American Heart Association

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.

Ivabradine: Valuable in HFrEF for a select few

Contributor: Mat Bull

Less is more when it comes to heart rate in HF. Ivabradine, a sinus node inhibitor, lowers heart rate, thereby decreasing myocardial demand. Some beta blockers have mortality benefit in HFrEF as shown by the MERIT-HF and COPERNICUS trials, and a side effect of these drugs is heart rate lowering. Thus, beta-blockers are standard of care in HFrEF; however, at maximally indicated doses, undesired side effects often occur. Since ivabradine targets very specific ion channels within the SA node, further heart rate reduction is possible. But which patients are eligible for this therapy? Read on.