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J Am Coll Cardiol, 2001; 37:1141-1148
© 2001 by the American College of Cardiology Foundation
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EXPERIMENTAL STUDY

Regional asynchrony during acute myocardial ischemia quantified by ultrasound strain rate imaging

Cristina Pislaru, MD*, Marek Belohlavek, MD, PhD{dagger}, Richard Y. Bae, MD{dagger}, Theodore P. Abraham, MD{dagger}, James F. Greenleaf, PhD* and James B. Seward, MD{dagger}

* Department of Physiology and Biophysics, Mayo Clinic and Foundation, Rochester, Minnesota, USA
{dagger} Division of Cardiovascular Diseases Internal Medicine, Mayo Clinic and Foundation, Rochester, Minnesota, USA

Manuscript received August 2, 2000; revised manuscript received November 6, 2000, accepted December 14, 2000.

Reprint requests and correspondence: Dr. Cristina Pislaru, Mayo Clinic, Ultrasound Research Lab, 200 First Street SW, Rochester, Minnesota 55905
Pislaru.Cristina{at}mayo.edu

OBJECTIVES

We propose a new method to easily quantify asynchronous wall motion due to postsystolic shortening (PSS). We also studied the relationship of the spatial and temporal extent of PSS to the extent of myocardium at ischemic risk after variable duration of ischemia.

BACKGROUND

Postsystolic shortening is a sensitive marker of asynchrony during ischemia. Current techniques for detection of asynchrony are either subjective, or invasive and time-consuming. Strain rate imaging (SRI) can noninvasively depict PSS as prolonged compression/expansion crossover.

METHODS

Nineteen open-chest pigs were scanned from apical views, before and after left anterior descending coronary artery occlusion. Strain rates were derived offline from tissue Doppler velocity cineloops. The time from electrocardiographic R-wave to the occurrence of compression/expansion crossover (TCEC) was calculated. Prolonged TCEC during ischemia was identified using a standardized analysis and both spatial (% of left ventricle) and temporal extent were quantified. The extent of myocardium at risk was measured in seven animals from dye-stained specimens.

RESULTS

Prolonged TCEC was found in all ischemic segments. There was a good correlation (r = 0.91; p < 0.001) and good agreement between the spatial distributions of prolonged TCEC and myocardium at risk. The extent of myocardium at risk was better approximated by TCEC measurement (36 ± 7% vs. 39 ± 8%, respectively; p = NS) than by wall motion analysis (47 ± 17%, p < 0.05). The duration of occlusion did not prolong TCEC.

CONCLUSIONS

Prolonged TCEC consistently occurs in ischemic myocardium and is apparently not affected by the duration of ischemia. Standardized analysis of TCEC in SRI closely quantifies the extent of ischemic myocardium. This new method may be a useful tool in other cardiac conditions associated with regional diastolic asynchrony.

Abbreviations and Acronyms
  LAD = left anterior descending coronary artery
  LV = left ventricle, left ventricular
  PSS = postsystolic shortening
  SD = standard deviation
  SRI = strain rate imaging
  TCEC = time to compression/expansion crossover
  WMS = wall motion score




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