title: Catheter-based transcoronary myocardial hypothermia attenuates arrhythmia and myocardial necrosis in pigs with acute myocardial infarction.
abstract: OBJECTIVE
  This study evaluated the efficacy of catheter-based transcoronary myocardial hypothermia (CTMH) in pigs with acute myocardial ischemia.
  
  
  BACKGROUND
  Although it has been suggested that hypothermia therapy can attenuate myocardial necrosis, few applications have been accepted for clinical use.
  
  
  METHODS
  This study comprises 2 substudies. In both studies, pigs underwent 60 min of coronary occlusion and 180 min of reperfusion. In study 1, after 15 min of coronary occlusion with an over-the-wire-type balloon (OTWB), pigs in the hypothermia group (H) (n = 13) were directly infused with 4 degrees C saline into the coronary artery through the OTWB wire lumen (2.5 ml/min) for 60 min. Pigs in the normothermia group (N) (n = 15) received the same amount of 36.5 degrees C saline. In study 2, pigs in the hypothermia-reperfusion group (HR) (n = 5) were infused with 4 degrees C saline through the infusion catheter (8 ml/min) for 30 min with a later start (60 min after coronary occlusion), whereas simple reperfusion was used for the reperfusion group (R) (n = 6).
  
  
  RESULTS
  Catheter-based transcoronary myocardial hypothermia was successful in both studies. In study 1, CTMH significantly decreased ventricular arrhythmia and the ratio of necrosis to ischemic risk area (H: 9 +/- 2%; N: 36 +/- 4%; p < 0.0001) with a significant reduction of enzyme leaks. In study 2, CTMH tended to reduce the ratio of necrosis (HR: 33 +/- 2%; R: 45 +/- 5%; p = 0.08). In both studies, CTMH significantly suppressed the increase of 8-iso-prostaglandin F(2alpha) while preserving the coronary flow reserve.
  
  
  CONCLUSIONS
  Catheter-based transcoronary myocardial hypothermia reduced myocardial necrosis while preserving coronary flow reserve, due, in part, to attenuation of oxidative stress.
authors.affiliation: Division of Cardiovascular and Respiratory Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
authors.forename: Hiromasa
authors.initials: H
authors.lastname: Otake
authors.forename: Junya
authors.initials: J
authors.lastname: Shite
authors.forename: Oscar Luis
authors.initials: OL
authors.lastname: Paredes
authors.forename: Toshiro
authors.initials: T
authors.lastname: Shinke
authors.forename: Ryohei
authors.initials: R
authors.lastname: Yoshikawa
authors.forename: Yusuke
authors.initials: Y
authors.lastname: Tanino
authors.forename: Satoshi
authors.initials: S
authors.lastname: Watanabe
authors.forename: Toru
authors.initials: T
authors.lastname: Ozawa
authors.forename: Daisuke
authors.initials: D
authors.lastname: Matsumoto
authors.forename: Daisuke
authors.initials: D
authors.lastname: Ogasawara
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Yokoyama
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000517:prevention & control* / Q000628:therapy; D002404:Catheterization; D003326:Coronary Circulation / Q000502:physiology; D004195:Disease Models, Animal; D005260:Female; D007036:Hypothermia, Induced / Q000295:instrumentation / Q000379:methods*; D008297:Male; D009203:Myocardial Infarction / Q000473:pathology* / Q000628:therapy*; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control* / Q000628:therapy; D009336:Necrosis / Q000473:pathology / Q000517:prevention & control; D011336:Probability; D012680:Sensitivity and Specificity; D013552:Swine