Metoprolol-Induced Changes in Myocardial 123I-Metaiodobenzylguanidine Uptake in Parkinson’s Disease
To the Editor:
In the November 14, 2000, issue of Circulation, de Milliano et al1 presented an interesting case of improved cardiac uptake of the radioiodinated norepinephrine analogue 123I-metaiodobenzylguanidine (MIBG) after administration of metoprolol for symptomatic orthostatic hypotension in a patient diagnosed with Parkinson’s disease. The authors attributed this finding to “restoration of functional nerve endings in the myocardium with metoprolol.” They went on to state, “MIBG is a structural analogue of norepinephrine and follows the same metabolic pathways as norepinephrine.”
This is not completely so. MIBG is indeed a norepinephrine analogue. It traces the uptake-1 transport for norepinephrine in the (presynaptic) sympathetic nerve terminals and subsequent vesicular storage.2 It also undergoes nonspecific binding (ie, nonneuronal, uptake-2 mechanism) in the myocardium. Importantly, this is where MIBG stops acting like norepinephrine. It is not metabolized by catechol-O-methyltransferase or monoamine oxidase. The improved uptake observed presumably relates to an indirect increase in uptake-1 mechanism after administration of metoprolol.
de Milliano PAR, van Eck-Smit BLF, de Groot AC, et al. Metoprolol-induced changes in myocardial 123I-metaiodobenzylguanidine uptake in Parkinson’s disease. Circulation. 2000; 102: 2553–2554.
Wieland DM, Brown LE, Rogers WL, et al. Myocardial imaging with a radioiodinated norepinephrine storage analog. J Nucl Med. 1981; 22: 22–31.