Differences Between Ischemic and Non-Ischemic Cardiomyopathy in Heart Failure Related Cardiogenic Shock.

Background: Heart failure-related cardiogenic shock (HF-CS) accounts for a growing proportion of cardiogenic shock (CS) related admissions to contemporary cardiac intensive care units. Limited data exists comparing non-ischemic (NICM) and ischemic cardiomyopathies (ICM) in this setting.

Methods And Results: We sought to examine the differences in patient characteristics, in-hospital treatments, and outcomes among individuals admitted with ICM and NICM HF-CS.

β-Blockade Prevents Post-Ischemic Myocardial Decompensation Via βAR-Dependent Protective Sphingosine-1 Phosphate Signaling.

Background: Although β-blockers increase survival in patients with heart failure (HF), the mechanisms behind this protection are not fully understood, and not all patients with HF respond favorably to them. We recently showed that, in cardiomyocytes, a reciprocal down-regulation occurs between β-adrenergic receptors (ARs) and the cardioprotective sphingosine-1-phosphate (S1P) receptor- (S1PR).

Objectives: The authors hypothesized that, in addition to salutary actions due to direct βAR-blockade, agents such as metoprolol (Meto) may improve post-myocardial infarction (MI) structural and functional outcomes via restored S1PR signaling, and sought to determine mechanisms accounting for this effect.

Context-dependent memory following recurrent hypoglycaemia in non-diabetic rats is mediated via glucocorticoid signalling in the dorsal hippocampus.

Aims/hypothesis: Recurrent hypoglycaemia is primarily caused by repeated over-administration of insulin to patients with diabetes. Although cognition is impaired during hypoglycaemia, restoration of euglycaemia after recurrent hypoglycaemia is associated with improved hippocampally mediated memory. Recurrent hypoglycaemia alters glucocorticoid secretion in response to hypoglycaemia; glucocorticoids are well established to regulate hippocampal processes, suggesting a possible mechanism for recurrent hypoglycaemia modulation of subsequent cognition.