Feasibility of endovascular cooling as an adjunct to primary percutaneous coronary intervention (results of the LOWTEMP pilot study)

Kandzari, David E.; Chu, Alan; Brodie, Bruce R.; Stuckey, Thomas; Hermiller, James; Vetrovec, George W.; Hannan, Karen L.; Krucoff, Mitchell W.; Christenson, Robert H.; Gibbons, Raymond J.; Sigmon, Kristina N.; Garg, Jyostna; Hasselblad, Victor; Collins, Kenneth P.; Harrington, Robert A.; Berger, Peter B.; Chronos, N.; Hochman, Judith S.; Califf, Robert M.

doi:10.1016/j.amjcard.2003.11.038

Cited by 71 publications

(45 citation statements)

References 10 publications

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“…Myocardial temperature at the time of angioplasty and coronary recanalization was often well above the target temperature (average of only 1.1°C drop before reperfusion). As a result, the ischemic myocardium was reperfused at a temperature above the cooling target, with further hypothermia induced after reperfusion (9,18).…”

Section: Discussionmentioning

confidence: 99%

Hypothermia-induced cardioprotection using extended ischemia and early reperfusion cooling

Shao

Chang

Chan

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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timing of therapeutic hypothermia for cardiac ischemia is unknown. Our prior work suggests that ischemia with rapid reperfusion (I/R) in cardiomyocytes can be more damaging than prolonged ischemia alone. Also, these cardiomyocytes demonstrate protein kinase C (PKC) activation and nitric oxide (NO) signaling that confer protection against I/R injury. Thus we hypothesized that hypothermia will protect most using extended ischemia and early reperfusion cooling and is mediated via PKC and NO synthase (NOS). Chick cardiomyocytes were exposed to an established model of 1-h ischemia/3-h reperfusion, and the same field of initially contracting cells was monitored for viability and NO generation. Normothermic I/R resulted in 49.7 Ϯ 3.4% cell death. Hypothermia induction to 25°C was most protective (14.3 Ϯ 0.6% death, P Ͻ 0.001 vs. I/R control) when instituted during extended ischemia and early reperfusion, compared with induction after reperfusion (22.4 Ϯ 2.9% death). Protection was completely lost if onset of cooling was delayed by 15 min of reperfusion (45.0 Ϯ 8.2% death). Extended ischemia/early reperfusion cooling was associated with increased and sustained NO generation at reperfusion and decreased caspase-3 activation. The NOS inhibitor N -nitro-L-arginine methyl ester (200 M) reversed these changes and abrogated hypothermia protection. In addition, the PKC⑀ inhibitor myr-PKC⑀ v1-2 (5 M) also reversed NO production and hypothermia protection. In conclusion, therapeutic hypothermia initiated during extended ischemia/early reperfusion optimally protects cardiomyocytes from I/R injury. Such protection appears to be mediated by increased NO generation via activation of protein kinase C⑀; nitric oxide synthase.

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Section: Discussionmentioning

confidence: 99%

Hypothermia-induced cardioprotection using extended ischemia and early reperfusion cooling

Shao

Chang

Chan

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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“…11 However, 2 randomized clinical trials failed to show positive results with hypothermia as an adjunct therapy to primary coronary intervention in patients with acute myocardial infarction. [12][13][14] In subgroup analysis, the patients who reached a temperature of Ͻ35°C before reperfusion and had significant anterior wall myocardial infarction showed a reduction in infarct size, suggesting the benefit of inducing hypothermia before reperfusion.…”

mentioning

confidence: 99%

Intra–Cardiopulmonary Resuscitation Hypothermia With and Without Volume Loading in an Ischemic Model of Cardiac Arrest

et al. 2009

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Background-We investigated the effects of intra-cardiopulmonary resuscitation (CPR) hypothermia with and without volume loading on return to spontaneous circulation and infarction size in an ischemic model of cardiac arrest. Methods and Results-Using a distal left anterior descending artery occlusion model of cardiac arrest followed by resuscitation with a total of 120 minutes of occlusion and 90 minutes of reperfusion, we randomized 46 pigs into 5 groups and used myocardial staining to define area at risk and myocardial necrosis. Group A had no intervention. Immediately after return of spontaneous circulation, group B received surface cooling with cooling blankets and ice. Group C received intra-CPR 680Ϯ23 mL of 28°C 0.9% normal saline via a central venous catheter. Group D received intra-CPR 673Ϯ26 mL of 4°C normal saline followed by surface cooling after return of spontaneous circulation. Group E received intra-CPR and hypothermia after return of spontaneous circulation with an endovascular therapeutic hypothermia system placed in the right atrium and set at a target of 32°C. Intra-CPR volume loading with room temperature (group C) or iced saline (group D) significantly (PϽ0.05) decreased coronary perfusion pressure (group C, 12.8Ϯ4.78 mm Hg; group D, 14.6Ϯ9.9 mm Hg) compared with groups A, B, and E (20.6Ϯ8.2, 20.1Ϯ7.8, and 21.3Ϯ12.4 mm Hg). Return of spontaneous circulation was significantly improved in group E (9 of 9) compared with groups A plus B and C (10 of 18 and 1 of 8). The percent infarction to the area at risk was significantly reduced with intra-CPR hypothermia in groups D (24.3Ϯ4.2%) and E (4Ϯ3.4%) compared with groups A (72Ϯ5.1%) and B (67.3Ϯ4.2%). Conclusions-Intra-CPR hypothermia significantly reduces myocardial infarction size.

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“…It can be used also for controlling normothermia after the rewarming phase and guide the patients through the whole early post-resuscitation period. Cooling efficacy and safety was documented not only for cardiac arrest patients but also for patients with traumatic brain injury, stroke and acute myocardial infarction (Diringer et al, 2004;Schmutzhard et al, 2002;Lyden et al, 2005;Guluma et al, 2008;Georgiadis et al, 2001;Keller et al, 2003;De Georgia et al, 2004;Dixon et al, 2002;Kandzari et al, 2004;Stone et al, 2006). Dixon et al randomized 42 patients with AMI to primary PCI with or without endovascular cooling (target core temperature 33 degrees C) for 3 hours after reperfusion.…”

Section: Cooling Methodsmentioning

confidence: 99%

Therapeutic Hypothermia in Cardiac Arrest Survivors

Škulec¹

2012

Coronary Interventions

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Feasibility of endovascular cooling as an adjunct to primary percutaneous coronary intervention (results of the LOWTEMP pilot study)

Cited by 71 publications

References 10 publications

Hypothermia-induced cardioprotection using extended ischemia and early reperfusion cooling

Hypothermia-induced cardioprotection using extended ischemia and early reperfusion cooling

Intra–Cardiopulmonary Resuscitation Hypothermia With and Without Volume Loading in an Ischemic Model of Cardiac Arrest

Therapeutic Hypothermia in Cardiac Arrest Survivors

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