Volume 1 Issue 1, January 2022

How do we measure the impact of scientific research? A new study discusses the current publication culture, diverse animal models that are commonly used in cardiovascular studies, the comparison between basic and clinical research paths, and the role of authors and reviewers in bringing these two paths together.

Aortic-intima-resident macrophages (MAC^AIRs) share the vessel luminal lining with endothelial cells in areas of turbulent flow and protrude into the arterial blood stream to clean the inner arterial surface via phagocytosis, shield nearby endothelial cells from activation by thrombin and prevent microthrombus formation.

In this issue of Nature Cardiovascular Research, Aung and colleagues¹ use breathalyser data to identify dates associated with high concentrations of blood alcohol, which matched days with excess emergency department presentations for atrial fibrillation. This study strengthens the existing evidence that binge drinking is responsible for atrial fibrillation in ‘holiday heart’.

This Review discusses the physical concepts and descriptions of the structures that determine myocardial stiffness, different techniques used to estimate myocardial stiffness, and their application in clinical medicine.

In this epidemiological analysis, Marcus et al. show that acute alcohol consumption is associated with a higher risk of discrete atrial fibrillation episodes, as well as for new-onset (incident) atrial fibrillation, in the general population.

Sick heart and vessels skew hematopoiesis toward inflammatory myeloid cells. Rhode et al. show that hypertension, atherosclerosis and myocardial infarction cause endothelial dysfunction in bone marrow (BM), which in return causes overproduction of inflammatory myeloid cells and systemic leukocytosis in mice. This process is mediated by VEGF signaling, IL-6 and versican production by the BM endothelium.

Sustained cardiac function depends on circadian REV-ERBs. Here, Dierickx et al. show that circadian nuclear receptors REV-ERBα and β are indispensable to establish the transcriptional program that controls cardiac metabolism and NAD⁺ production. Deregulation of REV-ERBs leads to dilated cardiomyopathy and premature death.

Borlaug et al. show that, among patients where heart failure was excluded, an increasing H₂FPEF score was associated with greater left atrial dilation, left ventricular hypertrophy and more severe diastolic dysfunction.

Hernandez et al. show that aortic intima resident macrophages (Mac^AIR) seed the mouse aorta at birth, self-replicate and line the aortic lumen together with the endothelium, protecting the aorta from clot formation in regions of disturbed flow by clearing fibrin deposits and blunting thrombin activity.

Koplev et al. apply interactive system analyses to infer and characterize gene-regulatory networks (GRNs) active within and across tissues that cause cardiometabolic disease and coronary artery disease (CAD). By including GWAS in the integrative analysis, the provided multiorgan framework of GRNs is suggested to explain significantly more heritability of CAD than what has been achieved by analyzing GWAS alone.