A Pilot Study of Rapid Cooling by Cold Saline and Endovascular Cooling Before Reperfusion in Patients With ST-Elevation Myocardial Infarction

Department of Coronary Heart Disease, Skane University Hospital, Lund University, Lund, Sweden.
Circulation Cardiovascular Interventions (Impact Factor: 6.98). 10/2010; 3(5):400-7. DOI: 10.1161/CIRCINTERVENTIONS.110.957902
Source: PubMed

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: Unique identifier: NCT00417638.

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    • "Malgré de nombreux travaux de recherche sur ce thème, les mécanismes permettant l'amélioration du pronostic neurologique après arrêt cardiaque, ne sont à ce jour qu'incomplètement élucidés. L'hypothèse ancienne reposant sur le fait que la diminution de la consommation cérébrale en oxygène permet le rétablissement d'une meilleure adéquation entre apports et demandes énergétiques [5] ne semble pas pouvoir expliquer en totalité le bénéfice du contrôle ciblé de la température entre 32 • et 34 • C. Alors que l'arrêt cardiaque représente une situation « quasi expérimentale » d'ischémie reperfusion, il est probable que tous les mécanismes permettant de lutter contre ces phénomènes sont associés : • diminution des phénomènes de mort cellulaire, ainsi que des anomalies mitochondriales [6] [7] ; • diminution des espèces radicalaires responsables du stress oxydatif [8] ; • protection de la barrière hémato-encéphalique [9] ; • diminution de la pression intracrânienne [10] ; • diminution de la température dans les zones atteintes de thermo-pooling (certaines zones cérébrales peuvent présenter une température supérieure à la température centrale ; ce phénomène pouvant alors aggraver les lésions neuronales dans ces territoires [11]) ; • diminution des lésions endothéliales [12] ; • diminution de la taille de zone myocardique infarcie en cas d'arrêt cardiaque consécutif à une occlusion coronaire [13] ; • effet systémique de l'hypothermie permettant une amélioration des paramètres hémodynamiques agissant possiblement sur le syndrome post arrêt cardiaque [14] [15], ainsi que sur les agressions cérébrales secondaires d'origine systémiques. "
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    • "Recently, several large randomized trials have reported the beneficial effects of hypothermia in cardiac arrest victims (with ventricular fibrillation as the initial cardiac rhythm) (Bernard et al., 2002; Hypothermia after Cardiac Arrest Study Group, 2002), asphyctic newborns (Shankaran et al., 2005; Azzopardi et al., 2009), and other patient populations in which the benefits of applied therapeutic hypothermia continue to grow (Villar and Slutsky, 1993; Hartemink et al., 2004; Bernard, 2009; Dietrich, 2009). More specifically, indications such as the induction of mild hypothermia in stroke victims (Linares and Mayer, 2009) or in awake patients with myocardial infarction (Gotberg et al., 2010) are currently being rigorously evaluated. Nevertheless , especially in conscious, unintubated patients, the ability to induce therapeutic hypothermia without pharmacological interventions can be difficult, as the human body possesses vigorous thermoregulatory defenses. "
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    Circulation Cardiovascular Interventions 10/2010; 3(5):397-9. DOI:10.1161/CIRCINTERVENTIONS.110.958546 · 6.98 Impact Factor
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