TY - JOUR
T1 - Regional cardiac adrenergic function using I-123 meta-iodobenzylguanidine tomographic imaging after acute myocardial infarction
AU - McGhie, A. Iain
AU - Corbett, James R.
AU - Akers, Marvin S.
AU - Kulkarni, Padmakur
AU - Sills, Michael N.
AU - Kremers, Mark
AU - Buja, L. Maximilian
AU - Durant-Reville, Marc
AU - Parkey, Robert W.
AU - Willerson, James T.
N1 - Funding Information:
From the Departments of Internal Medicine (Cardiology Division), Pathology, and Radiology (Nuclear Cardiology Division), at the University of Texas SouthwesternM edical Center in Dallas, Texas and the University of Texas Medical School and Texas Heart Institute in Houston, Texas. This study was supported in part by the National Heart, Lung, and Blood Institute Ischemic SCOR HL17669, Bethesda,M ary-land and the Moss Heart Fund, Dallas, Texas. Dr. A. Iain McGhie was a recipient of a Royal College of Physicianso f Edinburgh/Glaxo 1987-88 Traveling Fellowship. Manuscript receivedA ugust 21, 1990;r evised manuscript received and acceptedO ctober 1, 1990.
PY - 1991/2/1
Y1 - 1991/2/1
N2 - The effect of acute myocardial infarction (AMI) on regional cardiac adrenergic function was studied in 27 patients mean ± standard deviation 10 ± 4 days after AMI. Regional adrenergk function was evaluated noninvasively with I-123 meta-iodobenzylguanidine (MIBG) using a dedicated 3-detector tomograph. Four hours after its administration, there was reduced MIBG uptake in the region of infarction, 0.38 ± 0.31 counts/pixel/mCi × 103 compared with 0.60 ± 0.30 counts/pixel/mCi × 103 and 0.92 ± 0.35 counts/pixel/mCi × 103 in the zones bordering and distant from the infarct area, respectively, p < 0.001. In all patients, the area of reduced MIBG uptake after 4 hours was more extensive than the associated thallium-201 perfusion defect with defect scores of 52 ± 22 and 23 ± 18%, respectively, p < 0.001. After anterior wall AMI, the 4-hour MIBG defect score was 70 ± 13% and the degree of mismatch between myocardial perfusion and MIBG uptake was 30 ± 9% compared with 39 ± 17 and 21 ± 17% after inferior AMI, p < 0.001 and p = 0.016, respectively. The 4-hour MIBG defect score correlated inversely with the predischarge left ventricular ejection fraction, r = -0.73, p < 0.001. Patients with ventricular arrhythmia of ≥1 ventricular premature complexes per hour, paired ventricular premature complexes or ventricular tachycardia detected during the late hospital phase had higher 4-hour MIBG defect scores, 62.5 ± 15.0%, than patients with no detectable complex ventricular ectopic activity and a ventricular premature complex frequency of <1 per hour, 44.6 ± 23.4%, p = 0.036. These data suggest that after acute AMI in humans (1) the abnormality in adrenergic function is more extensive than the associated abnormality in myocardial perfusion; (2) anterior wall AMI is associated with greater disruption of cardiac adrenergic function than other infarcts; (3) the severity of cardiac adrenergic dysfunction correlates with the degree of left ventricular dysfunction; and (4) the abnormality in regional adrenergic function may be associated with the presence of ventricular ectopic activity after AMI.
AB - The effect of acute myocardial infarction (AMI) on regional cardiac adrenergic function was studied in 27 patients mean ± standard deviation 10 ± 4 days after AMI. Regional adrenergk function was evaluated noninvasively with I-123 meta-iodobenzylguanidine (MIBG) using a dedicated 3-detector tomograph. Four hours after its administration, there was reduced MIBG uptake in the region of infarction, 0.38 ± 0.31 counts/pixel/mCi × 103 compared with 0.60 ± 0.30 counts/pixel/mCi × 103 and 0.92 ± 0.35 counts/pixel/mCi × 103 in the zones bordering and distant from the infarct area, respectively, p < 0.001. In all patients, the area of reduced MIBG uptake after 4 hours was more extensive than the associated thallium-201 perfusion defect with defect scores of 52 ± 22 and 23 ± 18%, respectively, p < 0.001. After anterior wall AMI, the 4-hour MIBG defect score was 70 ± 13% and the degree of mismatch between myocardial perfusion and MIBG uptake was 30 ± 9% compared with 39 ± 17 and 21 ± 17% after inferior AMI, p < 0.001 and p = 0.016, respectively. The 4-hour MIBG defect score correlated inversely with the predischarge left ventricular ejection fraction, r = -0.73, p < 0.001. Patients with ventricular arrhythmia of ≥1 ventricular premature complexes per hour, paired ventricular premature complexes or ventricular tachycardia detected during the late hospital phase had higher 4-hour MIBG defect scores, 62.5 ± 15.0%, than patients with no detectable complex ventricular ectopic activity and a ventricular premature complex frequency of <1 per hour, 44.6 ± 23.4%, p = 0.036. These data suggest that after acute AMI in humans (1) the abnormality in adrenergic function is more extensive than the associated abnormality in myocardial perfusion; (2) anterior wall AMI is associated with greater disruption of cardiac adrenergic function than other infarcts; (3) the severity of cardiac adrenergic dysfunction correlates with the degree of left ventricular dysfunction; and (4) the abnormality in regional adrenergic function may be associated with the presence of ventricular ectopic activity after AMI.
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U2 - 10.1016/0002-9149(91)90552-V
DO - 10.1016/0002-9149(91)90552-V
M3 - Article
C2 - 1990785
AN - SCOPUS:0026033725
SN - 0002-9149
VL - 67
SP - 236
EP - 242
JO - The American journal of cardiology
JF - The American journal of cardiology
IS - 4
ER -