| 1. |
- 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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| 2. |
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| 3. |
- 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. |
- Rundgren, Malin, et al.
(författare)
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The Inflammatory Marker suPAR After Cardiac Arrest.
- 2015
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Ingår i: Therapeutic hypothermia and temperature management. - : Mary Ann Liebert Inc. - 2153-7933 .- 2153-7658. ; 5:2, s. 89-94
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Tidskriftsartikel (refereegranskat)abstract
- Background: Soluble urokinase plasminogen activator receptor (suPAR) is released in response to inflammatory stimuli, and plasma levels are associated with long-term outcomes. The ischemia/reperfusion injury caused by cardiac arrest (CA) and resuscitation triggers an inflammatory response. This pilot study aimed at investigating suPAR levels in relation to outcome after CA and mild induced hypothermia. Methods: suPAR levels were measured at 6, 36, and 72 hours in patients treated with hypothermia after CA. suPAR levels were analyzed in relation to survival after 6 months. Receiver operating characteristic curve (ROC)-analyses were performed, and area under the curve (AUC) was calculated. Time to return of spontaneous circulation (ROSC) was correlated to suPAR levels. Results: Fifty-five patients (40 male, median 65 years) were included, and 33 (60%) were alive after 6 months. The suPAR levels were significantly higher in nonsurviving patients compared with survivors at 6 and 36 hours (p=0.006 and 0.034 respectively), but not at 72 hours. The suPAR levels increased from 6 to 72 hours (p<0.0001). Time to ROSC correlated positively with suPAR levels at 6 hours (p=0.003) but not at 36 and 72 hours. ROC analysis shoved an AUC of 0.76 at 6 hours. In the subgroup of CA of cardiac cause, the AUC was 0.84. Conclusion: suPAR levels at 6 and 36 hours after CA were significantly higher in nonsurviving patients compared with survivors; however, the overlap in suPAR levels between the outcome groups was substantial, reducing the prognostic value. There was a significant increase in suPAR levels during the first 72 hours after CA.
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| 5. |
- Sparv, David, et al.
(författare)
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Safety, Feasibility, and Hemodynamic Effects of Mild Hypothermia in Transcatheter Aortic Valve Replacement: The TAVR-CHILL Trial.
- 2015
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Ingår i: Therapeutic hypothermia and temperature management. - : Mary Ann Liebert Inc. - 2153-7933 .- 2153-7658. ; 5:4, s. 209-216
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Tidskriftsartikel (refereegranskat)abstract
- The safety, feasibility, and hemodynamic effects of mild hypothermia (MH) induced by transnasal cooling were studied in transcatheter aortic valve replacement (TAVR). MH is a common therapy following cardiac arrest and seems to have favorable effects in myocardial infarction and on hemodynamic stability. In TAVR, hemodynamic instability is common during rapid pacing. Twenty subjects undergoing TAVR were randomized 1:1 to hypothermia or normothermia. Hemodynamic endpoints were mean arterial blood pressure and required dosage of vasoactive and inotropic drugs. Patients were followed up at 6 months. All patients in the MH group (n=10) reached the target temperature of 34°C before first rapid pacing. Tympanic and urinary bladder temperature remained significantly lower in the MH group during the procedure. No adverse effects of cooling were observed. Mean arterial pressure was higher in the MH group (90±20 mm Hg) than in the control group (71±13 mm Hg) at the start of the procedure, at first rapid pacing (94±19 vs. 80±16 mm Hg), and at balloon aortic valvuloplasty (90±17 vs. 73±14 mm Hg). Less norepinephrine was administered to the hypothermia group. Transnasal cooling during TAVR was safe and well tolerated. We observed a more stable hemodynamic profile in the MH group, indicated by higher blood pressure and lower levels of vasoactive drugs required. A larger study of patients with severe ventricular dysfunction is required to more comprehensively investigate the hemodynamic effects of transnasal cooling in TAVR.
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