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Is reducing low-density lipoprotein cholesterol all that matters?
  1. Alastair James Moss
  1. British Heart Foundation Cardiovascular Research Centre, University of Leicester, Leicester, UK
  1. Correspondence to Dr Alastair James Moss, British Heart Foundation Cardiovascular Research Centre, University of Leicester, Leicester LE3 9QP, UK; alastairmoss{at}

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Current international guidance recommends reducing an individual’s cardiovascular risk by aggressively lowering low-density lipoprotein cholesterol (LDL-C). A central tenet of the latest European Society of Cardiology guidance on the management of dyslipidaemias is the lowering of the targets for LDL-C in high risk (<1.8 mmol/L), very-high risk (<1.4 mmol/L) and individuals who experience recurrent cardiovascular events (<1.0 mmol/L).1 There are an increasing number of tools that can be deployed to achieve these goals including specific lifestyle interventions, the initiation of high-intensity statins, and adjuvant therapy with ezetimibe or a proprotein convertase subtilisin/kexin 9 (PCSK9) inhibitor. In this regard, as previously highlighted in Heart, there is considerable scope for improvement as more than half of patients in the UK do not attain an optimal therapeutic reduction in LDL-C.2 What remains unclear with respect to cardiovascular risk modification is whether aggressive reduction of LDL-C is the only target that matters?

In this issue of Heart, Dhar and colleagues examined the association between neopterin, a novel marker of macrophage inflammation, and the incidence of myocardial infarction.3 Neopterin is a by-product of the guanosine triphosphate-biopterin pathway found in activated macrophages. Neopterin is secreted from macrophages following interferon-gamma-mediated T-cell stimulation thereby providing a surrogate measure of plaque inflammation.4 In this post hoc analysis from a prospective observation study in Norway, 4130 patients underwent invasive coronary angiography as part of …

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  • Contributors AJM is the sole contributor of this study.

  • Funding AJM is supported by a British Heart Foundation Accelerator Award Clinical Lectureship (Grant AA/18/3/34220).

  • Competing interests None declared.

  • Patient and public involvement Patients and/or the public were not involved in the design, conduct, reporting or dissemination plans of this research.

  • Patient consent for publication Not required.

  • Provenance and peer review Commissioned; internally peer reviewed.

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