Myocardial hibernation in coronary artery disease
Tóm tắt
Coronary artery disease (CAD) is very prevalent in Western societies and is a leading cause of mortality and morbidity. Despite decreases in mortality rates from CAD over the past 30 years, ischemic heart failure remains an important problem because people with CAD are now living longer. Hibernating myocardium may be defined as reversible left ventricular dysfunction due to chronic CAD that shows improvement in function after revascularization. Many patients with ischemic cardiomyopathy have areas of hibernating myocardium, and thus can potentially show improvement in left ventricular regional and global function if they are revascularized. Whether hibernating myocardium represents an adaptive response to hypoperfusion in the face of chronic ischemia or whether it is a degenerative process is not entirely clear. Clearly, ultrastructural changes of de-differentiaton are seen, and include loss of sarcomeres and the appearance of small mitochondria and glycogen accumulation. Although the mechanisms underlying the changes in morphology and depressed contractility, and the factors governing recovery of function are not clear, changes in adrenergic receptor density, cytokine upregulation, and the degree of fibrosis may all play a role. Identification of viability is commonly performed with dobutamine echocardiography or nuclear imaging. Because patients with extensive CAD and poor left ventricular systolic function are high-risk candidates for coronary bypass surgery, the preoperative identification of viability provides important prognostic information. Patients with viable myocardium who are treated with revascularization rather than medical therapy have better outcomes in terms of survival, left ventricular function, symptoms, and exercise capacity.
Tài liệu tham khảo
Diamond GA, Forrester JS, deLuz PL, Wyatt HL, Swan HJ: Post-extrasystolic potentiation of ischemic myocardium by atrial stimulation. Am Heart J 1978, 95:204–209.
Rahimtoola SH: The hibernating myocardium. Am Heart J 1989, 117:211–221.
Horn HR, Teichholz LE, Cohn PF, Herman MV, Gorlin R: Augmentation of left ventricular contraction pattern in coronary artery disease by an inotropic catecholamine. The epinephrine ventriculogram. Circulation 1974, 49:1063–1071.
Dyke SH, Cohn PF, Gorlin R, Sonnenblick EH: Detection of residual myocardial function in coronary artery disease using post-extra systolic potentiation. Circulation 1974, 50:694–699.
Heyndrickx GR, Millard RW, McRitchie RJ, Maroko PR, Vatner SF: Regional myocardial functional and electrophysiological alterations after brief coronary artery occlusion in conscious dogs. J Clin Invest 1975, 56:978–985.
Braunwald E, Kloner RA: The stunned myocardium: prolonged, postischemic ventricular dysfunction. Circulation 1982, 66:1146–1149.
Renkin J, Wijns W, Ladha Z, Col J: Reversal of segmental hypokinesis by coronary angioplasty in patients with unstable angina, persistent T wave inversion, and left anterior descending coronary artery stenosis. Additional evidence for myocardial stunning in humans. Circulation 1990, 82:913–921.
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.
Camici PG, Rimoldi O: Blood flow in myocardial hibernation. Curr Opin Cardiol 1998, 13:409–414.
Ross J, Jr: Myocardial perfusion-contraction matching. Implications for coronary heart disease and hibernation. Circulation 1991, 83:1076–1083.
Firoozan S, Wei K, Linka A, et al.: A canine model of chronic ischemic cardiomyopathy: characterization of regional flow-function relations. Am J Physiol 1999, 276:H446-H455.
St. Louis JD, Hughes GC, Kypson AP, et al.: An experimental model of chronic myocardial hibernation. Ann Thorac Surg 2000, 69:1351–1357.
Baer FM, Theissen P, Voth E, et al.: Morphologic correlate of pathologic Q waves as assessed by gradient-echo magnetic resonance imaging. Am J Cardiol 1994, 74:430–434.
Brunken R, Tillisch J, Schwaiger M, et al.: Regional perfusion, glucose metabolism, and wall motion in patients with chronic electrocardiographic Q wave infarctions: evidence for persistence of viable tissue in some infarct regions by positron emission tomography. Circulation 1986, 73:951–963.
Afridi I, Kleiman NS, Raizner AE, Zoghbi WA: Dobutamine echocardiography in myocardial hibernation. Optimal dose and accuracy in predicting recovery of ventricular function after coronary angioplasty. Circulation 1995, 91:663–670.
Cwajg JM, Cwajg E, Nagueh SF, et al.: End-diastolic wall thickness as a predictor of recovery of function in myocardial hibernation: relation to rest-redistribution T1-201 tomography and dobutamine stress echocardiography. J Am Coll Cardiol 2000, 35:1152–1161.
Yong Y, Nagueh SF, Shimoni S, et al.: Deceleration time in ischemic cardiomyopathy: relation to echocardiographic and scintigraphic indices of myocardial viability and functional recovery after revascularization. Circulation 2001, 103:1232–1237.
Shan K, Bick RJ, Poindexter BJ, et al.: Relation of tissue Doppler derived myocardial velocities to myocardial structure and beta-adrenergic receptor density in humans. J Am Coll Cardiol 2000, 36:891–896.
Larrazet F, Pellerin D, Prigent A, et al.: Quantitative analysis of hibernating myocardium by dobutamine tissue Doppler echocardiography. Am J Cardiol 2001, 88:418–422.
Rambaldi R, Poldermans D, Bax JJ, et al.: Doppler tissue velocity sampling improves diagnostic accuracy during dobutamine stress echocardiography for the assessment of viable myocardium in patients with severe left ventricular dysfunction. Eur Heart J 2000, 21:1091–1098.
He ZX, Verani MS, Liu XJ: Nitrate-augmented myocardial imaging for assessment of myocardial viability. J Nucl Cardiol 1995, 2:352–357.
Gallagher KP, Matsuzaki M, Koziol JA, Kemper WS, Ross J, Jr: Regional myocardial perfusion and wall thickening during ischemia in conscious dogs. Am J Physiol 1984, 247:H727-H738.
Nagueh SF, Mikati I, Weilbaecher D, et al.: Relation of the contractile reserve of hibernating myocardium to myocardial structure in humans. Circulation 1999, 100:490–496.
Dakik HA, Howell JF, Lawrie GM, et al.: Assessment of myocardial viability with 99mTc-sestamibi tomography before coronary bypass graft surgery: correlation with histopathology and postoperative improvement in cardiac function. Circulation 1997, 96:2892–2898.
Shan K, Bick RJ, Poindexter BJ, et al.: Altered adrenergic receptor density in myocardial hibernation in humans: a possible mechanism of depressed myocardial function. Circulation 2000, 102:2599–2606.
Botker HE, Lassen JF, Hermansen F, et al.: Electromechanical mapping for detection of myocardial viability in patients with ischemic cardiomyopathy. Circulation 2001, 103:1631–1637.
Nagueh SF, Vaduganathan P, Ali N, et al.: Identification of hibernating myocardium: comparative accuracy of myocardial contrast echocardiography, rest-redistribution thallium-201 tomography and dobutamine echocardiography. J Am Coll Cardiol 1997, 29:985–993.
Swinburn JM, Lahiri A, Senior R: Intravenous myocardial contrast echocardiography predicts recovery of dysynergic myocardium early after acute myocardial infarction. J Am Coll Cardiol 2001, 38:19–25.
Baer FM, Theissen P, Crnac J, et al.: Head to head comparison of dobutamine-transoesophageal echocardiography and dobutamine-magnetic resonance imaging for the prediction of left ventricular functional recovery in patients with chronic coronary artery disease. Eur Heart J 2000, 21:981–991.
Kim RJ, Wu E, Rafael A, et al.: The use of contrast-enhanced magnetic resonance imaging to identify reversible myocardial dysfunction. N Engl J Med 2000, 343:1445–1453.
Borgers M, Ausma J: Structural aspects of the chronic hibernating myocardium in man. Basic Res Cardiol 1995, 90:44–46.
Schwarz ER, Schaper J, Vom DJ, et al.: Myocyte degeneration and cell death in hibernating human myocardium. J Am Coll Cardiol 1996, 27:1577–1585.
Elsasser A, Schlepper M, Klovekorn WP, et al.: Hibernating myocardium: an incomplete adaptation to ischemia. Circulation 1997, 96:2920–2931.
Lai T, Fallon JT, Liu J, et al.: Reversibility and pathohistological basis of left ventricular remodeling in hibernating myocardium. Cardiovasc Pathol 2000, 9:323–335.
Bartling B, Hoffmann J, Holtz J, et al.: Quantification of cardioprotective gene expression in porcine short-term hibernating myocardium. J Mol Cell Cardiol 1999, 31:147–158.
Kaprielian RR, Gunning M, Dupont E, et al.: Downregulation of immunodetectable connexin43 and decreased gap junction size in the pathogenesis of chronic hibernation in the human left ventricle. Circulation 1998, 97:651–660.
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.
Bounous EP, Mark DB, Pollock BG, et al.: Surgical survival benefits for coronary disease patients with left ventricular dysfunction. Circulation 1988, 78:1151–1157.
Veterans Administration Coronary Artery Bypass Surgery Cooperative Study Group (VACABG): Eleven-year survival in the Veterans Administration randomized trial of coronary bypass surgery for stable angina. The Veterans Administration Coronary Artery Bypass Surgery Cooperative Study Group. N Engl J Med 1984, 311:1333–1339.
Swan HJ, Chatterjee K, Corday E, et al.: Clinical conference: Myocardial revascularization for acute and chronic coronary heart disease. Ann Intern Med 1973, 79:851–866.
Eitzman D, al Aouar Z, Kanter HL, et al.: Clinical outcome of patients with advanced coronary artery disease after viability studies with positron emission tomography. J Am Coll Cardiol 1992, 20:559–565.
Di Carli MF, Davidson M, Little R, et al.: Value of metabolic imaging with positron emission tomography for evaluating prognosis in patients with coronary artery disease and left ventricular dysfunction. Am J Cardiol 1994, 73:527–533.
Haas F, Haehnel CJ, Picker W, et al.: Preoperative positron emission tomographic viability assessment and perioperative and postoperative risk in patients with advanced ischemic heart disease. J Am Coll Cardiol 1997, 30:1693–1700.
Afridi I, Grayburn PA, Panza JA, et al.: Myocardial viability during dobutamine echocardiography predicts survival in patients with coronary artery disease and severe left ventricular systolic dysfunction. J Am Coll Cardiol 1998, 32:921–926.
Chaudhry FA, Tauke JT, Alessandrini RS, et al.: Prognostic implications of myocardial contractile reserve in patients with coronary artery disease and left ventricular dysfunction. J Am Coll Cardiol 1999, 34:730–738.
Vanoverschelde JL, Depre C, Gerber BL, et al.: Time course of functional recovery after coronary artery bypass graft surgery in patients with chronic left ventricular ischemic dysfunction. Am J Cardiol 2000, 85:1432–1439.
Shivalkar B, Maes A, Borgers M, et al.: Only hibernating myocardium invariably shows early recovery after coronary revascularization. Circulation 1996, 94:308–315.
Schwarz ER, Schoendube FA, Kostin S, et al.: Prolonged myocardial hibernation exacerbates cardiomyocyte degeneration and impairs recovery of function after revascularization. J Am Coll Cardiol 1998, 31:1018–1026.
Meluzin J, Cerny J, Frelich M, et al.: Prognostic value of the amount of dysfunctional but viable myocardium in revascularized patients with coronary artery disease and left ventricular dysfunction. Investigators of this Multicenter Study. J Am Coll Cardiol 1998, 32:912–920.
Pagley PR, Beller GA, Watson DD, Gimple LW, Ragosta M: Improved outcome after coronary bypass surgery in patients with ischemic cardiomyopathy and residual myocardial viability. Circulation 1997, 96:793–800.
Kaprielian RR, Gunning M, Dupont E, et al.: Downregulation of immunodetectable connexin43 and decreased gap junction size in the pathogenesis of chronic hibernation in the human left ventricle. Circulation 1998, 97:651–660.
Nagueh SF, Zoghbi WA: Stress echocardiography for the assessment of myocardial ischemia and viability. Curr Prob Cardiol 1996, 21:497.