Research Highlights in 2019

Engineered chimeric antigen receptor (CAR) T cells can be applied to reduce cardiac fibrosis and restore function in a mouse model of hypertensive heart failure, according to a new study published in Nature.

Addition of ticagrelor to the treatment regimen of patients with stable coronary artery disease and diabetes with or without previous percutaneous coronary intervention significantly improved outcomes.

Two studies reveal new details of the mechanisms underlying the benefits of the angiotensin receptor–neprilysin inhibitor sacubitril–valsartan in patients with heart failure and reduced ejection fraction, suggesting that sacubitril–valsartan induces reverse cardiac remodelling but has no effect in reducing central aortic stiffness.

In patients with STEMI and multivessel coronary artery disease, a strategy of revascularizing both the culprit lesion and any angiographically significant nonculprit lesions achieves better outcomes than a strategy of revascularizing only the culprit lesion.

A novel machine-learning-derived biomarker that can detect structural changes in perivascular fat improved cardiac risk prediction beyond traditional prediction tools.

Lifelong genetic exposure to lower levels of both LDL cholesterol and systolic blood pressure is associated with an independent, additive and dose-dependent decrease in the risk of major coronary events.

Genotype-guided selection of oral P2Y₁₂ inhibitor therapy (clopidogrel versus prasugrel or ticagrelor) can reduce the incidence of bleeding in patients who have undergone primary percutaneous coronary intervention.

A new study shows that clonal haematopoiesis of indeterminate potential (CHIP)-driver mutations in DNMT3A or TET2 are associated with increased medium-term mortality in patients with severe aortic stenosis undergoing transcatheter aortic valve implantation.

The 2-year results of the MITRA-FR trial confirm the 1-year findings showing that addition of percutaneous mitral valve repair to medical treatment does not reduce the risk of death or hospitalization for heart failure compared with medical treatment alone in patients with heart failure and severe secondary mitral regurgitation

The PARAGON-HF trial indicates that sacubitril–valsartan does not have a significant benefit in patients with heart failure with preserved ejection fraction (HFpEF) for reducing hospitalizations for heart failure and death from cardiovascular causes. However, the trial suggests a potential benefit in patients with low left ventricular ejection fraction and in women.

A novel, community-based model of care led by non-physician health workers significantly reduced blood pressure levels and risk of cardiovascular disease.

In the PolyIran study, a fixed-dose polypill strategy was more effective than non-pharmacological interventions in reducing the risk of cardiovascular events.

In patients with acute heart failure, treatment with serelaxin, a recombinant form of human relaxin 2, did not reduce the incidence of cardiovascular death or worsening heart failure.

Treatment with resolvin D4, a specialized pro-resolving mediator, significantly attenuated thrombus burden in a mouse model of deep vein thrombosis.

The transcription factor FOXP1 downregulates activation of the endothelial NLRP3 inflammasome and suppresses vascular inflammation, protecting against atherosclerosis. Upregulation of FOXP1 expression is a novel anti-atherogenic effect of simvastatin.

A new study shows that the loss of an enzyme in humans during evolution might be a contributing factor to the increased predisposition to atherosclerosis in humans compared with other animals

Three independent regulatory pathways contribute to neovascular growth during developmental coronary vessel growth and ischaemic injury.

Activation of the PDGF pathway is involved in the pathogenesis of dilated cardiomyopathy caused by mutations in LMNA; this new finding suggests that inhibition of PDGFRβ is a novel therapeutic target for patients with this condition.

Both systolic and diastolic hypertension independently contribute to the risk of adverse cardiovascular events, even though systolic hypertension has a greater effect on cardiovascular outcomes, and this relationship is not altered by the threshold used for the definition of hypertension.

Two studies reporting novel insights into fibroblast identity and activation dynamics provide an important step forward in our understanding of cardiac fibrosis and the quest to develop new anti-fibrotic strategies