Abnormal Sympathetic Innervation of Viable Myocardium and the Substrate of Ventricular Tachycardia After Myocardial Infarction

Sasano, Tetsuo; Abraham, M. Roselle; Chang, Kuan Cheng; Ashikaga, Hiroshi; Mills, Kevin J.; Holt, Daniel P.; Hilton, John; Nekolla, Stephan G.; Dong, Jun; Lardo, Albert C.; Halperin, Henry R.; Dannals, Robert F.; Marbán, Eduardo; Bengel, Frank M.

doi:10.1016/j.jacc.2008.02.062

Cited by 159 publications

(117 citation statements)

References 29 publications

Supporting

Mentioning

114

Contrasting

Unclassified

Order By: Relevance

“…Furthermore, the postsynaptic effects of sympathetic HA have been found to be positively related to the firing activities of sympathetic nerves (19). The overactivation of cardiac sympathetic nerves in ischemic hearts, as reported in previous studies, further correlates with ischemiainduced ventricular arrhythmias (11)(12)(13)21,22). Therefore, it is rational to speculate that sympathetic HA, in addition to norepinephrine (NE), is also released and plays certain pathophysiological roles in ischemia-induced ventricular arrhythmias.…”

mentioning

confidence: 74%

Arrhythmogenic Effect of Sympathetic Histamine in Mouse Hearts Subjected to Acute Ischemia

et al. 2011

Mol Med

View full text Add to dashboard Cite

mentioning

confidence: 74%

Arrhythmogenic Effect of Sympathetic Histamine in Mouse Hearts Subjected to Acute Ischemia

et al. 2011

Mol Med

View full text Add to dashboard Cite

“…15,16 Indeed, in dogs, the induction of sustained ventricular tachycardia after myocardial infarction has been shown to be associated with a larger area of myocardial perfusion-innervation mismatch as assessed by [13N]-ammonia and [11C]-epinephrine positron emission tomography. 17 Abidov et al were the first to report on the prognostic significance of the HR change after adenosine infusion. 18 In their study, the hemodynamic response of 3,444 patients who underwent adenosine MPI was assessed.…”

mentioning

confidence: 99%

Heart rate response during vasodilator stress myocardial perfusion imaging: Mechanisms and implications

Hage

Iskandrian

2010

Journal of Nuclear Cardiology

View full text Add to dashboard Cite

See related article, pp. 617-624Myocardial perfusion imaging (MPI) using adenosine, dipyridamole, or regadenoson (a selective A 2A receptor agonist) is an established method for detecting coronary artery disease (CAD) and risk stratification. 1 In high-risk populations, as in those with diabetes mellitus (DM) or chronic kidney disease, MPI has been shown to be a powerful predictor of risk, but nevertheless, patients with normal myocardial perfusion are at higher risk than those without DM or chronic kidney disease. 2,3 Thus, there continues to be a need to extract more useful prognostic data from stress MPI especially in high-risk populations.A blunted heart rate (HR) response to exercise stress has been known to be an independent predictor of poor outcome and is used clinically in conjunction with other prognostic variables such as perfusion defects, left ventricular (LV) ejection fraction (EF) and volumes, exercise time, and symptoms during exercise to derive an overall assessment of risk in a particular patient. 4 In patients undergoing stress testing, for one reason or another, with adenosine or regadenoson (and dipyridamole, which acts indirectly by increasing interstitial levels of endogenous adenosine), there is a modest increase in HR and a modest decrease in blood pressure (BP). The increase in HR has been traditionally attributed to a reflex response to the vasodilatory effect on the systemic circulation and the resultant increase in sympathetic discharge. 5,6 The true mechanism of HR increase, however, is more complicated and involves direct stimulation of the sympathetic nervous system. 7 The administration of adenosine as a bolus, as done for the interruption of supra-ventricular tachycardias, has a negative chronotropic effect on the atrio-ventricular node via stimulation of the A1 receptor. This is in contradistinction to its effect on the A 2A receptor when given as an infusion in stress MPI studies where it induces an increase in HR. 5,8 The development of selective A 2A receptor agonists (such as regadenoson) has allowed for the dissection of the effects of adenosine on the multiple receptors. A well-done pivotal study in rats by Dhalla et al 7 that used regadenoson in combination with a selective A 2A receptor antagonist, B-blocker, a ganglionic blocker (to block the sympathetic nervous system), and a direct vasodilator (nitroprusside) demonstrated the dissociation of tachycardia and hypotension (secondary to peripheral vasodilation) responses to regadenoson. This and other data (reviewed in Ref. 9 ) confirm that A 2A receptor agonists cause a direct stimulation of the autonomic nervous system, which results in sinus tachycardia independent of the baroreflex mechanism. Thus, the change in HR in response to A 2A receptor agonists can be used to evaluate autonomic function.In order to evaluate the HR response to adenosine and regadenoson in relation to DM (since there is a high prevalence of autonomic dysfunction in patients with DM), we used data from the ADenoscan Versus RegAdenosoN Comparativ...

show abstract

“…35 In addition to global cardiac sympathetic activity assessed with 123 I-mIBG scintigraphy, there is evidence that, in ischemic HF, regional innervation/perfusion mismatch with a larger defect size on 123 I-mIBG SPECT than on myocardial perfusion imaging SPECT predisposes to ventricular arrhythmias. [36][37][38] In a large prospective study in 116 CHF patients, eligible for ICD implantation for both primary and secondary prevention of sudden cardiac death (SCD), ¹²³I-mIBG SPECT was shown to be an independent predictor of appropriate ICD therapy and cardiac death. 39 The cumulative incidence of appropriate ICD therapy during 3 years of follow-up was significantly higher when a relatively large ¹²³I-mIBG SPECT defect (median summed score ≥ 26) was present.…”

Section: Review Articlementioning

confidence: 99%

The use of Cardiac 123I-mIBG Scintigraphy in Clinical Practice: The Necessity to Standardize!

Rocha¹,

Alves²,

Verschure³

et al. 2017

International Journal of Cardiovascular Sciences

View full text Add to dashboard Cite

show abstract

Abnormal Sympathetic Innervation of Viable Myocardium and the Substrate of Ventricular Tachycardia After Myocardial Infarction

Abstract: 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.

Cited by 159 publications

References 29 publications

Arrhythmogenic Effect of Sympathetic Histamine in Mouse Hearts Subjected to Acute Ischemia

Arrhythmogenic Effect of Sympathetic Histamine in Mouse Hearts Subjected to Acute Ischemia

Heart rate response during vasodilator stress myocardial perfusion imaging: Mechanisms and implications

The use of Cardiac 123I-mIBG Scintigraphy in Clinical Practice: The Necessity to Standardize!

Contact Info

Product

Resources

About