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Biomarkers and ST-elevation myocardial infarction
  1. Christian Mueller
  1. Correspondence to Professor Christian Mueller,
    Department of Cardiology, University Hospital Basel, Petersgraben 4, Basel CH-4031, Switzerland; chmueller{at}uhbs.ch

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In the recent Heart paper, Cuculi et al1 from Oxford University challenge two conventional wisdoms in clinical cardiology: first, biomarkers do not have a role in the management of patients presenting with suspected ST-elevation myocardial infarction (STEMI); and second, in the absence of cardiogenic shock, there is no remaining unmet clinical need in STEMI as contemporary coronary reperfusion strategies yield excellent patient outcomes.

In their investigation, the authors report the course of plasma neuropeptide Y levels in patients undergoing successful percutaneous coronary intervention (PCI) and relate these to non-invasive and invasive measures of the success of myocardial reperfusion and the coronary microcirculation.1 In the vast majority of patients with STEMI, a complete thrombotic occlusion in the epicardial segment of one of the coronary arteries results in ischaemia and cell death of a large amount of cardiomyocytes supplied by that artery. To salvage cardiomyocytes at risk, therapy must not only reopen the epicardial occlusion, but also restore and sustain blood flow on the myocardial level.1–3 While contemporary PCI seems near perfect in achieving the former, microcirculatory ‘no-reflow’ can be identified in nearly one-third of STEMI patients.1–3 Seduced by the impressive pictures of ‘normalised’ epicardial arteries after coronary stenting, many cardiologists may not have attributed enough attention to the coronary microcirculation in the last decade. Cuculi et al1 report that patients with angiographic no-reflow, incomplete ST resolution and impaired coronary flow reserve, have significantly higher neuropeptide Y levels. Could this finding have diagnostic or therapeutic implications?

Neuropeptide Y seems to be secreted by multiple tissues.1 ,4–6 It is abundant in the peripheral sympathetic nervous system, where following prolonged sympathetic activation, it is released from cardiac sympathetic nerve endings along with the main neurotransmitter norepinephrine, where it can act as a co-transmitter and local neuromodulator of several aspects of cardiac function.1 ,4–6 In contrast to norepinephrine and other plasma catecholamines, neuropeptide Y seems to have very little circadian variation, which would render neuropeptide Y a potentially suitable diagnostic tool.6 ,7

The Cuculi paper reminds us that microcirculatory ‘no-reflow’ seems to have two components: a mechanical component and a functional vasoactive component. While thrombus aspiration and our current antithrombotic medical therapies effectively target the former, the latter has yet to become a therapeutic target. The important work by Cucculi for sure will inspire additional research into therapeutic interventions targeting neuropeptide Y, endothelin-1, thromboxane A2 and other vasoactive factors that might be causally involved in the functional component of mircovascular dysfunction in STEMI.

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Footnotes

  • Competing interests Professor Mueller has received research grants from the Swiss National Science Foundation, the European Union, the Swiss Heart Foundation, Abbott, Alere, Beckman Coulter, BRAHMS, Critical Diagnostics, Nanosphere, Roche, Siemens, 8sense, and the Department of Internal Medicine, of the University Hospital Basel, as well as speaker honoraria from Abbott, Alere, Brahms, Novartis, Roche, and Siemens.

  • Patient consent Obtained.

  • Provenance and peer review Commissioned; internally peer reviewed.

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