Carbon-11 hydroxyephedrine with positron emission tomography for serial assessment of cardiac adrenergic neuronal function after acute myocardial infarction in humans.
OBJECTIVE
The purpose of this study was to assess the extent and reversibility of neuronal abnormalities in patients with an acute myocardial infarction.


BACKGROUND
Previous experimental studies have described ischemic injury to sympathetic neurons exceeding the area of myocardial necrosis. Carbon-11 (C-11) hydroxyephedrine (HED) is a norepinephrine analogue that can be used for the noninvasive evaluation of neuronal integrity using positron emission tomography.


METHODS
We studied 14 volunteers and 16 patients experiencing a first acute myocardial infarction. Positron emission tomographic imaging was used to quantitatively compare regional perfusion, as assessed with nitrogen-13 ammonia, with myocardial retention of C-11 hydroxyephedrine early after myocardial infarction as well as > 6 months after the acute event.


RESULTS
C-11 hydroxyephedrine and flow images demonstrated homogeneous tracer retention in volunteers but were abnormal in all patients. C-11 hydroxyephedrine abnormalities were more extensive than those for blood flow assessed by semiquantitative polar map analysis (31 +/- 15% vs. 17 +/- 17% left ventricle; p < 0.05), particularly in five patients with non-Q wave infarction (31 +/- 11% vs. 3.5 +/- 2.5% left ventricle; p = 0.008). Eleven patients with Q wave infarction had matched defects (28 +/- 17% vs. 21 +/- 17% left ventricle; p = NS). C-11 hydroxyephedrine tissue retention fraction was quantified in three tissue zones: zone 1 (abnormal rest flow) had retention fraction 0.037 +/- 0.022-min; zone 2 (normal rest flow but decreased carbon-11 hydroxyephedrine retention) had retention fraction 0.068 +/- .034-min, and zone 3 (normal flow and carbon-11 hydroxyephedrine retention) had retention fraction 0.087 +/- 0.041-min (p = 0.0004). Follow-up studies at 8 +/- 3 months in eight patients revealed no change in extent of abnormalities or absolute tissue tracer retention in infarct and peri-infarct territories.


CONCLUSIONS
The results of abnormal regional sympathetic innervation in patients with infarction confirm previous experimental data and suggest persistent neuronal damage in infarct and peri-infarct territories, without evidence of reinnervation of reversibly injured myocardium.
Allman
K C
KC
Department of Internal Medicine, University of Michigan, Ann Arbor.
Wieland
D M
DM
Muzik
O
O
Degrado
T R
TR
Wolfe
E R
ER
Schwaiger
M
M
D000320:Adrenergic Fibers / Q000502:physiology*; D000328:Adult; D000368:Aged; D001342:Autonomic Nervous System Diseases / Q000000981:diagnostic imaging* / Q000209:etiology; D002250:Carbon Radioisotopes; D016022:Case-Control Studies; D003326:Coronary Circulation; D004809:Ephedrine / Q000031:analogs & derivatives*; D005260:Female; D005500:Follow-Up Studies; D006321:Heart / Q000000981:diagnostic imaging* / Q000294:innervation / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000150:complications / Q000000981:diagnostic imaging* / Q000503:physiopathology; D013566:Sympathomimetics; D014055:Tomography, Emission-Computed
D002250:Carbon Radioisotopes; D013566:Sympathomimetics; C065363:3-hydroxyephedrine; D004809:Ephedrine