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Bivalirudin in acute myocardial infarction: NICE guidance
  1. Gregg W Stone
  1. Correspondence to Dr Gregg W Stone, Department of Cardiology, Columbia University Medical Center, New York-Presbyterian Hospital, The Cardiovascular Research Foundation, 111 E 59th St, 11th Floor, New York, NY 10022, USA; gs2184{at}columbia.edu

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ST-segment elevation myocardial infarction (STEMI) is typically caused by acute thrombotic occlusion of an epicardial coronary artery, resulting in a wave front of myonecrosis from the subendocardium to the subepicardium, which is complete within several hours1 (although this time course can be substantially delayed by intermittent flow in the infarct artery and collateral vessels to the infarct zone).2 With this understanding, the treatment of STEMI shifted from strategies to reduce myocardial oxygen demand to approaches to rapidly re-establish patency of the infarct artery, either pharmacologically with fibrinolytic treatment or mechanically with primary percutaneous coronary intervention (PCI). For nearly two decades controversy raged as to whether the greater patency rates and reduced risks of life-threatening haemorrhagic complications achieved with primary PCI warranted the delays inherent in its implementation. This debate has largely been laid to rest by the performance of 23 randomised trials demonstrating that compared with fibrinolytic treatment, primary PCI results in reduced early and late mortality, reinfarction, recurrent ischaemia, intracranial haemorrhage, all-cause stroke and infarct size.3 4 As a result, primary PCI has become the worldwide standard of care for STEMI, when performed expeditiously at a skilled interventional facility. The delineation of factors delaying time to reperfusion with PCI has facilitated great strides in reducing system delays, resulting in shorter door-to-balloon times and enhanced survival.5

In addition to rapid intervention, favourable clinical outcomes after primary PCI in STEMI depend on restoring epicardial coronary artery patency, a prerequisite to normal myocardial perfusion and metabolism. Platelet activation is heightened in patients with acute coronary syndromes, and thrombus which forms early after plaque rupture is platelet-rich. By dissecting tissue planes and exposing collagen, and releasing tissue factor and other chemokines to the bloodstream, the PCI procedure itself further enhances platelet activation. Moreover, red blood cells soon become adherent …

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