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| 2. |
- Erlinge, David, et al.
(författare)
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Therapeutic Hypothermia for the Treatment of Acute Myocardial Infarction-Combined Analysis of the RAPID MI-ICE and the CHILL-MI Trials
- 2015
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Ingår i: Therapeutic Hypothermia and Temperature Management. - : Mary Ann Liebert Inc. - 2153-7658 .- 2153-7933. ; 5:2, s. 77-84
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Tidskriftsartikel (refereegranskat)abstract
- In the randomized rapid intravascular cooling in myocardial infarction as adjunctive to percutaneous coronary intervention (RAPID MI-ICE) and rapid endovascular catheter core cooling combined with cold saline as an adjunct to percutaneous coronary intervention for the treatment of acute myocardial infarction CHILL-MI studies, hypothermia was rapidly induced in conscious patients with ST-elevation myocardial infarction (STEMI) by a combination of cold saline and endovascular cooling. Twenty patients in RAPID MI-ICE and 120 in CHILL-MI with large STEMIs, scheduled for primary percutaneous coronary intervention (PCI) within <6 hours after symptom onset were randomized to hypothermia induced by rapid infusion of 600-2000mL cold saline combined with endovascular cooling or standard of care. Hypothermia was initiated before PCI and continued for 1-3 hours after reperfusion aiming at a target temperature of 33 degrees C. The primary endpoint was myocardial infarct size (IS) as a percentage of myocardium at risk (IS/MaR) assessed by cardiac magnetic resonance imaging at 4 +/- 2 days. Patients randomized to hypothermia treatment achieved a mean core body temperature of 34.7 degrees C before reperfusion. Although significance was not achieved in CHILL-MI, in the pooled analysis IS/MaR was reduced in the hypothermia group, relative reduction (RR) 15% (40.5, 28.0-57.6 vs. 46.6, 36.8-63.8, p=0.046, median, interquartile range [IQR]). IS/MaR was predominantly reduced in early anterior STEMI (0-4h) in the hypothermia group, RR=31% (40.5, 28.8-51.9 vs. 59.0, 45.0-67.8, p=0.01, median, IQR). There was no mortality in either group. The incidence of heart failure was reduced in the hypothermia group (2 vs. 11, p=0.009). Patients with large MaR (>30% of the left ventricle) exhibited significantly reduced IS/MaR in the hypothermia group (40.5, 27.0-57.6 vs. 55.1, 41.1-64.4, median, IQR; hypothermia n=42 vs. control n=37, p=0.03), while patients with MaR<30% did not show effect of hypothermia (35.8, 28.3-57.5 vs. 38.4, 27.4-59.7, median, IQR; hypothermia n=15 vs. control n=19, p=0.50). The prespecified pooled analysis of RAPID MI-ICE and CHILL-MI indicates a reduction of myocardial IS and reduction in heart failure by 1-3 hours with endovascular cooling in association with primary PCI of acute STEMI predominantly in patients with large area of myocardium at risk. (ClinicalTrials.gov id NCT00417638 and NCT01379261).
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- Graffagnino, Carmelo, et al.
(författare)
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Current Advances in the Use of Therapeutic Hypothermia
- 2015
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Ingår i: Therapeutic hypothermia and temperature management. - : Mary Ann Liebert Inc. - 2153-7933 .- 2153-7658. ; 5:1, s. 9-12
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 4. |
- Mohammad, Moman A, et al.
(författare)
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Proteomics in Hypothermia as Adjunctive Therapy in Patients with ST-Segment Elevation Myocardial Infarction : A CHILL-MI Substudy
- 2017
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Ingår i: Therapeutic hypothermia and temperature management. - : Mary Ann Liebert Inc. - 2153-7933 .- 2153-7658. ; 7:3, s. 152-161
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Tidskriftsartikel (refereegranskat)abstract
- Cardiovascular and inflammatory biomarkers in therapeutic hypothermia have been studied in cardiac arrest, but data on patients with ST-segment elevation myocardial infarction (STEMI) treated with therapeutic hypothermia are currently unavailable. A multiplex proximity extension assay allowed us to measure 157 cardiovascular disease (CVD) and inflammatory disease-related biomarkers in patients from the international, multicenter, and randomized trial; CHILL-myocardial infarction (MI) and to explore the associations of cardiovascular and inflammatory biomarkers. Blood samples were obtained from 119 patients with STEMI, randomized to hypothermia as adjunctive therapy to percutaneous coronary intervention (PCI) or standard care with PCI only. Blood samples were obtained at baseline (0 hour), 6, 24, and 96 hours post PCI, and stored at -80°C until they were analyzed by PROSEEK Multiplex CVD and PROSEEK Multiplex INF (Olink Bioscience, Uppsala, Sweden). Peak values from 6, 24, and 96 hours postrandomization were compared between treatment groups. One hundred fifty-seven cardiovascular and inflammatory biomarkers were evaluated. Peak values of four biomarkers (BDNF, DNER, CCL20, MMP3) were reduced in the hypothermia group as compared with the control group. In addition, seven markers were slightly elevated in the hypothermia group (OPG, FGF21, FS, IL12B, PRL, TIM, IL6). In a prespecified subgroup analysis of anterior infarctions, two additional markers were reduced (PTX3 and SELE). In this explorative proteomic study from the randomized trial CHILL-MI, four biomarkers were identified as having reduced peak plasma values in patients with STEMI treated with therapeutic hypothermia as adjunctive therapy to PCI as compared with patients treated with standard care of PCI. In addition, seven biomarkers were elevated in the group treated with hypothermia therapy. The effect of hypothermia on biomarker peak values was modest, possibly due to a low reduction in mean body temperature. Whether a faster and deeper cooling results in more pronounced effects is yet to be established.
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