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- EMERALD, enhanced myocardial efficacy and removal by aspiration of liberated debris
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- ICE-IT, intravascular cooling adjunctive to percutaneous coronary intervention
- LOW TEMP, lowering adverse outcomes with temperature regulation
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- NICAMI, non-invasive surface cooling thermoregulator system to induce mild hypothermia in acute myocardial infarction
- POZNAN, percutaneous transvenous transplantation of autologous myoblasts in the treatment of postinfarction heart failure
- RESEARCH, rapamycin-eluting stent evaluated at Rotterdam Cardiology Hospital
- TOPCARE-AMI, transplantation of progenitor cells and regeneration enhancement in acute myocardial infarction
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- acute myocardial infarction
- drug eluting stents
- infarct angioplasty
- percutaneous coronary intervention
The primary goal of treatment in acute myocardial infarction is to salvage jeopardised myocardium, preserve ventricular function, and improve long term survival.1 Since de Wood’s landmark observations ushered in the modern reperfusion era, the main focus of treatment in this field has been on methods to restore blood flow to the ischaemic myocardium. With contemporary angioplasty techniques, normal epicardial coronary flow can be achieved in most patients, and for this reason catheter based reperfusion is now widely accepted as the preferred treatment for acute myocardial infarction (AMI). Despite these advances, however, many patients have relatively poor recovery of ventricular function in the infarct zone, attributable to suboptimal restoration of flow at a tissue level. Mechanisms contributing to this “myocardial no reflow” phenomenon are not well understood, but are thought to include ischaemia induced microvascular damage, distal embolisation, and reperfusion injury.2–6 Studies utilising sensitive measures of myocardial perfusion such as ST segment resolution, contrast echocardiography, and cardiac magnetic resonance imaging have demonstrated worse clinical outcomes in patients with poor tissue level flow.7,8,9,10 These observations have prompted the search for new pharmacologic and mechanical approaches to enhance tissue level perfusion and improve myocardial salvage during reperfusion treatment.
MYOCARDIAL PROTECTION (MECHANICAL)
Systemic hypothermia
Myocardial temperature is an important factor influencing the extent of necrosis after coronary artery occlusion.11,12 In experimental studies, mild hypothermia has been shown to significantly reduce infarct size (fig 1).13–15 Cooling appears to protect the myocardium by lowering metabolic demand in the risk region, as well as reducing myocyte apoptosis and increasing production of heat shock proteins. Several innovative endovascular cooling systems have been developed, in which a catheter in placed in the inferior vena cava via the femoral vein to cool the patient centrally.16 Compared with surface cooling techniques, these systems are …
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No conflict of interest to disclose