Heart failure

Due to various possible causes, blood moves through the heart and body at a slower rate, and pressure in the heart increases. As a result, the heart cannot pump enough oxygen and nutrients to meet the body's needs. The chambers of the heart may respond by stretching to hold more blood to pump through the body or by becoming stiff and thickened. This helps to keep the blood moving, but the heart muscle walls may eventually weaken and become unable to pump as efficiently. As a result, the kidneys may respond by causing the body to retain fluid (water) and salt. If fluid builds up in the arms, legs, ankles, feet, lungs, or other organs, the body becomes congested, and congestive heart failure is the term used to describe the condition.

• Metabolic syndrome, high-sensitivity C-reactive protein and the risk of heart failure: the Kailuan cohort study
• Heart Rate Variability, Microvascular Dysfunction, and Inflammation: Exploring the Potential of taVNS in Managing Heart Failure in Type 2 Diabetes Mellitus
• Matrix Metalloproteinases: Pathophysiologic Implications and Potential Therapeutic Targets in Cardiovascular Disease
• Contemporary insights into elamipretide's mitochondrial mechanism of action and therapeutic effects
• The citrus flavonoid nobiletin prevents the development of doxorubicin-induced heart failure by inhibiting apoptosis
• One for multiple: Physics-informed synthetic data boosts generalizable deep learning for fast MRI reconstruction
• [Retracted] Effect of apelin on the cardiac hemodynamics in hypertensive rats with heart failure
• Blood transfusion in percutaneous left atrial appendage occlusion: a nationwide analysis of incidence, predictors, and outcomes

Mitigation of cardiac autonomic dysregulation by neuromodulation technologies is emerging as a new therapeutic modality of heart failure (HF). This progress has necessitated the identification of a biomarker for the quantification of sympathovagal balance, the potential target of 'neuromodulation' strategies. The currently available autonomic nervous system assessment parameters do not truly reflect the sympathovagal balance of the ventricle. Protein kinase A (PKA) is an intracellular enzyme that plays a major role in the pathophysiology of functional and structural ventricular remodeling in HF. Interestingly, sympathetic and parasympathetic activations exert reciprocal influence on the activity of PKA ¹⁾.