8,226 research outputs found
Funding: International Society for Heart Research, European Section/Servier Research Fellowship
No full textNitroxyl (HNO) for treatment of acute heart failure
No full textThe loss of contractile function is a hallmark of heart failure. Although increasing intracellular Ca2+ is a possible strategy for improving contraction, current inotropic agents that achieve this by raising intracellular cAMP levels, such as β-agonists and phosphodiesterase inhibitors, are generally deleterious when administered as long-term therapy due to arrhythmia and myocardial damage. Nitroxyl donors have been shown to improve cardiac function in normal and failing dogs, and in isolated cardiomyocytes they increase fractional shortening and Ca2+ transients, independently from cAMP/PKA or cGMP/PKG signaling. Instead, nitroxyl targets cysteines in the EC-coupling machinery and myofilament proteins, reversibly modifying them to enhance Ca2+ handling and myofilament Ca2+ sensitivity. Phase I-IIa trials with CXL-1020, a novel pure HNO donor, reported declines in left and right heart filling pressures and systemic vascular resistance, and increased cardiac output and stroke volume index. These findings support the concept of nitroxyl donors as attractive agents for the treatment of acute decompensated heart failure. © 2014 Springer Science+Business Media
Low-intensity pulsed ultrasound (LIPUS) in heart failure with preserved ejection fraction (HFpEF): lupus in fabula?
No full textCardiac Toxicity in Patients Treated With Immune Checkpoint Inhibitors: It Is Now Time for Cardio-Immuno-Oncology
No full text
Mechanisms of Cardiovascular Damage Induced by Traditional Chemotherapy
No full textTraditional chemotherapeutics are essential tools in the management of cancer patients. Nevertheless, these drugs are burdened by some degree of cardiovascular toxicity. Anthracycline-induced toxicity has been historically the most studied, but also the use of other drugs can be limited by a certain risk of cardiac and vascular toxicities. Here we acknowledge the main mechanistic insights, and we describe the different aspects of cardiotoxicity of these drugs, highlighting the different cellular compartments and cardiovascular components affected
Molecular Mechanisms of Cardiovascular Damage Induced by Anti-HER-2 Therapies
No full textIn the last two decades, newer biological drugs have been designed in order to “target” specific proteins involved in cancer proliferation and overcome the increased risk of cardiovascular toxicity associated with “broad-spectrum” classic chemotherapeutics. Unfortunately, these proteins are also important for the maintenance of cardiovascular homeostasis. The humanized anti-ErbB2 antibody, trastuzumab, is the prototypical biological drug first introduced in antineoplastic protocols for the treatment of ErbB2+ breast cancer. Indeed, not only is this protein overexpressed in several breast cancers, but also it plays a major role in the cardiovascular system in cell growth, including myocyte growth, and inhibition of apoptosis and can modulate the oxidative damage induced by anthracyclines. Hence, patients treated with trastuzumab developed systolic dysfunction, especially when administered with or shortly after doxorubicin
- …
