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Heart-on-a-chip: a revolutionary organ-on-chip platform for cardiovascular disease modeling.
J Transl Med
January 2025
Aerospace Medical Center, Aerospace Center Hospital, Beijing, China.
Heart-on-a-chip (HoC) devices have emerged as a powerful tool for studying the human heart's intricate functions and dysfunctions in vitro. Traditional preclinical models, such as 2D cell cultures model and animal model, have limitations in accurately predicting human response to cardiovascular diseases and treatments. The HoC approach addresses these shortcomings by recapitulating the microscale anatomy, physiology, and biomechanics of the heart, thereby providing a more clinically relevant platform for drug testing, disease modeling, and personalized therapy.
View Article and Find Full Text PDFBTKi-induced cardiovascular toxicity in CLL: Risk mitigation and management strategies.
Blood Rev
January 2025
Clinic of Hematology, University Clinical Centre of Serbia, Serbia; Faculty of Medicine, University of Belgrade, Serbia. Electronic address:
Targeted therapies, consisting of Bruton tyrosine kinase inhibitors (BTKis) or BCL-2 inhibitors, are the mainstay of contemporary treatments for chronic lymphocytic leukemia (CLL). The most common adverse effects (AEs) of BTKis are fatigue, bruising, infection, hematological and cardiovascular AEs. While AEs during treatment are usually mild (grades 1 and 2), grade 3 and 4 AEs have been detected in some patients, necessitating additional medical care and temporary or permanent drug discontinuation.
View Article and Find Full Text PDFPredictors of Mortality in Venoarterial Extracorporeal Membrane Oxygenation Regardless of Early Left Ventricular Unloading: A National Experience.
J Cardiothorac Vasc Anesth
January 2025
Department of Anesthesia, Cardiothoracic Surgery/Cardiac ICU Section, Heart Hospital, Hamad Medical Corporation, Doha, Qatar; Department of Critical Care Medicine, Beni Suef University, Egypt; Weill Cornell Medical College, Doha, Qatar.
Objective: The use of an intra-aortic balloon pump (IABP) has been suggested to unload the left ventricle while on venoarterial extracorporeal membrane oxygenation (VA-ECMO) for cardiogenic shock (CS), leading to possibly improved in-hospital mortality. However, the predictors of mortality on dual mechanical circulatory support have not yet been evaluated, especially in real-world clinical settings. Therefore, a case-control study was conducted to determine the rate of all-cause mortality associated with VA-ECMO use regardless of left ventricular (LV) unloading, and with early LV unloading in the setting of CS, and to identify the predictors of mortality associated with VA-ECMO, with concurrent early LV unloading.
View Article and Find Full Text PDFEngineered Strategies to Interfere with Macrophage Fate in Myocardial Infarction.
ACS Biomater Sci Eng
January 2025
Central Laboratory, The Fifth Affiliated Hospital, Southern Medical University, Guangzhou, Guangdong 510910, China.
Myocardial infarction (MI), a severe cardiovascular condition, is typically triggered by coronary artery disease, resulting in ischemic damage and the subsequent necrosis of the myocardium. Macrophages, known for their remarkable plasticity, are capable of exhibiting a range of phenotypes and functions as they react to diverse stimuli within their local microenvironment. In recent years, there has been an increasing number of studies on the regulation of macrophage behavior based on tissue engineering strategies, and its regulatory mechanisms deserve further investigation.
View Article and Find Full Text PDFSevere pulmonary arterial hypertension and cardiogenic shock in acute systemic lupus erythematosus.
BMJ Case Rep
January 2025
Department of Allergy, Immunology and Respiratory Medicine, Alfred Hospital, Melbourne, Victoria, Australia.
We describe a woman in her late 20s with newly diagnosed systemic lupus erythematosus (SLE), who presented with fulminant pulmonary arterial hypertension (PAH) requiring inotropic and extracorporeal support. She was established on triple pulmonary vasodilator therapy with concurrent aggressive immunosuppression; however, treatment was complicated by infection and diffuse alveolar haemorrhage, necessitating delays in immunosuppression and withdrawal of epoprostenol. Despite this, with ongoing suppression of her SLE, her pulmonary haemodynamics improved, with normal pressures on right heart catheterisation several months later allowing stepdown to sildenafil monotherapy.
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