American Heart Association

Challenges in Employing Neuregulin-1 as a Heart Failure Therapy

Contributor: Ike Chinyere

Mechanisms of the Multitasking Endothelial Protein NRG-1 as a Compensatory Factor During Chronic Heart Failure

Study Link: Mechanisms of the Multitasking Endothelial Protein NRG-1 as a Compensatory Factor During Chronic Heart Failure

Superior Survival in Women with HFpEF but Worse HF Symptoms & Quality of Life

Contributor: Sadaf Sharfaei

Sex-Related Differences in Heart Failure With Preserved Ejection Fraction

Study Link: Sex-Related Differences in Heart Failure With Preserved Ejection Fraction

Rat Model Suggests Sacubitril/Valsartan may be Effective in Pulmonary Hypertension

Contributor: Ike Chinyere

Study Link: Treatment of Pulmonary Hypertension With Angiotensin II Receptor Blocker and Neprilysin Inhibitor Sacubitril/Valsartan

Disparities in Rates of Admission to Primary Cardiology Service Among Black and Latinx Patients

Contributor: Sadaf Sharfaei

Identification of Racial Inequities in Access to Specialized Inpatient Heart Failure Care at an Academic Medical Center

Study Link: Identification of Racial Inequities in Access to Specialized Inpatient Heart Failure Care at an Academic Medical Center

Adenosine-induced vasodilation is impaired and may be a therapeutic target in HFpEF

Contributor: Seyedeh Maryam Hosseini, MD

Heart failure with preserved ejection fraction is characterized by impaired cardiovascular reserve and coronary microvascular dysfunction. Tissue hypoxia activates endogenous adenosine secretion leading to vasodilation of the myocardial microvasculature. By increasing tissue perfusion in working myocardium, adenosine responds to increased metabolic demand. Davila et al. demonstrate that this adenosine vasodilation mechanism is impaired in HFpEF due to up-regulation of the adenosine kinase (ADK) enzyme gene. ADK changes adenosine to its inactive form. Increasing endogenous adenosine by inhibiting the ADK enzyme pharmacologically may have therapeutic potential to improve coronary vasodilation, myocardial perfusion and LV diastolic dysfunction in HFpEF.