTnT plasma concentration > 81% from the baseline value should be considered as high-risk patients for cardiotoxicity and need more precise cardiac monitoring and early preventive medical intervention strategies.

Background/Objectives: Venous thromboembolism (VTE) is a major cardiovascular complication in cancer patients and the leading cause of morbidity and mortality. The aim of the study was to evaluate the incidence, timing, clinical predictors, and management of VTE in patients with breast cancer (BC), undergoing oncological therapy, and to propose a risk-adapted strategy for thrombosis monitoring and prevention. Methods: In this retrospective single-center study, 116 women with histologically confirmed BC (stages I–IV) treated between 2021 and 2024 were included. Patients were divided according to the occurrence of objectively confirmed VTE. Clinical characteristics, comorbidities, laboratory parameters, cancer-related factors, and treatment modalities were analyzed. Univariate and multivariate logistic regression analyses were performed to identify independent predictors of VTE. Results: VTE occurred in 25 patients (21.6%), predominantly within the first 12 months after cancer diagnosis. Patients who developed VTE were significantly older and more frequently had hypertension, dyslipidemia, hyperglycemia, anemia, and leukocytosis. Multivariate analysis identified age ≥ 55 years, poor performance status (ECOG ≥ 3), and elevated glucose level as independent predictors of VTE. Deep vein thrombosis of the lower and upper extremities was the most common manifestation (52%), while pulmonary embolism was present in 24% of cases, either alone or in combination (20%). Direct oral anticoagulants were the most frequently used long-term anticoagulant therapy. Conclusions: VTE is a clinically relevant and relatively frequent complication in patients with BC, particularly during the early period of anticancer treatment. Patient-related and metabolic factors play a key role in thrombosis risk, underscoring the need for individualized, risk-adapted approaches to VTE prevention and monitoring in these populations.

Background & Objectives: Venous thromboembolism (VTE) is a major cardiovascular complication in cancer patients and leading cause of morbidity and mortality. The aim of the study was to evaluate the incidence, timing, clinical predictors, and management of VTE in patients with breast cancer (BC), undergoing oncological therapy, and to propose a risk-adapted strategy for thrombosis monitoring and prevention. Methods: In this retrospective single-center study, 116 women with histologically confirmed BC (stages I–IV) treated between 2021 and 2024 were included. Patients were divided according to the occurrence of objectively confirmed VTE. Clinical characteristics, comorbidities, laboratory parameters, cancer-related factors, and treatment modalities were analyzed. Univariate and multivariate logistic regression analyses were performed to identify independent predictors of VTE. Results: VTE occurred in 25 patients (21.6%), predominantly within the first 12 months after cancer diagnosis. Patients who developed VTE were significantly older and more frequently had hypertension, dyslipidemia, hyperglycemia, anemia, and leukocytosis. Multivariate analysis identified age≥55 years, poor performance status (ECOG ≥3), and elevated glucose level as independent predictors of VTE. Deep vein thrombosis of the lower and upper extremities was the most common manifestation (52%), while pulmonary embolism was present in 24% of cases, either alone or in combination (20%). Direct oral anticoagulants were the most frequently used long-term anticoagulant therapy. Conclusions: VTE is a clinically relevant and relatively frequent complication in patients with BC, particularly during the early period of anticancer treatment. Patient-related and metabolic factors play a key role in thrombosis risk, underscoring the need for individualized, risk-adapted approaches to VTE prevention and monitoring in these populations.