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(Circulation. 1995;92:3527-3538.)
© 1995 American Heart Association, Inc.

Articles

³¹P Nuclear Magnetic Resonance Spectroscopic Imaging of Regions of Remodeled Myocardium in the Infarcted Rat Heart

Presented at the 66th Annual Scientific Sessions of the American Heart Association, Atlanta, Ga, November 8-11, 1993.

Jan Friedrich, DPhil; Carl S. Apstein, MD; Joanne S. Ingwall, PhD

From the NMR Laboratory for Physiological Chemistry, Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Mass, and the Cardiac Muscle Research Laboratory (C.S.A.), Whitaker Cardiovascular Institute, Boston University School of Medicine.

Correspondence to Jan Friedrich, DPhil, NMR Laboratory for Physiological Chemistry, Department of Medicine, Brigham and Women's Hospital, 221 Longwood Ave, Room 209, Boston, MA 02115.

Background The clinical course of a patient with a myocardial infarction (MI) depends largely on the ability of the noninfarcted region to remodel and compensate for the loss of the infarcted region. Previous studies have shown that the remaining viable myocardium remodels morphologically, functionally, and biochemically. The purpose of this study was to define the regional distribution of the biochemical remodeling that occurs after MI in rat hearts by use of a technique that could be applied noninvasively to human subjects.

Methods and Results Infarcts of the left ventricular apex and anterolateral wall were induced by occluding a coronary artery. Eight to 10 weeks after infarction, one-dimensional chemical shift imaging (CSI) was used to obtain ³¹P nuclear magnetic resonance (NMR) spectra of eight 2.5-mm-thick cross-sectional slices along the long axis (from base to apex) of isolated buffer-perfused rat hearts. Regional ATP and phosphocreatine (PCr) contents were compared in remodeled versus normal (sham) myocardium. Spin-echo ¹H MR images identified the mass of each slice, allowing calculations of metabolite amount per unit myocardium in each slice. ¹H MR images identify the hypertrophy of remodeled myocardium but do not discriminate between scar and viable tissue. In contrast, ³¹P CSI does distinguish viable tissue. Compared with shams, there was less ³¹P signal in the slices distal to the occlusion containing mainly scar tissue and increased signal intensity in slices proximal to the occlusion because of myocyte hypertrophy. The ATP signal intensity changed in direct proportion to the viable tissue mass in the slice, suggesting that the amount of ATP per unit mass in viable remodeled myocardium is the same as that of the shams. In contrast, the amount of PCr per unit mass in remodeled myocardium decreased. This decrease is uniform across the slices, correlates with infarct size, and parallels a similar decrease in tissue creatine content.

Conclusions ³¹P CSI of post-MI hearts shows that (1) PCr decreases uniformly (ie, independent of the distance from the scar) in the noninfarcted remodeled myocardium, and its amount inversely correlates with infarct size; and (2) the ATP signal provides a profile of viable myocardium and is a biochemical marker of morphological remodeling and hypertrophy that has occurred in noninfarcted regions. Thus, ³¹P CSI provides both a marker that tissue injury has occurred (decreased PCr) and a marker of the extent of remodeling in response to injury (ATP distribution) in a single set of noninvasive measurements.

Key Words: myocardial infarction • remodeling • myocardium • phosphocreatine • ATP

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