Methylene blue reduces monoamine oxidase expression and oxidative stress in human cardiovascular adipose tissue.

Cardiovascular diseases represent the major cause of morbidity mainly due to chronic heart failure. Epicardial (EAT) and perivascular adipose tissues (PVAT) are considered major contributors to the pathogenesis of cardiometabolic pathologies. Monoamine oxidases (MAOs) are mitochondrial enzymes recognized as sources of reactive oxygen species (ROS) in cardiometabolic pathologies.

Empagliflozin and dapagliflozin decreased atrial monoamine oxidase expression and alleviated oxidative stress in overweight non-diabetic cardiac patients.

The sodium-glucose-cotransporter 2 inhibitors (SGLT2i) are the blockbuster antidiabetic drugs that exert cardiovascular protection via pleiotropic effects. We have previously demonstrated that empagliflozin decreased monoamine oxidase (MAO) expression and oxidative stress in human mammary arteries. The present study performed in overweight, non-diabetic cardiac patients was aimed to assess whether the two widely prescribed SGLT2i decrease atrial MAO expression and alleviate oxidative stress elicited by exposure to angiotensin 2 (ANG2) and high glucose (GLUC).

Acquired Von Willebrand Factor Deficiency at Patient-Prosthesis Mismatch after AVR Procedure-A Narrative Review.

Acquired von Willebrand factor deficiency has been described in patients with aortic valve stenosis due to high shear forces developed during passage through the narrowed valve orifice, which determines structural changes in this molecule. Similar flow conditions are present in patients with an aortic prosthesis that presents a patient-prosthesis mismatch. Patient-prosthesis mismatch is described by the smaller effective orifice area of the prosthesis than the native valve, which would probably determine similar changes in the molecules of the von Willebrand factor, leading to acquiring von Willebrand deficiency.