Physiological basis for potassium (39K) magnetic resonance imaging of the heart.

Published

Journal Article

The potassium cation (K+) is fundamentally involved in myocyte metabolism. To explore the potential utility of direct MRI of the most abundant natural isotope of potassium, 39K, we compared 39K magnetic resonance (MR) image intensity with regional myocardial K+ concentrations after irreversible injury. Rabbits were subjected either to 40 minutes of in situ coronary artery occlusion and 1 hour of reperfusion (n=26) or to 24 hours of permanent occlusion (n=4). The hearts were then isolated and imaged by 39K MRI (n=10), or tissue samples were analyzed for regional 39K content by MR spectroscopy (n=9), K+ and Na+ concentrations by atomic emission spectroscopy (inductively coupled plasma atomic emission spectroscopy; n=5), or intracellular K+ content by electron probe x-ray microanalysis (n=6). Three-dimensional 39K MR images of the isolated hearts were acquired in 44 minutes with 3 x 3 x 3-mm resolution. 39K MR image intensity was reduced in infarcted regions (51.7+/-4. 8% of remote; P<0.001). The circumferential extent and location of regions of reduced 39K image intensity were correlated with those of infarcted regions defined histologically (r=0.97 and r=0.98, respectively). Compared with remote regions, tissue analysis revealed that infarcted regions had reduced 39K concentration (by MR spectroscopy, 40.5+/-9.3% of remote; P<0.001), reduced potassium-to-sodium ratio (by inductively coupled plasma atomic emission spectroscopy, 20.7+/-2.1% of remote; P<0.01), and reduced intracellular potassium (by electron probe x-ray microanalysis, K+ peak-to-background ratio 0.95+/-0.32 versus 2.86+/-1.10, respectively; P<0.01). We acquired the first 39K MR images of hearts subjected to infarction. In the pathophysiologies examined, potassium (39K) MR image intensity primarily reflects regional intracellular K+ concentrations.

Full Text

Duke Authors

Cited Authors

  • Fieno, DS; Kim, RJ; Rehwald, WG; Judd, RM

Published Date

  • April 30, 1999

Published In

Volume / Issue

  • 84 / 8

Start / End Page

  • 913 - 920

PubMed ID

  • 10222338

Pubmed Central ID

  • 10222338

International Standard Serial Number (ISSN)

  • 0009-7330

Language

  • eng

Conference Location

  • United States