A Pilot Study of Rapid Cooling by Cold Saline and Endovascular Cooling Before Reperfusion in Patients With ST-Elevation Myocardial Infarction
ABSTRACT Experimental studies have shown that induction of hypothermia before reperfusion of acute coronary occlusion reduces infarct size. Previous clinical studies, however, have not been able to show this effect, which is believed to be mainly because therapeutic temperature was not reached before reperfusion in the majority of the patients. We aimed to evaluate the safety and feasibility of rapidly induced hypothermia by infusion of cold saline and endovascular cooling catheter before reperfusion in patients with acute myocardial infarction.
Twenty patients with acute myocardial infarction scheduled to undergo primary percutaneous coronary intervention were enrolled in this prospective, randomized study. After 4 ± 2 days, myocardium at risk and infarct size were assessed by cardiac magnetic resonance using T2-weighted imaging and late gadolinium enhancement imaging, respectively. A core body temperature of <35°C (34.7 ± 0.3°C) was achieved before reperfusion without significant delay in door-to-balloon time (43 ± 7 minutes versus 40 ± 6 minutes, hypothermia versus control, P=0.12). Despite similar duration of ischemia (174 ± 51 minutes versus 174 ± 62 minutes, hypothermia versus control, P=1.00), infarct size normalized to myocardium at risk was reduced by 38% in the hypothermia group compared with the control group (29.8 ± 12.6% versus 48.0 ± 21.6%, P=0.041). This was supported by a significant decrease in both peak and cumulative release of Troponin T in the hypothermia group (P=0.01 and P=0.03, respectively).
The protocol demonstrates the ability to reach a core body temperature of <35°C before reperfusion in all patients without delaying primary percutaneous coronary intervention and that combination hypothermia as an adjunct therapy in acute myocardial infarction may reduce infarct size at 3 days as measured by MRI.
URL: http://www.clinicaltrials.gov. Unique identifier: NCT00417638.
- SourceAvailable from: Jean Baptiste Lascarrou[Show abstract] [Hide abstract]
ABSTRACT: Cardiac arrest is a public healthcare problem due to its frequency and high incidence of mortality. However, the development of a strategy for induced hypothermia produced in the aftermath of the recovery of cardiac activity allows a significant improvement in neurologic prognosis, especially when cardiac arrest occurs with a cardiac rhythm disturbance responsive to cardioversion. The indications of therapeutic hypothermia have been extended to abnormal rhythms unresponsive to cardioversion and to less frequent settings. New clinical trials are mandatory to improve the prognosis of these patients.Le Praticien en Anesthésie Réanimation 02/2013; 17(1):2–7. DOI:10.1016/j.pratan.2013.01.002
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ABSTRACT: Hypothermia has been linked to beneficial neurologic outcomes in different clinical situations and its therapeutic value is considered important. For example, in asphyctic neonates and in patients with out-of-hospital cardiac arrest (with ventricular fibrillation as the initial cardiac rhythm), rapid installation of hypothermia has been reported to add substantial therapeutic benefits over nonthermal standard treatments. Yet, in other groups of patients in which the application of therapeutic hypothermia may be applied with clinical benefits, the optimization of therapy remains less straightforward, as the body possesses vigorous defense mechanisms to protect it from inducing hypothermia, that is, especially in conscious patients and/or in those in which the hypothalamus remains intact, such as stroke patients or patients who suffer a myocardial infarction or spinal cord injury. This overview summarizes the body's primary reactions to hypothermia and the defense mechanisms available or evoked. Then, clinically applicable ways to overcome these forceful cold defenses of the body are described to ensure both an optimal induction process for therapeutic hypothermia and maximal subjective comfort for these conscious patients.06/2011; 1(2):77-85. DOI:10.1089/ther.2010.0010
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