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J Am Coll Cardiol, 2000; 36:2339-2346
© 2000 by the American College of Cardiology Foundation
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EXPERIMENTAL STUDY

Transmural contractile reserve after reperfused myocardial infarction in dogs

J.érôme Garot, MD*, David A. Bluemke, MD, PhD{dagger}, Nael F. Osman, PhD{ddagger}, Carlos E. Rochitte, MD*, Elias A. Zerhouni, MD{dagger}, Jerry L. Prince, PhD{ddagger} and João A. C. Lima, MD, FACC*

* Cardiology Division of the Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
{dagger} Department of Radiology of the Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
{ddagger} Department of Electrical and Computer Engineering of the Whiting School of Engineering, Johns Hopkins University, Baltimore, Maryland, USA

Manuscript received March 3, 2000; revised manuscript received June 23, 2000, accepted August 7, 2000.

Reprint requests and correspondence: Dr. João A.C. Lima, Cardiology Division, Blalock 569, Johns Hopkins Hospital, 600 North Wolfe Street, Baltimore, Maryland 21287-6568
jlima{at}mail.jhmi.edu

OBJECTIVES

The goal of this study was to characterize detailed transmural left ventricular (LV) function at rest and during dobutamine stimulation in subendocardial and transmural experimental infarcts.

BACKGROUND

The relation between segmental LV function and the transmural extent of myocardial necrosis is complex. However, its detailed understanding is crucial for the diagnosis of myocardial viability as assessed by inotropic stimulation.

METHODS

Short-axis tagged magnetic resonance images were acquired at five to seven levels encompassing the LV from base to apex in seven dogs 2 days after a 90-min closed-chest left anterior descending coronary occlusion, followed by reflow. Myocardial strains were measured transmurally in the entire LV by harmonic phase imaging at rest and 5 ig.kg–1.min–1 dobutamine. Risk regions were assessed by radioactive microspheres, and the transmural extent of the infarct was assessed by 2,3,5 triphenyltetrazolium chloride staining.

RESULTS

Circumferential shortening (Ecc), radial thickening (Err) and maximal shortening at rest were greater in segments with subendocardial versus transmural infarcts, both in subepicardium (–1.1 ± 1.0 vs. 2.5 ± 0.6% for Ecc, –0.5 ± 1.9 vs. –1.8 ± 1.0% for Err, p < 0.05) and subendocardium (–2.0 ± 1.4 vs. 2.8 ± 0.8%, 2.4 ± 1.7 vs. 0.0 ± 0.9%, respectively, p < 0.05). Under inotropic stimulation, risk regions retained maximal contractile reserve. Recruitable deformation was found in outer layers of subendocardial infarcts (p < 0.01 for Ecc and Err) but also in inner layers (p < 0.01). Conversely, no contractile reserve was observed in segments with transmural infarcts.

CONCLUSIONS

Under dobutamine challenge, recruitment of myofiber shortening and thickening was observed in inner layers of segments with subendocardial infarcts. These results may have important clinical implications for the detection of myocardial viability.

Abbreviations and Acronyms
  Ecc = circumferential shortening
  ECG = electrocardiogram
  Err = radial thickening
  E1 = maximal elongation
  E2 = maximal shortening
  HARP = harmonic phase imaging
  LV = left ventricular
  MBF = myocardial blood flow
  MI = myocardial infarction
  MRI = magnetic resonance imaging
  TTC = 2,3,5 triphenyltetrazolium chloride




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