American Heart Association

NT-proBNP is more predictive of unfavorable outcomes in HFpEF in the absence of AFib

Contributor: Martin Chacon

Does an increased NT-proBNP in patients with atrial fibrillation (AF) and HFpEF correspond to a higher risk for worse outcomes? Kristensen et al suggest increased NTproBNP levels do not show the same correlation with poor outcomes in patients with AF compared with those without AF. NT-proBNP is increased in AF patients independently from heart failure, therefore, its capacity to predict cardiovascular death or hospitalizations in HFpEF may be diminished.

Visual Abstract: Cardiac Troponin I and Cardiac Events in HFpEF Patients

Contributor: Ike Chinyere

Cardiac Troponin I and Risk of Cardiac Events in Patients With Heart Failure and Preserved Ejection Fraction

Study Link: Cardiac Troponin I and Risk of Cardiac Events in Patients With Heart Failure and Preserved Ejection Fraction

Visual Abstract: Spironolactone Reduces Albuminuria in HFpEF

Contributor: Ike Chinyere

Prognostic Value of Albuminuria and Influence of Spironolactone in Heart Failure With Preserved Ejection Fraction The TOPCAT Trial

Study Link: Prognostic Value of Albuminuria and Influence of Spironolactone in Heart Failure With Preserved Ejection Fraction: The TOPCAT Trial

Progenitor cells are decreased in heart failure and specific to HF type

Contributor: Mat Bull

Do progenitor cells matter for patients with HF? First, what is a progenitor cell? A progenitor cell is a stem cell that has potential to differentiate into multiple different cell types. Progenitor cells are classified by cluster of differentiation surface markers, which act as receptors and ligands to their target tissue. CD34+ progenitor cells have been shown to play a role in vascular and myocardial regeneration and in this article are shown to be an important biomarker in heart failure.

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.