title: Cyclic variation in ultrasonic myocardial integrated backscatter is due to phasic changes in the number of patent myocardial microvessels.
abstract: OBJECTIVE
  We tested the hypothesis that the cyclic variation in ultrasonic myocardial integrated backscatter (IBS) is due to cardiac contraction-induced changes in the number of patent myocardial microvessels.
  
  
  METHODS
  We performed experiments in open-chest dogs in which we increased the number of patent myocardial microvessels without changing cardiac contraction. We achieved this either by direct intracoronary administration of adenosine (group 1; n = 10) or by producing a noncritical coronary stenosis (group 2; n = 7).
  
  
  RESULTS
  At baseline, IBS was lowest in systole and highest in diastole. This cyclic variation in IBS was closely associated with the phasic changes in myocardial blood volume that were measured with myocardial contrast echocardiography. During adenosine administration, the diastolic IBS increased from -18.8 +/- 6.5 to -17.5 +/- 6.1 dB (P = .002), with an associated increase in the difference between the systolic and diastolic IBS from 3.8 +/- 1.1 to 4.6 +/- 1.0 dB (P = .009). After a noncritical stenosis was produced, diastolic IBS also increased from -26.6 +/- 8.3 to -25.2 +/- 7.3 dB (P = .001), with an associated increase in the difference between the systolic and diastolic IBS from 3.7 +/- 1.2 to 5.0 +/- 1.0 dB (P = .02). No change in IBS was noted in the bed that did not receive adenosine or the bed that had a stenosis.
  
  
  CONCLUSIONS
  The variation in IBS during the cardiac cycle is closely associated with the phasic changes in myocardial blood volume seen during cardiac contraction. When the number of patent myocardial arterioles is increased via adenosine or placement of a noncritical stenosis, diastolic IBS increases with a concomitant increase in IBS cyclic variation. These results may have important clinical applications for the noninvasive diagnosis of noncritical coronary stenosis at rest.
authors.affiliation: Division of Cardiovascular Medicine, Oregon Health and Science University, Portland, OR 97239, USA.
authors.forename: Antonio
authors.initials: A
authors.lastname: Micari
authors.forename: Marco
authors.initials: M
authors.lastname: Pascotto
authors.forename: Ananda R
authors.initials: AR
authors.lastname: Jayaweera
authors.forename: Jiri
authors.initials: J
authors.lastname: Sklenar
authors.forename: N Craig
authors.initials: NC
authors.lastname: Goodman
authors.forename: Sanjiv
authors.initials: S
authors.lastname: Kaul
mesh_terms: D000241:Adenosine / Q000494:pharmacology; D000818:Animals; D003287:Contrast Media; D003326:Coronary Circulation; D023921:Coronary Stenosis / Q000503:physiopathology; D004285:Dogs; D004452:Echocardiography; D004548:Elasticity; D005466:Fluorocarbons; D008833:Microcirculation; D008955:Models, Cardiovascular; D009200:Myocardial Contraction / Q000502:physiology*
chemical_list: D003287:Contrast Media; D005466:Fluorocarbons; C078626:perflexane; D000241:Adenosine