Clinical Application of I-123 MIBG Cardiac Imaging.
- Author:
Do Young KANG
1
Author Information
1. School of Nuclear Medicine, College of Medicine, Dong-A University, Busan, Korea. dykang@daunet.donga.ac.kr
- Publication Type:Review
- Keywords:
I-123 MIBG;
Cardiac Imaging;
Autonomic sympathetic dysfunction;
Cardiac neurotransmission
- MeSH:
3-Iodobenzylguanidine*;
Adrenergic Neurons;
Arrhythmias, Cardiac;
Cardiomyopathies;
Dementia;
Guanethidine;
Heart;
Heart Diseases;
Heart Failure;
Humans;
Lewy Bodies;
Myocardial Ischemia;
Neurodegenerative Diseases;
Neurons;
Neurotransmitter Agents;
Norepinephrine;
Parkinson Disease;
Prognosis;
Synaptic Transmission;
Tachycardia, Ventricular;
Tomography, Emission-Computed, Single-Photon;
Ventricular Dysfunction
- From:Korean Journal of Nuclear Medicine
2004;38(5):331-337
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Cardiac neurotransmission imaging allows in vivo assessment of presynaptic reuptake, neurotransmitter storage and postsynaptic receptors. Among the various neurotransmitter, I-123 MIBG is most available and relatively well- established. Metaiodobenzylguanidine (MIBG) is an analogue of the false neurotransmitter guanethidine. It is taken up to adrenergic neurons by uptake-1 mechanism as same as norepinephrine. As tagged with I-123, it can be used to image sympathetic function in various organs including heart with planar or SPECT techniques. I-123 MIBG imaging has a unique advantage to evaluate myocardial neuronal activity in which the heart has no significant structural abnormality or even no functional derangement measured with other conventional examination. In patients with cardiomyopathy and heart failure, this imaging has most sensitive technique to predict prognosis and treatment response of betablocker or ACE inhibitor. In diabetic patients, it allow very early detection of autonomic neuropathy. In patients with dangerous arrhythmia such as ventricular tachycardia or fibrillation, MIBG imaging may be only an abnormal result among various exams. In patients with ischemic heart disease, sympathetic derangement may be used as the method of risk stratification. In heart transplanted patients, sympathetic reinnervation is well evaluated. Adriamycin-induced cardiotoxicity is detected earlier than ventricular dysfunction with sympathetic dysfunction. Neurodegenerative disorder such as Parkinson's disease or dementia with Lewy bodies has also cardiac sympathetic dysfunction. Noninvasive assessment of cardiac sympathetic nerve activity with I-123 MIBG imaging may be improve understanding of the pathophysiology of cardiac disease and make a contribution to predict survival and therapy efficacy.
