American Heart Association

Impaired relaxation and elevated intracellular Ca2+ in contracting myocardium of hypertensive heart disease and HFpEF

Contributor: Steven Stroud

Relaxing can be hard in hypertensive heart disease (HHD). Specifically, for the stiff ventricle destined for HFpEF. Is it a problem with relaxation of myocytes, or is it due to stiffening from fibrosis?

Entry of Ca2+ into the myocyte begins a flood of stored Ca2+, stimulating contraction. The cell can relax only when this Ca2+ is taken away from the contractile apparatus. Along with SERCA and phospholamban, the sarcolemmal Na+/Ca2+ exchanger (NCX) handles this important duty.

Cathespin D–mediated autophagosome flux prevents cardiac remodeling and restrictive cardiomyopathy

Contributor: Steven Stroud

How does the heart clean up after a myocardial infarction? Autophagy. Wong et al identified the role of Cathespin D as a regulator of cardiac remodeling.

First, what is autophagy? Autophagy is derived from the Greek “auto” meaning self and “phagy” meaning eating. Pay close attention, as it is soon to be a familiar term in our field. Exciting new basic and translational research will be presented in CircHF in the coming months.

Peripheral venous pressure, a surrogate for central venous pressure

Contributor: Steven Stroud

Bedside assessment of volume status is an age-old practice for clinicians. Spoiler alert: we are not very good at it. So, is there an alternate, accurate, less invasive way to assess volume status in decompensated heart failure patients other than measurement of central hemodynamics? Well, every hospitalized patient gets (at least) one peripheral intravenous (IV) line. What if we transduced the peripheral venous pressure (PVP) to estimate central venous pressure (CVP)? Sperry and colleagues demonstrated that PVP was highly correlated with CVP (r=0.947). OK, but does that help me estimate  pulmonary catheter wedge pressure (PCWP)? PVP was mildly correlated (r=0.57) with PCWP, but patients with PVP >10mmHG did have a 100% positive predictive value of PCWP >20mmHg (n=13). Big news— worry less about keeping batteries in that little flashlight for the neck exam.

Rapid decline in high energy phosphate leads to exercise intolerance in HF patients

Contributor: Steven Stroud

Exercise intolerance is a hallmark of HF. We tend to blame the weak heart for not delivering enough oxygen to exercising muscles, but this is wrong.

Muscles without oxygen are hypoxic. This could happen because of poor cardiac output or because the skeletal muscle cells are not handling oxygen well. In other words, does low cardiac output cause fatigability or are there differences in skeletal muscle energetics in HF?

Decoupling between dPAP and PCWP predicts mortality and HF readmission among CF-LVAD patients

Contributor: Elise Vo

Decoupling of diastolic pulmonary artery pressure and PCWP (greater than 5 mmHg difference) during ramp testing in continuous flow LVAD patients is a significant predictor for HF hospitalization and all-cause mortality. This decoupling is also represented as the diastolic pressure gradient (dPAP-PCWP). dPAP and PCWP decoupling (increased DPG) may indicate intrinsic pulmonary vascular pathology and associated right ventricular strain.