Therapeutic Hypothermia in STEMI.

In this review article we tried to find an answer to the question, should local coronary hypothermia be a part of the early reperfusion strategy in patients with STEMI to prevent reperfusion injury, no-reflow phenomenon, and to reduce the infarct size and mortality. Hypothermia can save cardiomyocytes if achieved in a timely fashion before reperfusion. Intracoronary hypothermia can be adjunct to PCI by lessening ischemia/reperfusion injury on cardiomyocytes and reduction in infarct size. Reperfusion induced Calcium overload, generation of ROS and subsequent activation of Mitochondrial permeability transition pore (MPT) are major contributors to reperfusion injury. Hypothermia reduces calcium loading of the cell and maintains cellular energy and tissue level glucose which can scavenger ROS. Hypothermia reduces MPT activation and thus reduces infarct size. Systemic cooling trials failed to reduce infarct size, perhaps because the target temperature was not reached fast enough, and it was associated with systemic side effects. The need for rapid induction of hypothermia to <35 °C with the ethical concern of delaying reperfusion while cooling the patient and the inconsistency of endovascular cooling results lead to a belief that endovascular cooling may exceed the acceptable level of invasiveness in the context of other novels cardioprotective, regenerative and reperfusion therapies. Clinical trials showed the safety and feasibility of novel intracoronary hypothermia with rapid induction and maintenance of hypothermia using routine PCI equipment ahead of reperfusion. Two phases of cooling were applied without significant delay in the door to balloon time. Cooling of the coronary artery leads to cooling of its dependant myocardium without affecting adjacent myocardium. Heat transfer occurred by heat conduction during the occlusion phase and heat convention during the reperfusion phase. Fine-tuning of saline temperature and infusion rate helped to improve the protocol. The best duration of hypothermia before and after reperfusion is not known and needs further investigation. A balance between the undoubted cardioprotective effects of hypothermia with iatrogenic prolongation of ischemia time needs to be established. A reduction in infarct size was observed but needs to be validated with large randomized trials. Furthermore, it might be possible to augment the cardioprotective effects of intracoronary hypothermia by combination with other cardioprotective approaches such as antioxidant drugs and afterload reducing agents.