Effects of canine myocardial infarction on sympathetic efferent neuronal function: Scintigraphic and electrophysiologic correlates

Newman, David; Munoz, Luisa; Chin, Michael C.; Franz, Michael R.; Herre, John M.; Scheinman, Melvin M.; Botvinick, Elias H.; Dae, Michael W.

doi:10.1016/0002-8703(93)90661-r

Cited by 16 publications

(3 citation statements)

References 24 publications

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“…Our findings in CCC are concordant with other experimental and clinical studies that support the notion that regional myocardial sympathetic denervation is a mechanism for triggering ventricular arrhythmia in several forms of heart disease (12)(13)(14). Regional cardiac sympathetic denervation documented by 123 I-MIBG scintigraphy has been described in several other clinical settings characterized by a high density of ventricular arrhythmias and sudden death, such as arrhythmogenic right ventricular cardiomyopathy, congenital long QT syndrome, Brugada syndrome, and cardiomyopathy of other etiology (15)(16)(17).…”

Section: I-mibg Uptake Derangementssupporting

confidence: 91%

Sustained Ventricular Tachycardia Is Associated with Regional Myocardial Sympathetic Denervation Assessed with ¹²³I-Metaiodobenzylguanidine in Chronic Chagas Cardiomyopathy

Miranda¹,

Figueiredo²,

Maciel³

et al. 2011

J Nucl Med

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Cardiac sympathetic denervation and ventricular arrhythmia are frequently observed in chronic Chagas cardiomyopathy (CCC). This study quantitatively evaluated the association between cardiac sympathetic denervation and sustained ventricular tachycardia (SVT) in patients with CCC. Methods: We prospectively investigated patients with CCC and left ventricular ejection fraction (LVEF) greater than 35% with SVT (SVT group: n 5 15; mean age 6 SD, 61 6 8 y; LVEF, 51% 6 8%) and patients without SVT (non-SVT group: n 5 11; mean age 6 SD, 55 6 10 y; LVEF, 57% 6 10%). Patients underwent myocardial scintigraphy with 123 I-metaiodobenzylguanidine ( 123 I-MIBG) for the evaluation of sympathetic innervation and resting perfusion with 99m Tc-methoxyisobutylisonitrile ( 99m Tc-MIBI) for the evaluation of myocardial viability. A visual semiquantitative score was attributed for regional uptake of each radiotracer using a 17-segment left ventricular segmentation model (0, normal; 4, absence of uptake). A mismatch defect was defined as occurring in segments with a 99m Tc-MIBI uptake score of 0 or 1 and a 123 I-MIBG score of 2 or more. Results: Compared with the non-SVT group, the SVT group had a similar 99m Tc-MIBI summed score (6.9 6 7.5 vs. 4.4 6 5.2, respectively, P 5 0.69) but a higher 123 I-MIBG summed score (10.9 6 7.8 vs. 22.4 6 9.5, respectively, P 5 0.007) and a higher number of mismatch defects per patient (2.0 6 2.2 vs. 7.1 6 2.0, respectively, P , 0.0001). The presence of more than 3 mismatch defects was strongly associated with the presence of SVT (93% sensitivity, 82% specificity; P 5 0.0002). Conclusion: In CCC, the amount of sympathetically denervated viable myocardium is associated with the occurrence of SVT. Myocardial sympathetic denervation may participate in triggering malignant ventricular arrhythmia in CCC patients with relatively well-preserved ventricular function.

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Section: I-mibg Uptake Derangementssupporting

confidence: 91%

Sustained Ventricular Tachycardia Is Associated with Regional Myocardial Sympathetic Denervation Assessed with ¹²³I-Metaiodobenzylguanidine in Chronic Chagas Cardiomyopathy

Miranda¹,

Figueiredo²,

Maciel³

et al. 2011

J Nucl Med

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“…Subtraction of the area of perfusion defect at rest detected by perfusion study from the entire extent of defect detected by the new test at rest should allow detection of the reversible ischaemic territory. It has been shown that the uptake of iodine-123 metaiodobenzylguanidine (MIBG) is significantly reduced in the areas of myocardial infarction [9,10,11], and also in areas of acute and chronic ischaemia in canine experiments [12,13]. A decrease in MIBG uptake represents the loss of integrity of post-ganglionic, presynaptic neurones.…”

Section: Introductionmentioning

confidence: 99%

Concordance between rest MIBG and exercise tetrofosmin defects: possible use of rest MIBG imaging as a marker of reversible ischaemia

et al. 2001

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Perfusion imaging combined with pharmacological stress is the study of choice in patients with ischaemic heart disease who are incapable of exercising. Some medical conditions, however, can preclude the use of pharmacological stress. In these particular situations, availability of a diagnostic test which allows for the assessment of ischaemic territory at rest would be desirable. With the purpose of providing a marker of reversible ischaemia, we evaluated myocardial iodine-123 metaiodobenzylguanidine (MIBG) uptake in regions with fixed and reversible defects defined by exercise/rest perfusion study. Fifty-four male patients with ischaemic heart disease and previous myocardial infarction were studied by means of exercise/rest tetrofosmin and MIBG single-photon emission tomography (SPET). Regional tracer uptake was quantified and expressed as a percentage of maximum peak activity. Areas with denervated but perfused myocardium and areas with ischaemic myocardium were calculated. Regions with<75% of peak activity in the exercise perfusion study were divided into two groups according to whether the increase in peak activity in the respective rest study was >10% (reversible regional defect) or <10% (fixed regional defect). These percentages were compared with the percentages of the innervation study. The area of the innervation defect was significantly larger when the perfusion defect was reversible than when it was fixed. In regions with reversible perfusion defects, the size of the area of denervated but perfused myocardium was similar to the size of the area of ischaemic myocardium. In regions with reversible defects, the percentage of myocardial MIBG uptake was not significantly different from the percentage of tetrofosmin uptake at exercise, while it was significantly lower than the percentage of tetrofosmin uptake at rest. In regions with fixed defects, the percentage of myocardial MIBG uptake was significantly lower than the percentage of tetrofosmin uptake at exercise and at rest. In patients who developed angina during exercise test, the area of denervated but perfused myocardium was significantly larger than in patients without angina (4.1+/-2.4 vs 3.4+/-2.5, P=0.02). The same trend was observed with regard to the size of the innervation defect (8.6+/-2.4 vs 5.7+/-2.2, P=0.02). It is concluded that when the use of pharmacological stress is not possible in patients incapable of exercising, rest studies with MIBG combined with rest myocardial perfusion studies may be useful as a marker of reversible ischaemia.

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“…Thus, the infarcted zone is surrounded by viable myocardium that has lost its adrenergic innervation. This can be demonstrated both with electrophysiologic techniques (Kammerling et al ., 1987; Newman et al ., 1993), with positron emission tomography using C‐11 hydroxyephedrine (Allman et al ., 1993) or with single‐photon emission computed tomography (SPECT) using radiolabelled I 123 ‐metaiodobentzylguanidine (MIBG) (Kline et al ., 1981; Wieland et al ., 1981) – a guanethidine analogue sharing the uptake, storage and release mechanisms of norepinephrine. Adrenergic denervation per se or the resulting inhomogeneity of cardiac adrenergic innervation have been suggested to increase the risk of ventricular arrhythmias (Inoue & Zipes, 1987; Herre et al ., 1988).…”

Section: Introductionmentioning

confidence: 99%

Cardiac adrenergic innervation within the first 3 months after acute myocardial infarction

Simula

Lakka

Kuikka

et al. 2000

Clinical Physiology

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It is widely accepted that myocardial infarction results in adrenergic denervation of the infarcted and peri-infarcted myocardium. On the contrary, the concept of re-innervation of adrenergic nerve fibres is less well established. Although there is evidence of partial re-innervation occuring several months after myocardial infarction, the extent and time scale of re-innervation are only poorly known. In this study we investigated changes in cardiac adrenergic innervation and myocardial perfusion during the early convalescence period (the first 3 months) after an acute myocardial infarction. Single-photon emission computed tomographic imaging was conducted in 15 men 1 week and 3 months after an acute myocardial infarction with I123-metaiodobentzylguanidine (MIBG) and Tc99m-sestamibi (MIBI) to determine the extent of adrenergic denervation and impaired perfusion, respectively. A MIBG and MIBI defect was determined as regional uptake

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Effects of canine myocardial infarction on sympathetic efferent neuronal function: Scintigraphic and electrophysiologic correlates

Cited by 16 publications

References 24 publications

Sustained Ventricular Tachycardia Is Associated with Regional Myocardial Sympathetic Denervation Assessed with ¹²³I-Metaiodobenzylguanidine in Chronic Chagas Cardiomyopathy

Sustained Ventricular Tachycardia Is Associated with Regional Myocardial Sympathetic Denervation Assessed with ¹²³I-Metaiodobenzylguanidine in Chronic Chagas Cardiomyopathy

Concordance between rest MIBG and exercise tetrofosmin defects: possible use of rest MIBG imaging as a marker of reversible ischaemia

Cardiac adrenergic innervation within the first 3 months after acute myocardial infarction

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Effects of canine myocardial infarction on sympathetic efferent neuronal function: Scintigraphic and electrophysiologic correlates

Cited by 16 publications

References 24 publications

Sustained Ventricular Tachycardia Is Associated with Regional Myocardial Sympathetic Denervation Assessed with 123I-Metaiodobenzylguanidine in Chronic Chagas Cardiomyopathy

Sustained Ventricular Tachycardia Is Associated with Regional Myocardial Sympathetic Denervation Assessed with 123I-Metaiodobenzylguanidine in Chronic Chagas Cardiomyopathy

Concordance between rest MIBG and exercise tetrofosmin defects: possible use of rest MIBG imaging as a marker of reversible ischaemia

Cardiac adrenergic innervation within the first 3 months after acute myocardial infarction

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Sustained Ventricular Tachycardia Is Associated with Regional Myocardial Sympathetic Denervation Assessed with ¹²³I-Metaiodobenzylguanidine in Chronic Chagas Cardiomyopathy

Sustained Ventricular Tachycardia Is Associated with Regional Myocardial Sympathetic Denervation Assessed with ¹²³I-Metaiodobenzylguanidine in Chronic Chagas Cardiomyopathy