Results suggest that a complete evaluation, including a high-speed treadmill examination, should be conducted in horses with poor performance, regardless or whether horses do or do not have a history of abnormal respiratory noises and particularly if the horses have grade-II or -III left laryngeal hemiplegia.

Murmurs and arrhythmias are commonly detected in equine athletes. Assessing the relevance of these cardiovascular abnormalities in the performance horse can be challenging. Determining the impact of a cardiovascular disorder on performance, life expectancy, horse and rider or driver safety relative to the owner's future expectations is paramount. A comprehensive assessment of the cardiovascular abnormality detected is essential to determine its severity and achieve these aims. This consensus statement presents a general approach to the assessment of cardiovascular abnormalities, followed by a discussion of the common murmurs and arrhythmias. The description, diagnosis, evaluation, and prognosis are considered for each cardiovascular abnormality. The recommendations presented herein are based on available literature and a consensus of the panelists. While the majority of horses with cardiovascular abnormalities have a useful performance life, periodic reexaminations are indicated for those with clinically relevant cardiovascular disease. Horses with pulmonary hypertension, CHF, or complex ventricular arrhythmias should not be ridden or driven.

Sixty‐seven horses presented with atrial fibrillation (AF) from January I, 1980 to August 1, 1986. All horses were evaluated for the type and severity of the underlying cardiac disease and the probable duration of the arrhythmia. Fifty‐two (78%) of the horses were treated with quinidine sulfate and/or digoxin. The response to treatment was assessed in each horse. Horses were followed for periods extending from 8 months to 7 years. Standardbreds, young horses, and males predominated in the study group. There were more male horses (stallions and geldings) than mares. Most horses with AF had no evidence of other cardiac disease (56.7%). All performance horses without other cardiac disease were treated, and return to performance was significantly associated with conversion to sinus rhythm. Horses that did not convert with quinidine sulfate therapy, whose arrhythmia recurred, and that had side effects from quinidine sulfate therapy, had a longer history of poor performance. Tachycardia (heart rate > 60 beats/min) was significantly associated with the existence of congestive heart failure. The horses with congestive heart failure had a poor prognosis for life (7.7% survived) and a poor conversion to normal sinus rhythm (23.1 %). Mitral regurgitation (19 horses) was the most common underlying cardiac disease. Tricuspid regurgitation (15 horses), aortic regurgitation (3 horses), myocardial dysfunction (3 horses), and atrial septal defect (1 horse) also were diagnosed. Congestive heart failure was common in this group of horses with underlying cardiac disease.

Summary A retrospective study of 10 horses with bacterial endocarditis was performed in order to describe the echocardiography findings in horses with bacterial endocarditis, in conjunction with clinical signs and post mortem findings, and to evaluate the usefulness of echocardiography in the diagnosis of bacterial endocarditis and the formulation of a prognosis. Echocardiographic and post mortem examinations were performed in 7 horses. Post mortem examination alone was performed in 2 horses and echocardiographic examination alone performed in one horse. No breed or sex predilection was obvious. Mean age ± s.d. was 2.12 ± 3.32 years. Predominant clinical signs and abnormal clinical pathology data were fever, cardiac murmur, tachycardia, tachypnoea, hyperfibrinogenaemia, anaemia and leucocytosis. Pasteurella/Actinobacillus spp. and Streptococcus spp. were most commonly cultured. Vegetative lesions were found most frequently on the mitral valve and secondarily on the aortic valve. The location and number of lesions identified with echocardiography in the horses accurately described the lesions found on post mortem examination. Medical treatment was attempted in 50% of the horses. Serial echocardiography was used to assess the response to treatment in 2 horses. All horses with vegetative lesions of the mitral and/or aortic valve died or were subjected to euthanasia due to the severity of their cardiac disease. Both horses with tricuspid valve endocarditis were cured of the infection; one horse returned to racing after antimicrobial therapy and the other was subjected to euthanasia due to severe laminitis.

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...

Mares with uncomplicated pregnancies (n = 33) underwent transabdominal sonography to evaluate fetal well-being, obtain measurements of fetal size and characterize the intrauterine environment. Data from the last examination obtained prior to parturition were used for statistical analysis. All mares had one active fetus with good fetal tone. The maximal vertical depth of amniotic fluid (7.9 + 3.5 cm) was less than allantoic (13.4 + 4.4 cm) and fewer echogenic particles were detected in amniotic fluid. The maximal uteroplacental thickness was 1.38 k 0.23 cm (retrospective) and 1.15 ++ 0.24 cm (prospective). In 3 mares small anechoic spaces were imaged between the uterus and placenta. Fetuses had a regular cardiac rhythm with a mean heart rate of 75 2 7 beatslminute and breathing movements. The diameter of the fetal aorta (mean = 22.8 f 2.15 mm) was significantly correlated with neonatal foal weight (P < 0.0008, r = 0.72) and maternal prepartum weight (P < 0.002, r = 0.86). This information on the normal intrauterine environment and fetal well-being can be used to develop a biophysical profile specific for the equine fetus. V e t e r i n q Radiology

Mares with complicated pregnancies (illness, problems at parturition or delivery of an abnormal foal, n = 30) were scanned transabdominally from 298 days gestation to term in order to measure fetal size, evaluate fetal well-being and characterise the intrauterine environment. The results of the last scan obtained prior to parturition were compared to normal data obtained from fetuses of comparable gestational age to develop a biophysical profile specific for the equine fetus. Twelve mares produced a normal foal (positive outcome) and 18 mares delivered 19 abnormal foals (negative outcome). Both fetuses that were inactive throughout the entire scan and 4 of 5 fetuses with heart rate abnormalities were abnormal at birth. Three of 4 fetuses surrounded by decreased allantoic fluid quantities had a negative outcome. All mares with large anechoic spaces between the uterus and placenta (n = 3) and/or thickened uteroplacental units (n = 5) delivered abnormal foals. There was a significant correlation between fetal aortic diameter and neonatal foal weight in these complicated pregnancies (P<0.0001, r = 0.85). Fetal aortic diameters were predicted from maternal weight and 6 fetuses had smaller than predicted aortic diameters, all with negative outcomes. A biophysical profile of the equine fetus from 298 days gestational age to term was developed that included 6 factors related to pregnancy outcome: fetal heart rate, fetal aortic diameter, maximal fetal fluid depths, uteroplacental contact, uteroplacental thickness and fetal activity. The profile proved informative about fetal well-being, perinatal morbidity and perinatal mortality. A low score was a definite indication of an impending negative outcome; however, a high score was not assurance of a positive outcome. The utility of such a biophysical profile and future directions for research are discussed.

BackgroundAlthough atrial fibrillation (AF) can be successfully treated in horses, recurrence occurs frequently. In humans, atrial function after cardioversion can predict recurrence.ObjectivesTo examine the prognostic value of atrial mechanical function at 24 hours after cardioversion and other potential predictor variables for AF recurrence in horses.Animals117 horses treated for AF at 4 referral centers.MethodsRetrospective study. Inclusion criteria were successful cardioversion, echocardiography at 24 hours after cardioversion and ≥4 months follow‐up. To determine factors associated with AF recurrence, a multivariable survival model was built.Results133 AF episodes in 117 horses were included. AF recurred in 36/100 horses with a first AF episode and in 57/133 AF episodes overall. Factors associated with recurrence in horses with a first episode were previous unsuccessful treatment attempt (hazard ratio HR 2.36, 95% confidence interval CI 1.11–4.99, P = .025) and mild or moderate mitral regurgitation (HR 2.70, 95% CI 1.23–5.91, P = .013). When the last AF episode of all horses was included, previous AF (HR 2.53, 1.33–4.82, P = .005) and active left atrial fractional area change ≤9.6% (HR 3.43, 1.22–9.67, P = .020) were significant predictors.Conclusions and Clinical ImportanceThe only echocardiographic variable of left atrial function with significant prognostic value for recurrence was low active left atrial fractional area change. Further research is necessary to evaluate whether echocardiography at a later timepoint could provide more prognostic information.