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UNASSIGNED: The fatal cyclophosphamide cardiotoxicity is associated with high mortality in the adult population, and the study of its effects on children represents a gap in the field. This study aimed to evaluate the potential of global longitudinal strain (GLS) as a predictor of cardiovascular events among children with high-dose cyclophosphamide chemotherapy.
UNASSIGNED: This was a prospective cohort study of patients aged 14 years or younger who received high-dose (>120 mg/kg) cyclophosphamide chemotherapy recruited consecutively. Blood collection and echocardiography were performed 1 day before and after cyclophosphamide chemotherapy, and patients were followed up for 30 days with echocardiography. GLS and other echocardiography indicators were calculated accordingly. The primary outcome was the occurrence of cardiovascular events within 30 days after cyclophosphamide chemotherapy. The association between GLS and outcome was analyzed by using univariate and multivariable-adjusted Poisson regression.
UNASSIGNED: A total of 29 subjects were included. Among them, 10 patients (34.48%) developed cardiovascular events during a median follow-up of 10 (interquartile range, 5-13) days. Although similar before cyclophosphamide chemotherapy, GLS 1 day after cyclophosphamide chemotherapy was significantly lower in the cardiac injury group than in the noncardiac injury group (-18.33%±1.81% vs. -20.03%±1.49%, P=0.01). In the multivariable analysis adjusted for total cyclophosphamide dose (160 vs. 120-159 mg/kg) and global circumferential strain, GLS remained an independent predictor for cardiovascular events [incidence rate ratio: 1.46, 95% confidence interval: 1.02-2.09, P=0.04].
UNASSIGNED: GLS after cyclophosphamide chemotherapy may be a reliable indicator to predict cardiovascular events in patients receiving cyclophosphamide chemotherapy, which might be essential in optimizing treatment strategies for this high-risk patient group.

UNASSIGNED: Serum biomarkers have been investigated as predictive risk factors for cancer-related cardiovascular (CV) risk, but their analysis is limited to their baseline level rather than their overtime change. Besides historically validated causal factors, inflammatory and oxidative stress (OS) related markers seem to be correlated to CV events but this association needs to be further explored. We conducted an observational study to determine the predictive role of the longitudinal changes of commonly used and OS-related biomarkers during the cancer treatment period.
UNASSIGNED: Patients undergoing anticancer therapies, either aged 75+ years old or younger with an increased CV risk according to European Society of Cardiology guidelines, were enrolled. We assessed the predictive value of biomarkers for the onset of CV events at baseline and during therapy using Cox model, Subpopulation Treatment-Effect Pattern Plot (STEPP) method and repeated measures analysis of longitudinal data.
UNASSIGNED: From April 2018 to August 2021, 182 subjects were enrolled, of whom 168 were evaluable. Twenty-eight CV events were recorded after a median follow up of 9.2 months (Interquartile range, IQR: 5.1-14.7). Fibrinogen and troponin levels were independent risk factors for CV events. Specifically, patients with higher than the median levels of fibrinogen and troponin at baseline had higher risk compared with patients with values below the medians, hazard ratio (HR) = 3.95, 95% CI, 1.25-12.45 and HR = 2.48, 0.67-9.25, respectively. STEPP analysis applied to Cox model showed that cumulative event-free survival at 18 and 24 months worsened almost linearly as median values of fibrinogen increased. Repeated measure analysis showed an increase over time of D-Dimer (p-interaction event*time = 0.08), systolic (p = 0.07) and diastolic (p = 0.05) blood pressure and a decrease of left ventricular ejection fraction (p = 0.15) for subjects who experienced a CV event.
UNASSIGNED: Higher levels of fibrinogen and troponin at baseline and an increase over time of D-Dimer and blood pressure are associated to a higher risk of CV events in patients undergoing anticancer therapies. The role of OS in fibrinogen increase and the longitudinal monitoring of D-dimer and blood pressure levels should be further assessed.

With the successive development of chemotherapy drugs, good results have been achieved in clinical application. However, myocardial toxicity is the biggest challenge. Anthracyclines, immune checkpoint inhibitors, and platinum drugs are widely used. Targeted drug delivery, nanomaterials and dynamic imaging evaluation are all emerging research directions. This article reviews the recent literature on the use of targeted nanodrug delivery and imaging techniques to evaluate the myocardial toxicity of antineoplastic drugs, and discusses the potential mechanisms.

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UNASSIGNED: Cardiogenic shock (CS) is the leading cause of death among patients with acute myocardial infarction (AMI) and is managed with temporary mechanical circulatory support (tMCS) in advanced cases. Patients with cancer are at high risk of AMI and CS. However, outcomes of patients with cancer and AMI-CS managed with tMCS have not been rigorously studied.
UNASSIGNED: Adult patients with AMI-CS managed with tMCS from 2006 to 2018 with and without cancer were identified using the National Inpatient Sample. Propensity score matching (PSM) was performed for variables associated with cancer. Primary outcome was in-hospital death, and secondary outcomes were major bleeding and thrombotic complications.
UNASSIGNED: After PSM, 1287 patients with cancer were matched with 12,870 patients without cancer. There was an increasing temporal trend for prevalence of cancer among patients admitted with AMI-CS managed with tMCS (P trend < .001). After PSM, there was no difference in in-hospital death (odds ratio [OR], 1.00; 95% CI, 0.88-1.13) or thrombotic complications (OR, 1.10; 95% CI, 0.91-1.34) between patients with and without cancer. Patients with cancer had a higher risk of major bleeding (OR, 1.29; 95% CI, 1.15-1.46).
UNASSIGNED: Among patients with AMI-CS managed with tMCS, cancer is becoming increasingly frequent and associated with increased risk of major bleeding, although there was no difference in in-hospital death. Further studies are needed to further characterize outcomes, and inclusion of patients with cancer in trials of tMCS is needed.

Atrial fibrillation (AF) is more common in patients with malignancies than in general population. The pathophysiological processes include the pro-inflammatory condition and the exaggerated inflammatory reaction to chemotherapy, radiotherapy, and surgery interventions. Thus, it is pivotal to decrease morbidity and mortality in this group by providing appropriate care and prevention. In this subset, the risk of thromboembolic and bleeding events is high and the common risk score such as CHA2DS2-VASc and HAS-BLED employed in non-oncologic patients have limited evidence in cancer patients. A paucity of evidence in the setting in individuals having both malignancies and atrial fibrillation entangle the clinician when it comes to therapeutic management. Tailored management is recommended of anticoagulation treatment could be difficult, and there is. In this review, we try to explain the mechanism of AF in cancer patients as well as its management in this setting.

Over the years, advancements in the field of oncology have made remarkable strides in enhancing the efficacy of medical care for patients with cancer. These modernizations have resulted in prolonged survival and improved the quality of life for these patients. However, this progress has also been accompanied by escalation in mortality rates associated with anthracycline chemotherapy. Anthracyclines, which are known for their potent antitumor properties, are notorious for their substantial cardiotoxic potential. Remarkably, even after six decades of research, a conclusive solution to protect the cardiovascular system against doxorubicin-induced damage has not yet been established. A comprehensive understanding of the pathophysiological processes driving cardiotoxicity combined with targeted research is crucial for developing innovative cardioprotective strategies. This review seeks to explain the mechanisms responsible for structural and functional alterations in doxorubicin-induced cardiomyopathy.

UNASSIGNED: Takotsubo syndrome (TTS) is characterized by transient regional left ventricular (LV) dysfunction occurring in individuals exposed to physical or emotional stress. Various stressors are triggers for TTS in cancer patients, and anti-cancer drugs have recently been proposed as a trigger. Therefore, further studies are needed to clarify these triggers and avoid the unnecessary interruption of anti-cancer treatment.
UNASSIGNED: A 66-year-old woman presented with dyspnoea 10 days after the initiation of atezolizumab in combination with bevacizumab. She had previously received osimertinib as first-line therapy for recurrent lung cancer after primary resection and atezolizumab in combination with bevacizumab, paclitaxel, and carboplatin as second-line therapy. She was admitted due to electrocardiography abnormalities and elevated troponin I and brain natriuretic peptide levels. Echocardiography revealed circumferential severe LV hypokinesis at the mid-ventricular level, with preserved wall motion at the base and apex. Cardiac catheterization performed after the attenuation of symptoms with 20 mg of intravenous furosemide showed normal coronary arteries. Cardiac magnetic resonance imaging on Day 4 revealed increases in T1 and T2 values and extracellular volume fraction; however, neither myocardial infiltration of inflammatory cells or myocardial necrosis was observed in endomyocardial samples obtained on the day of her arrival. Atypical TTS was suspected, and she was treated with perindopril, bisoprolol, and spironolactone. Magnetic resonance imaging 1.5 months after the onset of TTS showed improvements in LV contractility, T1 and T2 values, and the extracellular volume fraction.
UNASSIGNED: A more detailed understanding of the relationship between anti-cancer drugs and TTS is crucial for preventing interruptions to anti-cancer therapy.