Peer-reviewed veterinary case report
Rotigaptide effects on atrial fibrillation in dogs with heart failure
By Shiroshita-Takeshita, Akiko et al.·Published in Circulation·2007·Department of Medicine and Research Center, Canada·View original on PubMed →
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Original publication title: Model-dependent effects of the gap junction conduction-enhancing antiarrhythmic peptide rotigaptide (ZP123) on experimental atrial fibrillation in dogs.
- Species:
- dog
Plain-English summary
A group of dogs with heart problems and abnormal heart rhythms (atrial fibrillation) were given a new drug called rotigaptide to see if it could help. While the drug improved how well the heart's electrical signals traveled in some cases, it didn't stop the abnormal rhythms in dogs with congestive heart failure or those with rapid heartbeats. However, it did help prevent worsening of heart rhythms during episodes of reduced blood flow to the heart. Overall, rotigaptide showed promise in specific situations but wasn't effective for all heart issues.
People also search for: dog atrial fibrillation treatment · congestive heart failure in dogs · rotigaptide for dog heart problems
Abstract
BACKGROUND: Abnormal intercellular communication caused by connexin dysfunction may be involved in atrial fibrillation (AF). The present study assessed the effect of the gap junctional conduction-enhancing peptide rotigaptide on AF maintenance in substrates that result from congestive heart failure induced by 2-week ventricular tachypacing (240 bpm), atrial tachypacing (ATP; 400 bpm for 3 to 6 weeks), and isolated atrial myocardial ischemia. METHODS AND RESULTS: Electrophysiological study and epicardial mapping were performed before and after rotigaptide administration in dogs with ATP and congestive heart failure, as well as in similarly instrumented sham dogs that were not tachypaced. For atrial myocardial ischemia, dogs administered rotigaptide before myocardial ischemia were compared with no-drug myocardial ischemia controls. ATP significantly shortened the atrial effective refractory period (P=0.003) and increased AF duration (P=0.008), with AF lasting >3 hours in all 6-week ATP animals. Rotigaptide increased conduction velocity in ATP dogs slightly but significantly (P=0.04) and did not affect the effective refractory period, AF duration, or atrial vulnerability. In dogs with congestive heart failure, rotigaptide also slightly increased conduction velocity (P=0.046) but failed to prevent AF promotion. Rotigaptide had no statistically significant effects in sham dogs. Myocardial ischemia alone increased AF duration and impaired conduction (based on conduction velocity across the ischemic border and indices of conduction heterogeneity). Rotigaptide prevented myocardial ischemia-induced conduction slowing and AF duration increases. CONCLUSIONS: Rotigaptide improves conduction in various AF models but suppresses AF only for the acute ischemia substrate. These results define the atrial antiarrhythmic profile of a mechanistically novel antiarrhythmic drug and suggest that gap junction dysfunction may be more important in ischemic AF than in ATP remodeling or congestive heart failure substrates.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/17224477/