(Circulation. 1996;94:2685-2688.)
© 1996 American Heart Association, Inc.
Articles |
the Departments of Internal Medicine (A.I.M.), University of TexasHouston and Cardiac Unit (A.W.), Massachusetts General Hospital, Boston.
Key Words: Editorials hibernation, myocardial myocardial viability imaging
| Introduction |
|---|
In the early 1980s, development of clinical methods for coronary revascularization (CABG/PTCA) was rapidly followed by presentation of data that indicated that dysfunctional myocardial segments supplied by vessels with reduced or seemingly absent flow could often recover function after flow was restored. The term "hibernating" has been used to describe myocytes that reside in regions that receive blood flow sufficient to support the low energyrequiring functions needed to maintain structural integrity but inadequate to sustain the high-energy requirements of contraction.1 The recognition that such regions exist and that clinical recovery is possible is particularly important in patients with poor ventricular function and has driven research for reliable, noninvasive methods to detect hibernation. A variety of such techniques is available and can be broadly divided into two groups2 3 : (1) radioactive tracers of perfusion that depend on the integrity of the sarcolemmal membrane for myocardial uptake and retention (eg, 201Tl or 82Rb) or on preservation of myocardial metabolism (eg, [18F] fluorodeoxyglucose [FDG]) to indicate viability and (2) stimulants of inotropic reserve, of which the most widely used is low-dose dobutamine stress echocardiography (LDDSE). Thus the nuclear techniques, with which there is greater experience, evaluate structural viability, whereas LDDSE defines viability on the basis of functional recovery. When assessing these techniques, it is important to remember that inherent in the definition of hibernation is ultimate recovery in function. Therefore, it is only after function has been restored that
This article has been cited by other articles:
![]() |
A. Keck, K. Hertting, Y. Schwartz, R. Kitzing, M. Weber, B. Leisner, C. Franke, E. Bahlmann, C. Schneider, T. Twisselmann, et al. Electromechanical mapping for determination of myocardial contractility and viability: A comparison with echocardiography, myocardial single-photon emission computed tomography, and positron emission tomography J. Am. Coll. Cardiol., September 18, 2002; 40(6): 1067 - 1074. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Tawakol, H. A. Skopicki, S. A. Abraham, N. M. Alpert, A. J. Fischman, M. H. Picard, and H. Gewirtz Evidence of reduced resting blood flow in viable myocardial regions with chronic asynergy J. Am. Coll. Cardiol., December 1, 2000; 36(7): 2146 - 2153. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. Holmvang, S. Fry, H. A. Skopicki, S. A. Abraham, N. M. Alpert, A. J. Fischman, M. H. Picard, and H. Gewirtz Relation Between Coronary "Steal" and Contractile Function at Rest in Collateral-Dependent Myocardium of Humans With Ischemic Heart Disease Circulation, May 18, 1999; 99(19): 2510 - 2516. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. Gepstein, A. Goldin, J. Lessick, G. Hayam, S. Shpun, Y. Schwartz, G. Hakim, R. Shofty, A. Turgeman, D. Kirshenbaum, et al. Electromechanical Characterization of Chronic Myocardial Infarction in the Canine Coronary Occlusion Model Circulation, November 10, 1998; 98(19): 2055 - 2064. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. A. Kloner, R. Bolli, E. Marban, L. Reinlib, and E. Braunwald Medical and Cellular Implications of Stunning, Hibernation, and Preconditioning : An NHLBI Workshop Circulation, May 19, 1998; 97(18): 1848 - 1867. [Full Text] [PDF] |
||||
|
Circulation Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1996 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |