Treatment of Atrial Fibrillation in the Horse with Intravenous Dihydroquinidine Gluconate

Gerber, H.; Chuit, P.; Schatzmann, H. J.

doi:10.1111/j.2042-3306.1971.tb04450.x

Cited by 14 publications

(8 citation statements)

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“…[1][2][3][4][6][7][8][9]14,17,[19][20][21][22][23][24][25][26][27] Quinidine sulfate is the drug of choice for conversion of horses with AF to sinus rhythm and is most successful when the duration of AF is short (less than 4 months), murmurs auscultated are less than grade III/ VI intensity, the resting heart rate is 560 beats/min, and there are no signs of congestive heart fail~re. '-~.~-ntravenous quinidine gluconate therapy 9.…”

Section: A Rhythmia Affecting Performance Inmentioning

confidence: 99%

Treatment of Atrial Fibrillation in Horses: New Perspectives

Reef

Reimer

Spencer

1995

Veterinary Internal Medicne

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Forty-one horses were treated for atrial fibrillation (AF) with 22 mg/kg quinidine sulfate via nasogastric tube every 2 hours until conversion t o sinus rhythm, a cumulative dose of 88 to 132 mg/kg had been administered in 2-hour increments, or the horse had adverse or toxic effects from the drug. Treatment intervals were prolonged t o every 6 hours if conversion had not occurred. Digoxin was administered before treatment if the horse had a fractional shortening 227% (3 horses), was prone t o tachycardia (resting heart rate 260 beats/min) (1 horse), or had a previous history of sustained tachycardia of over 100 beats/min during prior conversion (3 horses). Digoxin was administered during day 1 of quinidine sulfate treatment if the horse developed a sustained tachycardia of over 100 beats/min during treatment (1 1 horses) or on day 2 if conversion had not occurred (7 horses). Plasma quinidine concentrations within trial fibrillation (AF) is the most common ar-A rhythmia affecting performance in Conversion to sinus rhythm usually results in horses returning to their prior performance level. [1][2][3][4][6][7][8][9]14,17,[19][20][21][22][23][24][25][26][27] Quinidine sulfate is the drug of choice for conversion of horses with AF to sinus rhythm and is most successful when the duration of AF is short (less than 4 months), murmurs auscultated are less than grade III/ VI intensity, the resting heart rate is 560 beats/min, and there are no signs of congestive heart fail~re.'-~.~-ntravenous quinidine gluconate therapy 9. I 3 I 7.20-26 I has also been used successfully, particularly in horses with recent onset AF.3363'4,25-2x H orses with longer (>2 months) suspected duration of AF are less likely to convert to sinus rhythm with intravenous quinidine gluconate therapy.6 The success rate for conversion to sinus rhythm with quinidine sulfate therapy also decreases as the suspected duration of the arrhythmia increases.2 A standard treatment protocol for adult horses with AF is the administration of 10 g quinidine sulfate every 2 hours via nasogastric tube, until conversion to sinus rhythm occurs, a total dose of 40 to 60 g has been administered, or toxic signs are noIf conversion does not occur, this process can be repeated on days 2 and 3 . The use ofa test dose of 5 to 10 g quinidine sulfate before initiating treatment for AF has been r e p~r t e d .~-~.~.~~' l ' , e test dose is administered on the day preceding treatment or 2 hours before beginning treatment. If no adverse reactions are observed, quinidine sulfate therapy is continued at 10 g via nasogastric tube every 2 hours.Plasma quinidine concentration in horses peaks at 13 1 minutes after a single oral 10-g dose of quinidine sulfate (range, 45 to 180 minute^).^' The plasma-totissue distribution phase is thought to occur rapidly (within 30 minutes) in all domestic animal^.^'.^' Therefore, the administration of 10 g quinidine sulfate via nasogastric tube every 2 hours allows for stepwise titration of the drug in the horse, while monitoring carefully for adverse reac...

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Section: A Rhythmia Affecting Performance Inmentioning

confidence: 99%

Treatment of Atrial Fibrillation in Horses: New Perspectives

Reef

Reimer

Spencer

1995

Veterinary Internal Medicne

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“…In cases of sustained atrial fibrillation, conversion to normal sinus rhythm (cardioversion) is required for the horse to regain athletic performance 2,3 . Pharmacologic cardioversion, primarily with quinidine, has been practiced in horses for over 4 decades, 2–10 with efficacy approaching 85–90% 2,3,7,10 . However, quinidine is associated with frequent adverse effects ranging in severity from benign to fatal, 2,3,7,10 which has encouraged investigators to pursue alternatives to quinidine therapy to achieve cardioversion.…”

mentioning

confidence: 99%

Effect of Transvenous Electrical Cardioversion on Plasma Cardiac Troponin I Concentrations in Horses with Atrial Fibrillation

et al. 2009

Veterinary Internal Medicne

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Background: Whether electrical cardioversion of cardiac arrhythmias results in cardiomyocyte damage is unknown. Objective: To describe effect of transvenous electrical cardioversion (TVEC) on plasma cardiac troponin I (cTnI) concentration in horses.Animals: All horses presented to the Cornell University Hospital for Animals for cardioversion of atrial fibrillation between May 2006 and October 2008 were eligible for inclusion in the study. Owners of 14 horses elected for TVEC and each horse was then enrolled (16 procedures).Methods: Prospective observational study measuring concentrations of plasma cTnI before and after TVEC.Results: Median cTnI concentration increased from 0.045 ng/mL at baseline (range 0.0-0.20 ng/mL) to 0.11 ng/mL after TVEC (range 0.0-3.73 ng/mL) (P 5 .036). This increase was not associated with the number of shocks delivered, maximal energy delivered, cumulative energy delivered, chronicity of atrial fibrillation before cardioversion, or positioning of the pulmonary artery catheter.Conclusions: The increase in cTnI is unlikely to be clinically important. The increase might be correlated with persistent atrial dysfunction after TVEC, suggesting that a longer convalescent period after the procedure could be warranted.

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“…Wir applizierten CS intravenös, weil auf diesem Weg ein schneller und sicherer therapeutischer Spiegel zu erwarten ist (Deegen 1971, Gerber et al 1971, Deegen et al 1974, Neff et al 1972, Muir et al 1990, Stadler et al 1994. Wir bestimmten deshalb auch keine Chinidinplamsakonzentrationen während der Behandlung, weil wir mit der intravenösen Gabe von einer 100%-tigen Bioverfügbarkeit ausgingen.…”

Section: Diskussionunclassified