Objective—To compare the feasibility and repeatability of tissue Doppler imaging (TDI) for quantification of radial left ventricular (LV) velocity and deformation from different imaging planes and to correlate cardiac event timing data obtained by TDI to M-mode and pulsed-wave Doppler-derived time intervals in horses.
Animals—10 healthy adult horses.
Procedures—Repeated echocardiography was performed by 2 observers from right and left parasternal short-axis views at papillary muscle and chordal levels. The TDI measurements of systolic and diastolic velocity, strain rate, strain peak values, and timing were performed in 8 LV wall segments (LV free wall and interventricular septum from right parasternal views; left and right region of LV wall from left parasternal views). The inter- and intraobserver within- and between-day variability and measurement variability were assessed. The correlation between TDI-based measurements and M-mode and pulsed-wave Doppler-based time measurements was calculated.
Results—TDI measurements of velocity, strain rate, and strain were feasible in each horse, although deformation could often not be measured in the LV free wall. Systolic and diastolic time intervals could be determined with low to moderate variability, whereas peak amplitude variability ranged from low to high. The TDI-based time measurements were significantly correlated to M-mode and pulsed-wave Doppler measurements.
Conclusions and Clinical Relevance—TDI measurements of radial LV velocity and deformation were feasible with low to moderate variability in 8 LV segments. These measurements can be used for evaluating LV function in further clinical studies.
Objective—To investigate effects of IV administration of propafenone for naturally occurring and experimentally induced chronic atrial fibrillation in horses.
Animals—2 horses with naturally occurring atrial fibrillation and 4 horses with pacing-induced atrial fibrillation.
Procedures—Horses received a bolus of propafenone (2 mg/kg, IV over 15 minutes). If atrial fibrillation persisted after 20 minutes, a continuous infusion of propafenone (7 μg/kg/min) was given for 120 minutes. Before, during, and after treatment, plasma propafenone concentrations, hematologic and serum biochemical values, and electolyte concentrations analyses were determined and clinical signs were monitored. Surface ECGs were recorded. If propafenone treatment failed, quinidine sulfate was administered.
Results—Bolus and continuous infusion induced minimal adverse effects. During the 15-minute bolus administration, a slight increase in heart rate was observed and horses appeared more sensitive to external stimuli. Throughout treatment, no significant changes were observed in respiratory rate, QRS or corrected QT duration, or results of hematologic analyses. Although a significant increase in F-wave interval and atrial fibrillation cycle length was observed and plasma propafenone concentrations (569 to 1,268 ng/mL) reached the human therapeutic range (64 to 1,044 ng/mL), none of the horses cardioverted to sinus rhythm. Sinus rhythm could be restored in all horses via standard oral administration of quinidine.
Conclusions and Clinical Relevance—A slow IV bolus of 2 mg of propafenone/kg followed by a continuous infusion of 7 μg/kg/min over 2 hours was not an effective treatment for chronic atrial fibrillation in horses.
Objective—To determine the clinical effects and pharmacokinetics of amiodarone after single doses of 5 mg/kg administered orally or intravenously.
Animals—6 healthy adult horses.
Procedure—In a cross over study, clinical signs and electrocardiographic variables were monitored and plasma and urine samples were collected. A liquid chromatography–mass spectrometry method was used to determine the percentage of protein binding and to measure plasma and urine concentrations of amiodarone and the active metabolite desethylamiodarone.
Results—No adverse clinical signs were observed. After IV administration, median terminal elimination half-lives of amiodarone and desethylamiodarone were 51.1 and 75.3 hours, respectively. Clearance was 0.35 L/kg•h, and the apparent volume of distribution for amiodarone was 31.1 L/kg. The peak plasma desethylamiodarone concentration of 0.08 μg/mL was attained 2.7 hours after IV administration. Neither parent drug nor metabolite was detected in urine, and protein binding of amiodarone was 96%. After oral administration of amiodarone, absorption of amiodarone was slow and variable; bioavailability ranged from 6.0% to 33.7%. The peak plasma amiodarone concentration of 0.14 μg/mL was attained 7.0 hours after oral administration and the peak plasma desethylamiodarone concentration of 0.03 μg/mL was attained 8.0 hours after administration. Median elimination half-lives of amiodarone and desethylamiodarone were 24.1 and 58.6 hours, respectively.
Conclusion and Clinical Relevance—Results indicate that the pharmacokinetic distribution of amiodarone is multicompartmental. This information is useful for determining treatment regimens for horses with arrythmias. Amiodarone has low bioavailability after oral administration, does not undergo renal excretion, and is highly protein-bound in horses.