(Circulation. 1995;92:9-10.)
© 1995 American Heart Association, Inc.
Articles |
From the Division of Cardiovascular Disease, the Center for Nuclear Magnetic Resonance Research and Development, and the Department of Radiology, University of Alabama at Birmingham.
Correspondence to Dr Pohost, 311-THT, UAB Station, Birmingham, AL 35294-0006.
Key Words: Editorials spectroscopy imaging
| Introduction |
|---|
|
|
|---|
Yabe et al8 report a new clinical approach for evaluating myocardial viability. The method uses 31P-NMR spectroscopic imaging (SI) to quantify the high-energy phosphates ATP and phosphocreatine (PCr). The use of ATP concentration as a standard for assessing myocardial viability is not new.9 What is new is the ability to estimate ATP and PCr concentrations clinically and noninvasively in asynergic segments of myocardium.
Wall motion abnormalities associated with ischemic heart disease may be related to myocardial scar in patients with previous myocardial infarction, an irreversible situation, or to transient ischemic dysfunction ("stunning")10 or persistent ischemic dysfunction ("hibernation").11 Reversible or irreversible dysfunction can suggest the appropriate therapeutic strategy. With viable but dysfunctional myocardium, bypass graft surgery or catheterization laboratory intervention can lead to improved function and symptomatic state of the patientor even extension of longevity. With nonviable myocardium, there is no need for intervention, since it will have no significant benefit. If dysfunction is so extensive that severe heart failure is present, the ability to assess viability can encourage beneficial coronary artery intervention if substantial myocardium is viable or cardiac transplantation if it is not.
| The Comprehensive Cardiac NMR Examination |
|---|
|
|
|---|
| Problems With NMR SI as a Viability Assessment Approach |
|---|
|
|
|---|
The advantages of the 31P approach include (1) as demonstrated in the article by Yabe et al,8 the unique ability to noninvasively assess the concentration of important high-energy phosphates (ATP, PCr) (the only other approach is myocardial biopsy); (2) the lack of need to use expensive radiotracers; (3) the unique ability to assess myocardial energetics, coupled with the ability to assess morphology, function, perfusion, and, potentially, the extent of epicardial coronary artery disease, in a single system and in a single examination interval; (4) the totally noninvasive nature of the test; (5) the fact that NMR systems are widely distributed and can be upgraded to enable NMR spectroscopic imaging; and (6) the ability to make serial measurements without the cumulative effects of radioactive tracers.
Previous work by Yabe et al14 and by Weiss et al15 demonstrates reduction in the PCr/ATP during handgrip exerciseinduced acute ischemia in patients with CAD, while Yabe et al in the present article use the concentrations of PCr and ATP, and PCr/ATP at rest, to characterize myocardial tissue in patients with chronic ischemic heart disease as viable or nonviable. The present article did not examine the serial changes in 31P spectra that occur during an acute ischemic insult. For example, in laboratory animals, the 31P myocardial spectrum may appear different during an acute ischemic insult than in myocardium long after the ischemic insult. Scar with mainly fibrous tissue and a low density of cells would naturally have lower concentrations of high-energy phosphates. By contrast, ischemic but viable myocardium loses its PCrand, to a lesser extent, its ATP (and from laboratory animal studies, more dramatically, its PCr relative to its Pi). In fact, at higher magnetic fields, the severity of ischemic insult can be better assessed by loss of PCr relative to Pi. When viability is compromised acutely, ATP concentration falls dramatically. Thus, the appearance of the 31P spectrum is different during the acute ischemic insult versus long after the insult, in which irreversibly damaged myocardial cells and then myocardial scar are responsible for the 31P spectral pattern.
In conclusion, the article by Yabe et al8 describes and suggests the importance of 31P spectroscopic imaging methods to differentiate between viable and nonviable myocardium. The 31P-NMR spectroscopic imaging of ATP and PCr has great potential to be an important addition to our armamentarium for assessment of myocardial viability.
| Footnotes |
|---|
| References |
|---|
|
|
|---|
2. Kiat H, Maddahi J, Yang L, van Train K, Daley N, Wong C, Berman DS. Late reversibility of thallium 201 myocardial tomography deficit: an accurate measure of myocardial viability. J Am Coll Cardiol. 1988;12:1456-1463. [Abstract]
3. Dilsizian V, Rocco TP, Freedman NMT, Leon MB, Bonow RO. Enhanced detection of ischemic but viable myocardium by the reinjection of thallium after stress-redistribution imaging. N Engl J Med. 1990;323:141-146. [Abstract]
4. Berman DS, Kiat H, Friedman J, Wang FP, van Train K, Matzer L, Maddahi J, Germano G. Separate acquisition rest thallium 201/stress Tc99m sestamibi dual isotope myocardial perfusion SPECT: a clinical validation study. J Am Coll Cardiol. 1993;22:1455-1464. [Abstract]
5.
Smart SC, Sawada S, Ryan T, Segar D, Atherton L,
Berkovitz K, Bourdillon PDV, Feigenbaum H. Low-dose dobutamine
echocardiography detects reversible dysfunction
after thrombolytic therapy of acute myocardial
infarction. Circulation. 1993;88:405-415.
6.
Baer FM, Voth E, Schneider CA, Theissen P, Schicha H,
Sechtem U. Comparison of low-dose dobutamine-gradient-echo
magnetic resonance imaging and positron emission tomography with
[18F] fluorodeoxyglucose in patients with chronic
coronary artery disease: a functional and morphological
approach to the detection of residual myocardial viability.
Circulation. 1995;91:1006-1015.
7.
Brunken RC, Mody FV, Hawkins RA, Nienaber C, Phelps
ME, Schelbert HR. Positron emission tomography detects
metabolic viability in myocardium with
persistent 24-hour single-photon emission computer tomography
201Tl defects. Circulation. 1992;86:1357-1369.
8.
Yabe T, Mitsunami K, Inubushi T, Kinoshita M.
Quantitative measurements of cardiac phosphorus metabolites in
coronary artery disease by phosphorus-31 magnetic resonance
spectroscopy. Circulation. 1995;92:15-23.
9.
Jennings RB, Reimer KA, Hill ML, Mayer SE.
Total ischemia in dog hearts in vitro.
Circ Res. 1981;49:892-900.
10.
Bolli R. Myocardial `stunning' in man.
Circulation. 1992;86:1671-1691.
11. Rahimtoola SH. The hibernating myocardium. Am Heart J. 1989;117:211-221. [Medline] [Order article via Infotrieve]
12. Evanochko WT, Pohost GM. Myocardial nuclear magnetic resonance spectroscopy: present and future perspectives. In: Zaret BL, Kaufman L, Berson AS, Dunn RA, eds. Frontiers in Cardiovascular Imaging. New York, NY: Raven Press; 1993:101-112.
13. Hetherington HP, Luney DJE, Vaughan JT, Pan JW, Ponder SL, Tschendel O, Twieg DB, Pohost GM. 3-D 31P spectroscopic imaging of the human heart at 4.1T. Magn Reson Med. 1995;33:427-431. [Medline] [Order article via Infotrieve]
14.
Yabe T, Mitsunami K, Okada M, Morikawa S, Inabushi T,
Kinoshita M. Detection of myocardial ischemia by
magnetic resonance spectroscopy during handgrip exercise.
Circulation. 1994;89:1709-1716.
15. Weiss RG, Bottomley PA, Hardy CJ, Gerstenblith G. Regional myocardial metabolism of high energy phosphates during isometric exercise in patients with coronary artery disease. N Engl J Med. 1990;323:1593-1600.[Abstract]
This article has been cited by other articles:
![]() |
M. Saeed New Concepts in Characterization of Ischemically Injured Myocardium by MRI Experimental Biology and Medicine, May 1, 2001; 226(5): 367 - 376. [Abstract] [Full Text] |
||||
![]() |
P. A. Bottomley and R. G. Weiss Noninvasive Localized MR Quantification of Creatine Kinase Metabolites in Normal and Infarcted Canine Myocardium Radiology, May 1, 2001; 219(2): 411 - 418. [Abstract] [Full Text] |
||||
![]() |
G. M. Pohost and R. W. W. Biederman The Role of Cardiac MRI Stress Testing : "Make a Better Mouse Trap ... " Circulation, October 19, 1999; 100(16): 1676 - 1679. [Full Text] [PDF] |
||||
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
Circulation Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1995 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |