Article

Abnormal sympathetic innervation of viable myocardium and the substrate of ventricular tachycardia after myocardial infarction.

Division of Cardiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Journal of the American College of Cardiology (impact factor: 14.16). 07/2008; 51(23):2266-75. DOI:10.1016/j.jacc.2008.02.062 pp.2266-75
Source: PubMed

ABSTRACT The aim of this study was to characterize the relationship between impaired sympathetic innervation and arrhythmia with noninvasive biologic imaging in an animal model of post-infarct ventricular tachycardia (VT).
Innervation might be abnormal in the normally perfused borderzone of myocardial infarction, contributing to myocardial catecholamine overexposure and arrhythmogenic risk.
Myocardial infarction was induced by mid-left anterior descending coronary artery balloon occlusion in 11 pigs. Positron emission tomography (PET) of tissue perfusion and catecholamine uptake and storage was performed with [13N]-ammonia and [11C]-epinephrine 4 to 12 weeks later. Magnetic resonance imaging and invasive electrophysiology (electroanatomic mapping, basket catheter, VT inducibility) were performed within 1 week of PET.
When compared with a normal database of 9 healthy animals, reduced perfusion was observed in 37 +/- 7% of the left ventricle (LV). Epinephrine retention was reduced in 44 +/- 7% of LV, resulting in a perfusion/innervation mismatch of 7 +/- 4% LV. Sustained monomorphic VT was inducible in 7 of 11 animals. These animals showed a larger perfusion/innervation mismatch (10 +/- 4% vs. 4 +/- 2% LV for animals without VT; p = 0.02). Regionally, the degree of perfusion/innervation mismatch did not correlate with wall thickness or thickening but showed a significant correlation with reduced myocardial voltage (r = 0.93; p = 0.001) and with the site of earliest VT activation (chi-square 13.1; p < 0.001).
Noninvasive mapping of cardiac sympathetic nerve terminals reveals regionally impaired catecholamine uptake and storage in the normally perfused borderzone after experimental myocardial infarction. These areas might be useful to characterize the individual risk for ventricular arrhythmia.

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    Article: The role of nuclear imaging in the failing heart: myocardial blood flow, sympathetic innervation, and future applications.
    Mark J Boogers, Kenji Fukushima, Frank M Bengel, Jeroen J Bax
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    ABSTRACT: Heart failure represents a common disease affecting approximately 5 million patients in the United States. Several conditions play an important role in the development and progression of heart failure, including abnormalities in myocardial blood flow and sympathetic innervation. Nuclear imaging represents the only imaging modality with sufficient sensitivity to assess myocardial blood flow and sympathetic innervation of the failing heart. Although nuclear imaging with single-photon emission computed tomography (SPECT) is most commonly used for the evaluation of myocardial perfusion, positron emission tomography (PET) allows absolute quantification of myocardial blood flow beyond the assessment of relative myocardial perfusion. Both techniques can be used for evaluation of diagnosis, treatment options, and prognosis in heart failure patients. Besides myocardial blood flow, cardiac sympathetic innervation represents another important parameter in patients with heart failure. Currently, sympathetic nerve imaging with 123-iodine metaiodobenzylguanidine (123-I MIBG) is often used for the assessment of cardiac innervation. A large number of studies have shown that an abnormal myocardial sympathetic innervation, as assessed with 123-I MIBG imaging, is associated with increased mortality and morbidity rates in patients with heart failure. Also, cardiac 123-I MIBG imaging can be used to risk stratify patients for ventricular arrhythmias or sudden cardiac death. Furthermore, novel nuclear imaging techniques are being developed that may provide more detailed information for the detection of heart failure in an early phase as well as for monitoring the effects of new therapeutic interventions in patients with heart failure.
    Heart Failure Reviews 10/2010; 16(4):411-23. · 3.20 Impact Factor
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Keywords

11 animals
 
9 healthy animals
 
animal model
 
basket catheter
 
catecholamine uptake
 
earliest VT activation
 
experimental myocardial infarction
 
invasive electrophysiology
 
larger perfusion/innervation mismatch
 
left ventricle
 
Magnetic resonance imaging
 
mid-left anterior descending coronary artery balloon occlusion
 
myocardial catecholamine overexposure
 
noninvasive biologic imaging
 
perfused borderzone
 
perfusion/innervation mismatch
 
Positron emission tomography
 
post-infarct ventricular tachycardia
 
sympathetic innervation
 
wall thickness