Key result
Sympathetic hyperinnervation in dogs with myocardial infarction and atrioventricular block induced paroxysmal atrial fibrillation and tachycardia in 100% of experimental dogs vs 0% of controls.
Why the study?
Does the induction of sympathetic hyperinnervation in dogs with myocardial infarction and complete atrioventricular block create a model of paroxysmal atrial fibrillation and tachycardia?
Does the induction of sympathetic hyperinnervation in dogs with myocardial infarction and complete atrioventricular block create a model of paroxysmal atrial fibrillation and tachycardia?
Absolute Event Rate: 100% vs 0%
Induction of nerve sprouting and sympathetic hyperinnervation in dogs with complete atrioventricular block and myocardial infarction creates a high-yield model for studying paroxysmal atrial fibrillation and tachycardia.
Provides high-yield canine model for autonomic AF research; leaves open human translation.
Both autonomic nerve activity and electrical remodeling are important in atrial arrhythmogenesis. Therefore, dogs with sympathetic hyperinnervation, myocardial infarction (MI), and complete atrioventricular block (CAVB) may have a high incidence of atrial arrhythmias. We studied eight dogs (experimental group) with MI, CAVB, and sympathetic hyperinnervation induced either by nerve growth factor infusion (n = 4 dogs) or subthreshold electrical stimulation (n = 4 dogs) of the left stellate ganglion. Cardiac rhythm was continuously monitored by a Data Sciences International transmitter for 48 (SD 27) days. Three normal control dogs were also monitored. Six additional normal dogs were used for histology control. Paroxysmal atrial fibrillation (PAF) and paroxysmal atrial tachycardia (PAT) were documented in all dogs in the experimental group, with an average of 3.8 (SD 3) episodes/day, including 1.3 (SD 1.6) episodes of PAF and 2.5 (SD 2.2) episodes of PAT. The duration averaged 298 (SD 745) s (range, 7-4,000 s). There was a circadian pattern of arrhythmia onset (P < 0.01). Of 576 episodes of PAF and PAT, 236 (41%) episodes occurred during either sustained or nonsustained ventricular tachycardia (VT). Among these 236 episodes, 53% started before VT, whereas 47% started after the onset of VT. Normal dogs did not have either PAF or PAT. The hearts from the experimental group had a higher density of nerve structures immunopositive (P < 0.01) for three different nerve specific markers in both right and left atria than those of the control dogs. We conclude that the induction of nerve sprouting and sympathetic hyperinnervation in dogs with CAVB and MI creates a high yield model of PAF and PAT.
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Swissa et al. (2005) studied Paroxysmal atrial fibrillation and paroxysmal atrial tachycardia (n=17). Sympathetic hyperinnervation, myocardial infarction, and complete atrioventricular block vs. Normal control dogs was evaluated on Incidence of paroxysmal atrial fibrillation and paroxysmal atrial tachycardia. Sympathetic hyperinnervation in dogs with myocardial infarction and atrioventricular block induced paroxysmal atrial fibrillation and tachycardia in 100% of experimental dogs vs 0% of controls.
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