title: Radio frequency heating of chronic ovine infarct leads to sustained infarct area and ventricular volume reduction.
abstract: OBJECTIVE
  Myocardial infarct expansion and subsequent left ventricular remodeling are associated with increased incidence of congestive failure and mortality. Collagen is known to denature and contract when heated above 65 degrees C. We therefore tested the hypothesis that radio frequency heating of myocardial infarct tissue with application of a restraining patch causes a sustained reduction in myocardial infarct area and left ventricular volume.
  
  
  METHODS
  Thirteen male Dorset sheep underwent surgical coronary artery ligation. At least 14 weeks later, animals were randomized to either radio frequency infarct heating (95 degrees C) with application of a restraining patch or a sham operation. Before treatment, after treatment, and 10 weeks later, left ventricular volume was measured with transdiaphragmatic echocardiography and myocardial infarct area was measured with an array of sonomicrometry crystals.
  
  
  RESULTS
  Radio frequency infarct heating causes an acute decrease of 34% (-215 +/- 82 mm(2); P =.0002) in infarct area at end-diastole that is maintained at 10 weeks (-144 +/- 79 mm(2); P =.0002). Radio frequency infarct heating causes a downward trend in end-diastolic left ventricular volume measured by echocardiography of 20% (-15.7 +/- 6.3 mL; P = no significant difference) and end-systolic left ventricular volume of 32% (-17.1 +/- 9.8 mL; P =.09), which are significantly decreased at 10 weeks (-13.6 +/- 22.3 mL; P =.007 and -15.3 +/- 21.9 mL; P =.008, respectively). Radio frequency infarct heating causes an acute improvement in systolic function (P <.001), a sustained increase in left ventricular ejection fraction (+0.11%; P =.06), and preserved stroke volume.
  
  
  CONCLUSIONS
  Radio frequency heating of chronic left ventricular myocardial infarct causes a sustained reduction in infarct area and left ventricular volume. This technique may beneficially reverse infarct expansion and left ventricular remodeling after myocardial infarction.
authors.affiliation: Division of Cardiothoracic Surgery, Department of Surgery, San Francisco, USA. mark.ratcliffe@med.va.gov
authors.forename: M B
authors.initials: MB
authors.lastname: Ratcliffe
authors.forename: A W
authors.initials: AW
authors.lastname: Wallace
authors.forename: J R
authors.initials: JR
authors.lastname: Teerlink
authors.forename: J
authors.initials: J
authors.lastname: Hong
authors.forename: A
authors.initials: A
authors.lastname: Salahieh
authors.forename: S H
authors.initials: SH
authors.lastname: Sung
authors.forename: E C
authors.initials: EC
authors.lastname: Keung
authors.forename: R J
authors.initials: RJ
authors.lastname: Lee
mesh_terms: D000818:Animals; D002908:Chronic Disease; D003972:Diathermy; D006352:Heart Ventricles / Q000473:pathology*; D008297:Male; D009203:Myocardial Infarction / Q000473:pathology* / Q000628:therapy*; D012756:Sheep