American Heart Association

left ventricle

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.

Concentric left ventricular hypertrophy rarely leads to dilated cardiomyopathy

Contributor: Jennifer Huang

Does concentric left ventricular hypertrophy (LVH) progress to dilated cardiomyopathy (DCM)? It may not be as common as we previously thought and the transition may occur over decades.

1,386 participants of the Dallas Heart Study without baseline LV dilation were included. Ten percent of the participants had baseline LVH (7.2 g/mL0.67  for men and 5.8 g/mL0.67 for women). The study population had a mean age of 44 years, 57% women and 43% black patients. Of note, patients that developed cardiovascular disease during the study period (MI, CABG, PCI, stroke or HF) were not included in the final cohort of 1282. Baseline and follow up cardiac magnetic resonance imaging was performed a median of 7 years after baseline imaging.