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The essential omega-6 polyunsaturated fatty acid γ-linolenic acid present in maternal milk coordinates cardiac adaptation and survival in newborn mice, according to a new study.

Results from the MONITOR-HF trial show that remote monitoring of pulmonary artery pressure using the implantable CardioMEMS sensor in patients with chronic heart failure improves quality of life and reduces hospitalizations.

In this Consensus Statement, Dewey and the other members of the Quantitative Cardiovascular Imaging Study Group provide clinical consensus recommendations on the optimal use of different imaging techniques in various patient populations to detect and assess coronary artery stenosis and atherosclerosis.

In a mouse model of atherosclerosis, a selective monoclonal antibody that blocks the binding of LDL to activin receptor-like kinase 1 reduced plaque formation in the aorta.

Simvastatin improves endothelial cell function by inhibiting endothelial-to-mesenchymal transition through an epigenetic regulatory mechanism, according to a new study.

In this Review, Ritterhoff and Tian describe the metabolic reprogramming that occurs in cardiac hypertrophy and heart failure; discuss the contribution of metabolism to energy-generating and non-energy-generating functions, including signalling, protein function and gene expression regulation; and highlight the role of metabolism in non-cardiomyocytes and the potential to develop metabolic therapies for heart failure.

Acute coronary syndromes (ACS) are a major contributor to death from cardiovascular disease. In this Review, Timmis and colleagues present data on mortality from ACS for 122 countries and examine the regional and temporal changes in the epidemiology of ACS over the past 20 years.

In this Review, Jo and colleagues discuss blood flow-induced mechanisms involved in endothelial cell dysfunction and atherosclerosis, including the emerging concept of disturbed-flow-induced reprogramming of endothelial cells as a pro-atherogenic mechanism, and highlight the therapeutic potential of targeting of flow-sensitive genes, proteins and pathways.

Contemporary tools to predict cardiovascular risk lack accuracy on an individual-patient level. The use of single-cell RNA sequencing to identify specific leukocyte patterns might overcome some of these limitations, propelling us towards a precision medicine approach.

Findings from the VIRGO study reveal that young women with acute myocardial infarction are more likely to be rehospitalized within 1 year compared with similarly aged men.

Hyperphosphorylation of tau in the heart reduces the tyrosination of microtubules, leading to myocardial stiffness and heart failure. This novel mechanism of diastolic dysfunction parallels the aggregation of tau in the brain that leads to Alzheimer disease and might be amenable to treatment using monoclonal antibodies against tau.

In this Review, Kroemer and colleagues describe eight molecular hallmarks of cardiovascular ageing: disabled macroautophagy, loss of proteostasis, genomic instability, epigenetic alterations, mitochondrial dysfunction, cell senescence, dysregulated neurohormonal signalling and inflammation. Therapeutically targeting these hallmarks might attenuate residual cardiovascular risk in older individuals.

Individuals with type 2 diabetes mellitus are at high risk of developing cardiovascular disease (CVD). In the context of type 2 diabetes mellitus, Wong and Sattar discuss established and novel mechanisms of CVD, risk assessment and patient stratification, and strategies to reduce multiple risk factors to prevent CVD.

Pulmonary embolism is the leading cause of in-hospital death and the third most frequent cause of cardiovascular death. In this Review, Mahfoud and colleagues discuss the growing range of interventional, catheter-based approaches for the treatment of pulmonary embolism as well as risk stratification and patient selection for these procedures.

Clonal haematopoiesis of indeterminate potential (CHIP) is defined as an expansion of mutant blood stem cells in individuals without haematological malignancies. CHIP is linked to an increased risk of non-cancerous disorders such as atherosclerotic cardiovascular disease, possibly because mutant innate immune cells have pro-inflammatory phenotypes. Prospective studies are needed to determine whether individuals with CHIP might benefit from anti-inflammatory therapies.

IgM antibodies have gained much attention as risk markers of atherosclerotic cardiovascular disease, but the exact antigenic determinants and the full spectrum of functions remain to be defined. A better understanding of the potentially diverse nature of the antigens that they recognize will help to dissect the function of IgM in atherosclerosis.

In this Review, Gaillard and Jaddoe describe how maternal cardiovascular disorders, occurring before and during pregnancy, can influence cardiovascular health in the offspring from embryonic life until adulthood. Furthermore, the authors highlight critical periods for cardiovascular adaptations, including preconception, early pregnancy and infancy, and how the events occurring during these periods can have an effect on future cardiovascular health.

In this Review, Münzel and colleagues describe the exposome concept with a focus on environmental physical and chemical exposures and their effects on the burden of cardiovascular disease. Additionally, they discuss selected exposome studies and the relevance of the exposome concept for future health research and preventive medicine.

Lipophagy is a type of selective autophagy that targets lipid droplets for degradation. Since the discovery of lipophagy in 2009, research has uncovered a central role for this process in cellular lipid metabolism, including in atherogenic foam cells. Therefore, increasing lipophagy might be a therapeutic target to reverse lipid build-up in atherosclerosis.

Excessive salt intake is a known risk factor for cardiovascular disease commonly associated with hypertension. However, we propose that a high-salt diet can promote cardiovascular and other diseases independently of high blood pressure through inflammatory pathways that increase the production of myeloid cells.