Abstract
The objective of myocardial viability assessment is to identify prospectively patients with potentially reversible left ventricular dysfunction in whom prognosis may be favorably altered with coronary artery revascularization. The concept that impaired left ventricular function at rest may be reversible after revascularization is now well established. Pathophysiologic paradigms have emerged that describe the relationships between myocardial perfusion and ventricular function, leading to the concepts of stunning and hibernation. In these paradigms, myocardial function is depressed but myocytes remain viable, and therefore left ventricular dysfunction may be completely reversible. Considerable advances in basic research and clinical science since the 1980s have helped clarify the underlying mechanisms of the functional alterations in stunned and hibernating myocardium. These advances have altered clinical practice and have led to improved patient management and survival. However, despite significant advances in our understanding and medical management of patients with left ventricular dysfunction, the prevalence of heart failure and the resultant death rates have almost tripled since the 1970s.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Taegtmeyer H: Modulation of responses to myocardial ischemia: metabolic features of myocardial stunning, hibernation, and ischemic preconditioning. In Myocardial Viability: A Clinical and Scientific Treatise. Edited by Dilsizian V. Armonk, New York: Futura; 2000:25–36.
Risk stratification and survival after myocardial infarction. N Engl J Med 1983, 309:331–336.
Mock MB, Ringqvist I, Fisher LD, et al.: Survival of medically treated patients in the coronary artery surgery study (CASS) registry. Circulation 1982, 66:562–568.
Alderman EL, Fisher LD, Litwin P, et al.: Results of coronary artery surgery in patients with poor left ventricular function (CASS). Circulation 1983; 68:785–795.
Bonow RO, Dilsizian V: Thallium-201 for assessment of myocardial viability. Sem Nucl Med 1991, 21:230–241.
Elefteriades JA, Tolis G Jr, Levi E, et al.: Coronary artery bypass grafting in severe left ventricular dysfunction: excellent survival with improved ejection fraction and functional state.J Am Coll Cardiol 1993, 22:1411–1417.
Rahimtoola SH: A perspective on the three large multicenter randomized clinical trials of coronary bypass surgery for chronic stable angina. Circulation 1985, 72(suppl V):V123-V135.
Haas F, Haehnel CH, Picker W, et al.: Preoperative positron emission tomography viability assessment and perioperative and postoperative risk in patients with advanced ischemic heart disease. J Am Coll Cardiol 1997, 30:1693–1700.
Vatner S: Correlation between acute reduction in myocardial blood flow and function in conscious dogs. Circ Res 1980, 47:201–207.
Braunwald E, Kloner RA: The stunned myocardium: prolonged, postischemic ventricular dysfunction. Circulation 1982, 66:1146–1149.
Heyndrickx GR, Millard RW, McRitchie RJ, et al.: Regional myocardial functional and electrophysiological alterations after brief coronary artery occlusion in conscious dogs. JClin Invest 1975, 56:978–985.
Matsuzaki M, Gallagher KP, Kemper S, et al.: Sustained regional dysfunction produced by prolonged coronary stenosis: gradual recovery after reperfusion. Circulation 1983, 68:170–182.
Camici P, Araujo LI, Spinks T, et al.: Increased uptake of 18F-fluorodeoxyglucose in postischemic myocardium of patients with exercise-induced angina. Circulation 1986, 74:81–88.
Krebs H: The Pasteur effect and the relation between respiration and fermentation. Essays Biochem 1972, 8:1–34.
Borgers M, Ausma J: Structural aspects of the chronic hibernating myocardium in man. Basic Res Cardiol 1995, 90:44–46.
Zhao M, Zhang H, Robinson TF, et al.: Profound structural alterations of the extracellular collagen matrix in postischemic dysfunction (“stunned”) but viable myocardium.J Am Coll Cardiol 1987, 10:1322–1334.
Shirani J, Lee J, Quigg RJ, et al.: Relation of thallium uptake to morphologic features of chronic ischemic heart disease: evidence for myocardial remodeling in non-infarct myocardium. J Am Coll Cardiol 2001, 38:84–90.
Hirsch AT, Talsness CE, Schunkert H, et al.: Tissue-specific activation of cardiac angiotensin converting enzyme in experimental heart failure. Circ Res 1991, 69:475–482.
Lindpaintner K, Lu W, Niedermajer N, et al.: Selective activation of cardiac angiotensinogen gene expression in post-infarction ventricular remodeling in the rat.J Mol Cell Cardiol 1993, 25:133–143.
Meggs LG, Coupet J, Huang H, et al.: Regulation of angiotensin II receptors on ventricular myocytes after myocardial infarction in rats. Circ Res 1993, 72:1149–1162.
Harada K, Sugaya T, Murakami K, et al.: Angiotensin II type 1A receptor knockout mice display less left ventricular remodeling and improved survival after myocardial infarction. Circulation 1999, 100:2093–2099.
Dilsizian V, Shirani J, Lee YHC, et al.: Specific binding of [18F] fluorobenzoyl-lisinopril to angiotensin converting enzyme in human heart tissue of ischemic cardiomyopathy. Circulation 2001, 104:II–694.
Dilsizian V, Loredo ML, Ferrans VJ, et al.: Evidence for increased angiotensin II type I receptor immunoreactivity in peri-infarct myocardium of human explanted hearts.J Am Coll Cardiol 2002, 39:365A.
Rights and permissions
Copyright information
© 2003 Current Medicine, Inc.
About this chapter
Cite this chapter
Dilsizian, V. (2003). Myocardial Viability: Reversible Left Ventricular Dysfunction. In: Atlas of Nuclear Cardiology. Current Medicine Group, London. https://doi.org/10.1007/978-1-4615-6496-6_8
Download citation
DOI: https://doi.org/10.1007/978-1-4615-6496-6_8
Publisher Name: Current Medicine Group, London
Print ISBN: 978-1-4615-6498-0
Online ISBN: 978-1-4615-6496-6
eBook Packages: Springer Book Archive