Myocardial ischemia leads to alterations in myocardial substrate metabolism that have been shown to reflect severity of ischemic injury. The purpose of this study was to correlate oxidative metabolism with recovery of contractile function in patients with acute myocardial infarction.
Methods and Results
Regional blood flow and oxidative metabolism were assessed by dynamic positron emission tomography early after myocardial infarction treated with thrombolytic therapy in 18 patients. The extent of myocardial perfusion abnormality (carbon 11-labeled acetate uptake; relative amplitude ≤50%) was inversely correlated with the ejection fraction obtained within 8 hours of the onset of chest pain (r=0.81;p=0.01) but not clearly with that at follow-up 1 week later (r=0.64;p=0.09). Oxidative metabolism (carbon 11-labeled acetate; monoexponential clearance) was higher in periinfarct territories with early or late recovery of contractile function than in those without, but there was a large overlap in absolute values limiting the predictive power of a single measurement. Relatively preserved oxidative metabolism compared with perfusion in low-flow areas was predictive of early (day 1 to 1 week) and delayed (week 1 to beyond 1 month) recovery. Normal resting perfusion with regionally decreased oxidative metabolism predicted early recovery of contractile function.
Thus in patients studied with positron emission tomography early after myocardial infarction, comparison of regional perfusion and oxidative metabolism was more predictive of recovery in contractile function than was assessment of either one alone.
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Gruppo Italiano per lo studio della streptochinasi nell’ infarto miocardico (GISSI): Effectiveness of intravenous thrombolytic therapy in acute myocardial infarction. Lancet 1986; 1: 397–401.
ISIS-2 (Second International Study of Infarct Survival) Collaborative Group. Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. Lancet 1988; 2: 349–60.
Topol EJ, O’Neill WW, Langburd AB, et al. A randomized, placebo-controlled trial of intravenous recombinant tissue-type plasminogen activator and emergency coronary angioplasty in patients with acute myocardial infarction. Circulation 1987; 75: 420–8.
Topol EJ, Califf RM, George BS, et al. Coronary arterial thrombolysis with combined infusion of recombinant tissue-type plasminogen activator and urokinase in patients with acute myocardial infarction. Circulation 1988; 77: 1100–7.
Kloner R, DeBoer L, Darsee J, et al. Prolonged abnormalities of myocardium salvaged by reperfusion. Am J Physiol 1981; 64: H591–9.
Braunwald E, Kloner RA The stunned myocardium prolonged postischemic ventricular dysfunction. Circulation 1983; 66: 1146–9.
Shiins A, Tajik AJ, Smith HC, Lengyl M, Seward JB. Prognostic sigificance of regional wall motion abnormality in patients with prior myocardial infarction: a prospective correlative study of two dimensional echo-cardiography and angiography. Mayo Clin Proc 1986; 61: 254–62.
Pike VW, Eakins MN, Allan RM, Selwyn AP. Preparation of [1–11C] acetate: an agent for the study of myocardial metabolism by positron emission tomography. Int J Appl Radiat Isot 1982; 33: 505–12.
Brown M, Marshall DR, Sobel BE, Bergmann SR. Delineation of myocardial oxygen utilization with carbon-11-labelled acetate. Circulation 1987;76:687–96.
Brown MA, Myears DW, Bergmann SR. Validity of estimates of myocardial oxidative metabolism with carbon-11 acetate and positron emission tomography despite altered patterns of substrate utilization. J Nucl Med 1989; 30: 187–93.
Buxton DB, Schwaiger M, Nguyen A, Phelps ME, Schelbert HR. Radiolabeled acetate as a tracer of myocardial tricarboxylic acid cycle flux. Circ Res 1988; 63: 628–34.
Buxton DB, Nienaber CA, Luxen A, et al. Noninvasive quantitation of regional myocardial oxygen consumption in vivo with [1–11C] acetate and dynamic positron emission tomography. Circulation 1989; 79: 134–42.
Armbrecht JJ, Buxton DB, Brunken RC, Phelps ME, Schelbert HR. Regional myocardial oxygen consumption determined noninvasively in humans with [1–11C] acetate and dynamic positron tomography. Circulation 1989; 80: 863–72
Kotzerke J, Hicks RJ, Wolfe E, et al. Three-dimensional assessment of myocardial oxidative metabolism: a new approach for regional determination of PET-derived C-11 acetate kinetics. J Nucl Med 1990; 31: 1876–83.
Garcia EV, Van Train K, Maddahi J, et al. Quantification of rotational thallium-201 myocardial tomography. J Nucl Med 1985; 26: 17–26.
Hicks RJ, Herman WH, Wolfe E, Kotzerke J, Kuhl DE, Schwaiger M. Regional variation in oxidative and glucose metabolism in the normal heart: comparison of PET-derived C-11 acetate and FDG kinetics [Abstract]. J Nucl Med 1990; 31: 774.
Gropler RJ, Siegel BA, Geltman EM. Myocardial uptake of carbon-11 acetate as an indirect measurement of regional myocardial blood flow. J Nucl Med 1991; 32: 245–51.
Chan SY, Brunken RC, Phelps ME, Schelbert HR. Use of the metabolic tracer carbon-11 acetate for evaluation of regional myocardial perfusion. J Nucl Med 1991; 32: 665–72.
The Multicenter Postinfarction Research Group. Risk stratification and survival after acute myocardial infarction. N Engl J Med 1983; 409: 331–6.
Kelly MJ, Thompson PL, Quinlan MF. The prognostic significance of the left ventricular ejection fraction after myocardial infarction: a bedside radionuclide study. Br Heart J 1985; 53: 16–24.
Rigo P, Murray M, Strauss HW, et al. Left ventricular ejection fraction in acute myocardial infarction evaluated by gated scintigraphy. Circulation 1974; 50: 678–84.
Tillisch J, Brunken R, Marshall R, et al. Reversibility of cardiac wall motion abnormalities predicted by positron tomography. N Engl J Med 1986; 314: 884–8.
Tamaki N, Yonekura Y, Yamashita K, et al. Relation of left ventricular perfusion and wall motion with metabolic activity in persistent defects on thallium-201 tomography in healed myocardial infarction. Am J Cardiol 1988; 62: 202–8.
Brunken RC, Schwaiger M, Grover-McKay M, Phelps ME, Tillisch JH, Schelbert HR. Positron emission tomography detects tissue metabolic activity in myocardial segments with persistent thallium perfusion defects. J Am Coll Cardiol 1987; 10: 557–67.
Brunken RC, Kottou S, Nienaber CA, et al. PET detection of viable tissue in myocardial segments with persistent defects at T1-201 SPECT. Radiology 1989; 172: 65–73.
Dilsizian V, Rocco TP, Freeman 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: 141–6.
Henes CG, Bergmann SR, Walsh MN, Sobel BE, Geltman EM. Assessment of myocardial oxidative metabolic reserve with positron emission tomography and carbon-11 acetate. J Nucl Med 1989; 30: 1489–99.
Gobel FL, Nordstrom LA, Nelson RP, Jorgensen CR, Wang Y. The rate-pressure product at an index of myocardial oxygen consumption during exercise in patients with angina pectoris. Circulation 1978; 57: 549–56.
Nelson RR, Gobel FL, Jorgensen CR, Wang K, Wang Y, Taylor HL. Hemodynamic predictors of myocardial oxygen consumption during static and dynamic exercise. Circulation 1974; 50: 1179–89.
Hicks RJ, Savas V, Currie PJ, Kalff V, Kuhl DE, Schwaiger M. PET-derived C-11 acetate kinetics as a marker of metabolic performance in the pressure and volume loaded heart [Abstract]. J Nucl Med 1990; 31: 773.
Hicks RJ, Kalff V, Savas V, Starling MR, Schwaiger M. Assessment of right ventricular oxidative metabolism by positron emission tomography with C-11 acetate in aortic valve disease. Am J Cardiol 1991; 67: 753–7.
Hicks RJ, Savas V, Currie PJ, et al. Assessment of myocardial oxidative metabolism in aortic valve disease using positron emission tomography with C-11 acetate. Am Heart J 1992; 123: 653–64.
Chan SY, Warner-Stevenson L, Brunken RC, Krivokapich J, Phelps ME, Schelbert HR. Myocardial oxygen consumption in patients with idiopathic dilated cardiomyopathy [Abstract]. J Nucl Med 1990; 31: 773.
Armbrecht JJ, Buxton DB, Schelbert HR. Validation of [1–11C] acetate as a tracer for noninvasive assessment of oxidative metabolism with positron emission tomography in normal, ischemic, postischemic, and hyperemic canine myocardium. Circulation 1990; 81: 1595–605.
Kalff V, Hicks RJ, Hutchins G, Topol E, Schwaiger M. Use of carbon-11 acetate and dynamic positron emission tomography to assess myocardial oxygen consumption in patients with acute myocardial infarction receiving thrombolysis or coronary angioplasty. Am J Cardiol 1993; 71: 529–35.
Buck A, Wolpers HG, Hutchins GD, et al. Effect of C-11 acetate recirculation on estimates of myocardial oxygen consumption by PET. J Nucl Med 1991; 32: 1950–7.
Walsh MN, Geltman EM, Brown MA, et al. Noninvasive estimation of regional myocardial oxygen consumption by positron emission tomography with carbon-11 acetate in patients with myocardial infarction. J Nucl Med 1989; 30: 1798–808.
Vanoverschelde J-LJ, Melin JA, Bol A, et al. Regional oxidative metabolism in patients after recovery from reperfused anterior myocardial infarction. Circulation 1992; 85: 9–21.
Gropler RJ, Siegel BA, Sampathkumaran K, et al. Dependence of recovery of contractile function on maintenance of oxidative metabolism after myocardial infarction. J Am Coll Cardiol 1992; 19: 989–97.
Supported in part by National Institues of Health grant RO1 HL4107-01 “PET in Myocardial Infarction.” Completed under the tenure of an established investigatiorship of the American Heart Association (M.S.).
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Hicks, R.J., Melon, P., Kalff, V. et al. Metabolic imaging by positron emission tomography early after myocardial infarction as a predictor of recovery of myocardial function after reperfusion. J Nucl Cardiol 1, 124–137 (1994). https://doi.org/10.1007/BF02984084
- positron emission tomography
- myocardial infarction