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Cover image supplied by Oliver Soehnlein and Carlos Silvestre-Roig from the Institute for Cardiovascular Prevention (IPEK), Ludwig Maximilian University, Munich, Germany. The picture shows an advanced atherosclerotic lesion in a hypercholesterolaemic mouse, with staining for macrophages, smooth muscle cells, nuclei, and endothelium.
In 2017, several high-impact studies in thrombosis were published. Refinements were made in the optimal therapy for patients with stable atherosclerosis or with atrial fibrillation undergoing percutaneous coronary intervention. Risk scores to determine duration of antiplatelet therapy were developed. The potential risk of subclinical valve leaflet thrombosis was identified.
Important milestones in cardiac regenerative medicine that will define future research were reached in 2017: demonstration of adult cardiomyocyte renewal capacity, recognition of the importance of the extracellular matrix and the higher regenerative efficacy of repetitive dose protocols, and the publication of human data supporting paracrine effects of stem cell therapies and guidelines from TACTICS, the first international alliance on cardiac regenerative medicine.
Research on dyslipidaemias in 2017 reaffirmed the central role of reducing the levels of atherogenic apolipoprotein B-containing lipoproteins, predominantly LDL, in preventing ischaemic cardiovascular events. However, whether increasing HDL-cholesterol levels in isolation can reduce cardiovascular risk remains to be determined.
In 2017, genetic research on cardiovascular disease (CVD) produced seemingly paradoxical findings. Thanks to the continuous upscaling of genotyping and sequencing data, researchers have discovered that whereas numerous genetic variants among the general population can increase CVD risk, an individual can tolerate most severe genetic alterations.
In 2017, a cluster of papers have provided strong evidence in favour of the inflammation hypothesis in cardiovascular disease. From fundamental observations on clonal haematopoiesis to clinical evidence indicating that blocking an inflammatory cytokine mitigates heart disease, 2017 has been a watershed year.
The past year provided strong evidence on the use of the instantaneous wave-free ratio to determine the severity of coronary artery disease, the improving outcomes of contemporary percutaneous coronary intervention, the increased risk of thrombosis with bioresorbable vascular scaffolds, and the benefits of a simple revascularization strategy in cardiogenic shock.
This Review summarizes the latest findings on heart reverse remodelling, which demonstrate that despite apparent normalization of function, the molecular changes associated with heart failure persist in the reverse-remodelled heart. This myocardial remission is distinct from true recovery, in which both function and molecular makeup are normalized. These findings have implications for developing therapies to repair the failing heart.
Increased arterial stiffness influences pulse pressure, wave reflections, kidney function, and cardiovascular risk. In this Review, Safar describes the importance of arterial stiffness in the diagnosis and management of hypertension, using historical perspectives to emphasize the need for new treatment approaches in patients with essential hypertension.
Cardiovascular mortality among the almost 600 million people living in the Eastern Mediterranean region (EMR) has been proposed to increase more dramatically in the next decade than in any other region except Africa. Turk-Adawi and colleagues summarize the available data on cardiovascular disease burden, risk factors, and treatment modalities for the EMR population.
A range of drugs is available for symptomatic angina, but the optimal choice or combination of therapies is often uncertain, and contemporary guidelines do not necessarily provide definite recommendations. In this Consensus Statement, Ferrari and colleagues propose an individualized approach to angina treatment, which takes into consideration the patient, their comorbidities, and the underlying mechanism of disease.