Cardiovascular changes in horses with atrial fibrillation and high thyroid hormone concentration: a case-control study.

INTRODUCTION: Hyperthyroidism is a predisposing factor for atrial fibrillation (AF) in humans. The relationship between high thyroid hormone (TH) and AF in horses has not been evaluated. OBJECTIVES: The aim of this study is to identify whether (1) high TH concentrations were present in horses with AF, (2) other cardiovascular effects were observed in horses with high TH and AF, and (3) TH status affected recurrence rate. ANIMALS: Twenty-three horses presented with naturally occurring AF. METHODS: Prospective case-control clinical study. Thyroid hormone concentration was measured in horses presenting with AF. Heart rate, electrocardiogram, blood pressure, and an echocardiogram were recorded as part of their clinical workup. Recurrence rate was determined by owner/veterinarian follow-up. RESULTS: High TH concentration was found in 60% of horses with AF. Horses in the high TH group had a higher heart rate (P=0.001), systolic blood pressure (P=0.019), left ventricular free wall thickness (P=0.026), relative wall thickness (P=0.041) and were more likely to have periods of AF with a rapid ventricular response rate (P=0.022). All horses were successfully converted to normal sinus rhythm. The likelihood of recurrence was not different between groups. CONCLUSION: Elevated TH concentration can be found in horses with AF. Other cardiovascular effects of high TH concentrations in other species were also present in horses with AF and elevated TH concentrations. This study recommends measuring TH concentrations in horses presenting for AF with a history of thyroid or iodine supplementation. This study also cautions against TH or iodine supplementation in healthy performance horses.

Hypercapnia and hyperlactatemia were positively associated with higher-grade arrhythmias during peak exercise in horses during poor performance evaluation on a high-speed treadmill.

Cardiac arrhythmias are common in horses during exercise, especially immediately post-exercise. The objectives of this study were to: (1) describe the frequency and type of cardiac arrhythmias detected in horses during incremental high-speed treadmill exercise testing (ITET); (2) determine if arterial blood gas (ABG) changes at peak and immediately post-exercise were associated with arrhythmias; and (3) determine whether upper or lower airway disease was associated with exercising cardiac arrhythmias. Horses (n = 368) presenting for an ITET underwent resting and exercising upper airway endoscopy, resting, exercising and post-exercise electrocardiography, resting and post-exercise echocardiography and exercising ABG. Arrhythmias were graded by the most severe arrhythmia present. Grade 1 arrhythmias were defined as one or two atrial (APCs) or ventricular premature complexes (VPCs), or one APC and one VPC, detected in 6.9% at peak and 16% at 0-2 min post exercise.. Grade 2 arrhythmias were >2 APCs or VPCs, or both, detected in 5.8% at peak and 16.6% at 0-2 min post exercise. Grade 3 included complex arrhythmias (couplets, triplets, R on T, multiform complexes or paroxysmal atrial or ventricular tachycardia), detected in 4.4% at peak and 7.3% at 0-2 min post exercise. Both partial pressure of arterial CO2 (PaCO2; P = 0.008) and lactate (P = 0.031) were significantly associated with arrhythmias occurring at peak exercise, but not immediately post-exercise. As PaCO2 and lactate increased, arrhythmia severity increased. Blood pH was significantly associated with grades 2 and 3 arrhythmias at 0-2 min post ITET (OR = 0.0002; P < 0.001). There was no significant association between grades 2 and 3 cardiac arrhythmias, inflammatory airway disease (IAD), or exercise-induced pulmonary hemorrhage (EIPH). When adjusted for lactate concentration (P = 0.06), higher PaCO2 concentrations in horses with and without exercising upper respiratory tract (URT) obstruction were associated with higher likelihood of grades 2 and 3 arrhythmias (P < 0.01). This study demonstrated that at peak exercise, with severe hypercapnia and hyperlactatemia, there was increased risk for grades 2 or 3 cardiac arrhythmias and, as the PaCO2 and lactate values increased further, the severity of those arrhythmias increased.

Assessing gastrointestinal motility in healthy horses comparing auscultation, ultrasonography and an acoustic gastrointestinal surveillance biosensor: a randomised, blinded, controlled crossover proof of principle study.

BACKGROUND: Auscultation and ultrasonography are noninvasive techniques used to assess gastrointestinal motility in horses. Recently, noninvasive acoustic gastrointestinal surveillance (AGIS) biosensors evaluating intestinal motility have been validated in humans. OBJECTIVES: To compare AGIS to auscultation and ultrasonography for detecting decreased motility after xylazine administration. STUDY DESIGN: Randomised, blinded, controlled cross-over proof of principle study. METHODS: Six healthy horses were evaluated under fasted and nonfasted conditions and randomly assigned to receive treatment with 0.4 mg/kg xylazine or an equivalent volume of 0.9% NaCl intravenously. After a 48-h washout period, the process was repeated with the alternate treatment. Motility was assessed pre and posttreatment. Borborygmi were assessed in each abdominal quadrant and graded on a scale of 0-3, with 3 being continuous borborygmi. Duodenal, jejunal and caecal contractions were assessed ultrasonographically in consistent locations. Four AGIS biosensors were applied in standardised locations (duodenum, caecum, ventral midline, right dorsal colon). The biosensors measure acoustic signals and data were recorded in transport metric. Data were analysed using cross-classified multilevel random effects logistic regression including area under the receiver operator characteristic curve (AUC ROC). Sensitivity, specificity and accuracy were calculated for each modality. RESULTS: All three modalities detected a reduction in gastrointestinal motility following xylazine administration with AUC ROC being 0.85, 0.84 and 0.86 for auscultation, ultrasonography and AGIS respectively. The sensitivity, specificity and accuracy for auscultation was 88, 71 and 75%; for ultrasonography was 67, 63 and 64%; and for AGIS was 69, 70 and 70%, respectively. MAIN LIMITATIONS: The study was performed in normal healthy horses and application of this device to clinical patients warrants further investigation. CONCLUSIONS: In this proof of principle study, AGIS was able to discriminate between horses given xylazine from those given 0.9% NaCl with comparable accuracy as auscultation and ultrasonography. The Summary is available in Spanish - see Supporting Information.

Occurrence of cardiac arrhythmias in Standardbred racehorses.

REASONS FOR PERFORMING STUDY: Cardiac arrhythmias are a recognised but poorly characterised problem in the Standardbred racehorse. Frequency data could aid the development of cardiac arrhythmia screening programmes. OBJECTIVES: To characterise the occurrence of cardiac arrhythmias in Standardbreds prior to racing and in the late post race period using a handheld, noncontinuous recording device. STUDY DESIGN: Prospective, observational study, convenience sampling. METHODS: Noncontinuous electrocardiographic recordings were obtained over a 12 week period from Standardbred horses competing at a single racetrack. Electrocardiograms were obtained before racing and between 6 and 29 min after the race using a handheld recording device. Prevalence of arrhythmias was calculated for all horses and overall frequency of arrhythmias was calculated for race starts and poor performers. Univariate logistic regression analysis was used to identify risk factors for cardiac arrhythmias. RESULTS: A total of 8657 electrocardiogram recordings were obtained from 1816 horses. Six horses had atrial fibrillation after racing (prevalence = 0.11%, frequency = 0.14%), one horse had supraventricular tachycardia before racing (prevalence = 0.06%, frequency = 0.02%), and 2 horses had ventricular tachyarrhythmias after racing (prevalence = 0.06%, frequency = 0.05%). The frequency of atrial fibrillation among race starts with poor performance was 1.3-2.0%. Increasing age was a significant risk factor for the presence of atrial premature contractions before racing and atrial fibrillation and ventricular ectopy after racing. CONCLUSIONS: Both physiological and pathological cardiac arrhythmias can be detected in apparently healthy Standardbred horses in the prerace and late post race period using noncontinuous recording methods. Future studies should examine cumulative training or racing hours as a risk factor for cardiac arrhythmia. The prevalence and frequency information may be useful for track veterinarians and regulatory personnel following trends in cardiac arrhythmias.

The Association of Fibrinous Pleural Effusion with Survival and Complications in Horses with Pleuropneumonia (2002-2012): 74 Cases.

BACKGROUND: Fibrinous parapneumonic pleural effusions are associated with decreased efficacy of pleural fluid drainage and increased risk of medical treatment failure in people, but similar associations have not been established in horses. HYPOTHESIS/OBJECTIVES: We hypothesized that fibrin deposition in the pleural cavity of horses with parapneumonic effusions increases the risk of poor outcome. ANIMALS: Seventy four horses with bacterial pleuropneumonia diagnosed by culture and cytology of tracheal aspirates, pleural fluid, or both, and pleural effusion diagnosed by ultrasonographic examination. METHODS: Retrospective study of cases was from 2002 to 2012. Information obtained from the medical records included signalment, history, sonographic findings, treatments, and outcome. The primary outcome investigated was survival and secondary outcomes were development of complications and surgical intervention. Fisher's exact test and logistic regression were applied for categorical variables. A t-test was used to find differences in continuous variables between groups. RESULTS: Seventy four horses met study criteria and 50 (68%) survived. Fibrinous pleural effusion was associated with higher respiratory rate and pleural fluid height at admission, necrotizing pneumonia, increased number of indwelling thoracic drains required for treatment, and decreased survival. CONCLUSIONS AND CLINICAL IMPORTANCE: Fibrin accumulation in parapneumonic effusions is associated with increased mortality. Direct fibrinolytic treatment might be indicated in affected horses.

Risk factors for recurrence of atrial fibrillation in horses after cardioversion to sinus rhythm.

BACKGROUND: Although atrial fibrillation (AF) can be successfully treated in horses, recurrence occurs frequently. In humans, atrial function after cardioversion can predict recurrence. OBJECTIVES: To examine the prognostic value of atrial mechanical function at 24 hours after cardioversion and other potential predictor variables for AF recurrence in horses. ANIMALS: 117 horses treated for AF at 4 referral centers. METHODS: Retrospective 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. RESULTS: 133 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 IMPORTANCE: The 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.

Complications of a permanent transvenous pacing catheter in a horse.

Gross and histopathological findings in a 9-year-old horse implanted with permanent transvenous pacing cardiac catheters, 18 and 34 months before its death, are described. Lesions consisting of extensive fibrino-haemorrhagic thrombi with large numbers of bacterial colonies were present along the electrode wires and on mural and valvular endocardial surfaces of the right heart. There was a locally extensive area of suppurative endocarditis around the attachment site of the atrial electrode, which was loosely attached by a thin band of membranous tissue to the endocardium. The ventricular electrode was firmly embedded in the myocardium and was surrounded by a dense area of fibrous connective tissue in which multifocal mineralized areas were seen. Histologically, there was evidence of terminal bacteraemia. The observed lesions are discussed with respect to findings in man and other animals with similar cardiac implants.

Bacterial endocarditis in horses: ten cases (1984-1995).

A retrospective study of 10 horses with bacterial endocarditis was performed in order to describe the echocardiographic findings in horses with bacterial endocarditis, in conjunction with clinical signs and post mortem findings, and to evaluate the usefulness 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.

Severe mitral regurgitation in horses: clinical, echocardiographic and pathological findings.

Forty-three horses with mitral regurgitation (MR) and congestive heart failure were examined, using M-mode, 2-dimensional real-time and Doppler echocardiography. There was no breed or sex predisposition when compared to the general hospital population. The mean +/- s.d. age of affected horses was 7.6 +/- 8.1 years. Horses with MR and congestive heart failure had significant increases in mean values for left ventricular chamber size, left atrial size and heart rate and significant decreases in interventricular septal and left ventricular free wall thickness. Significant increases in pulmonary artery diameter were detected compared to aortic diameter. Mean values for fractional shortening were not significantly different from normal. All horses had a Grade 3-6/6 holosystolic or pansystolic murmur with its point of maximal intensity in the mitral to aortic valve area. Atrial fibrillation was found at presentation in 24 horses with MR and congestive heart failure. One horse presented with atrial tachycardia and subsequently developed atrial fibrillation. Seven horses had ventricular premature contractions. Exercise intolerance (n = 34), respiratory signs (n = 31), and fever (n = 21) were the most common presenting signs. Thickening of the left atrioventricular valve leaflets, endocarditis, flail valve leaflets, rupture of a chorda tendineae, and mitral valve prolapse were detected echocardiographically. Doppler echocardiography confirmed the presence of a large systolic regurgitant jet in the left atrium in all horses in which it was used, and in many horses, concurrent tricuspid and pulmonary regurgitation was detected. All horses died or were subjected to euthanasia due to the severity of their MR and/or lack of response to therapy. Post mortem examinations were performed in 35 horses and confirmed the echocardiographic findings. The echocardiographic detection of a flail mitral valve leaflet was significantly associated with the detection of a ruptured chorda tendineae at post mortem examination. There was a significant association between echocardiographic detection of a dilated pulmonary artery and its presence at post mortem examination. M-mode, 2-dimensional real-time, and Doppler echocardiography should be used to accurately characterise the valvular abnormalities and assess the severity of mitral regurgitation. Pulmonary artery dilatation, an echocardiographic indication of severe pulmonary hypertension, should be considered a grave prognostic indicator and may indicate impending pulmonary artery rupture.

Treatment of atrial fibrillation in horses: new perspectives.

Forty-one horses were treated for atrial fibrillation (AF) with 22 mg/kg quinidine sulfate via nasogastric tube every 2 hours until conversion to 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 to every 6 hours if conversion had not occurred. Digoxin was administered before treatment if the horse had a fractional shortening < or = 27% (3 horses), was prone to tachycardia (resting heart rate > or = 60 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 (11 horses) or on day 2 if conversion had not occurred (7 horses). Plasma quinidine concentrations within 1 hour of conversion of AF to sinus rhythm ranged from 1.7 to 7.5 micrograms/mL (mean, 4.05 +/- 1.6) and ranged from 1.7 to 4.7 micrograms/mL in 97% of horses. Most horses (92%) with plasma quinidine concentrations > 5 micrograms/mL exhibited an adverse or toxic effect of quinidine sulfate (clinical or electrocardiographic). There was no statistical association between plasma quinidine concentrations and sustained tachycardia (> 100 beats/min), diarrhea, or colic. Ataxia and upper respiratory tract stridor were significantly associated with plasma quinidine concentrations. In most instances (98%) conversion did not occur while toxic or adverse effects of quinidine sulfate were present or when plasma quinidine concentrations were > 5 micrograms/mL.

Factors affecting prognosis and conversion in equine atrial fibrillation.

Sixty-seven horses presented with atrial fibrillation (AF) from January 1, 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 greater than 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.

An echocardiographic study of atrial fibrillation in horses: before and after conversion to sinus rhythm.

Two-dimensional and M-mode echocardiograms were recorded from 41 horses before they were successfully treated for atrial fibrillation. In addition, these examinations were performed in a subgroup of 20 horses after treatment, and the results were compared with pretreatment values. Atrial fibrillation in this group of horses was associated with a reduction of mean left ventricular fractional shortening (mean 31% +/- 5.24%), and 22 of the 41 horses were below the reference range. The remaining mean M-mode variables were within the normal reference range, although 12 horses had increased left ventricular lumen dimensions in systole, and 8 horses had decreased left ventricular ejection times. Abnormal motion of the mitral valve was present in all horses and was characterized by the absence of A peaks, which were replaced by small diastolic undulations in 55% of the horses. In horses 1 to 20, after conversion to sinus rhythm, the mean fractional shortening increased (35.34% +/- 5.4%, P = .004), but there were no significant differences in heart rate or left ventricular lumen diameters in systole or diastole. These results suggest that ventricular function may be compromised by the presence of atrial fibrillation. However, this improved after correction of the arrhythmia.

Echocardiographic evaluation of equine aortic insufficiency.

Echocardiographic evaluation of 23 horses with aortic insufficiency was performed, using M-mode (n = 23) and 2-dimensional real-time echocardiography (n = 14 of 23). Echocardiograms were evaluated for abnormalities of aortic and mitral valves and alterations in motion of these valves. Changes in left ventricular chamber size and function, as well as aortic root size, were evaluated. The presence of other cardiac disease was also evaluated. Horses with aortic insufficiency had significant increases (P less than 0.01) in mean values of left ventricular chamber size, aortic root diameter, and shortening fraction. Left ventricular free wall thickness also was significantly decreased (P less than 0.01). Valvular abnormalities were seen echocardiographically in all 23 horses. Eighteen horses with aortic insufficiency had thickened valves, whereas two horses had lesions associated with vegetative endocarditis. High-frequency vibrations of the septal leaflet of the mitral valve were noticed in all horses, whereas similar vibrations of the aortic valve were seen in six horses. The presence of a bounding arterial pulse correlated significantly (P less than 0.05) with increased left ventricular chamber size at end diastole and shortening fraction, indicating a marked left ventricular volume overload. A reliable diagnosis of aortic insufficiency can be made with the detection of bounding arterial pulses in concert with a holodiastolic decrescendo grade II to V/V murmur with maximal intensity over the aortic valve area, radiating toward the left cardiac apex.

Ultrasonography of umbilical structures in clinically normal foals.

The umbilical arteries, urachus, and umbilical vein were scanned ultrasonographically in 13 clinically normal foals that ranged in age from 6 hours to 4 weeks. Sonograms were obtained using a 7.5-MHz sector scanner transducer placed across the midline of the ventral portion of the foal's abdominal wall. The umbilical vein was scanned from the umbilical stalk to its entrance into the hepatic parenchyma. The mean (+/- SD) diameter of the umbilical vein was 0.61 +/- 0.20 cm immediately cranial to the umbilical stalk, 0.52 +/- 0.19 cm midway between the umbilicus and liver, and 0.6 +/- 0.19 cm at the liver. The urachus and umbilical arteries were scanned from the umbilical stalk to the apex of the urinary bladder and had a mean total diameter of 1.75 +/- 0.37 cm at the bladder apex. The umbilical arteries also were scanned along either side of the bladder and had a mean diameter of 0.85 +/- 0.21 cm. These measurements and the ultrasonographic appearance of the internal umbilical structures from clinically normal foals can be used as references to diagnose abnormalities of the umbilical structures in neonatal foals.

Three-dimensional sonographic imaging of the equine superficial digital flexor tendon.

In a feasability study, a technique for constructing 3-dimensional sonographic images of the superficial digital flexor tendon (SDFT) was established in 6 clinically normal horses and applied to 7 horses with injured SDFT. Two-dimensional B-mode sonographic images were recorded on videotape as the sonographic transducer was manually moved along the palmar aspect of the metacarpal region. Selected videofields were digitized, and 3-dimensional images were constructed, using a computer work station and dedicated software program. The 3-dimensional images were of high quality and presented qualitative clinical information in unique fashion. Indication of the extent of SDFT injuries was excellent. Such 3-dimensional images would be especially useful in explaining to owners and trainers the importance of the injury to their horse and would have a role in monitoring tendon healing and in the assessment of various treatments.

Pharmacokinetics of digoxin administered to horses with congestive heart failure.

Nine horses with (naturally acquired) congestive heart failure were treated with 2.2 micrograms of digoxin/kg of body weight by the IV route, followed by 11 micrograms/kg administered orally every 12 hours thereafter. Furosemide was administered IV concurrently with IV administered digoxin every 12 hours. Serum concentration of digoxin was measured after the first (IV) and seventh (orally administered) dose. After IV administration, digoxin disposition was described by a 2-compartment model, with a rapid distribution phase (t1/2 alpha = 0.17 hour), followed by a slower elimination phase (beta = 0.096 +/- 0.055 h-1, t1/2 beta = 7.2 hours, where beta is the exponential term from the elimination phase of the concentration vs time curve). Bioavailability after oral administration was 21.2 +/- 10.8%. After the seventh orally administered dose, serum concentration of digoxin peaked 1 to 2 hours later, and was 1.9 +/- 0.7 ng/ml (mean +/- SD). In 4 horses, a second increase in serum digoxin concentration was observed 4 to 8 hours after the initial peak, which possibly was evidence of enterohepatic recycling of the drug. Response to treatment included reduction in heart rate, peripheral edema, and pulmonary edema, but these could not be attributed to the digoxin alone because the horses were treated concurrently with furosemide.

Pulsed-wave Doppler evaluation of intracardiac blood flow in 30 clinically normal Standardbred horses.

Pulsed-wave Doppler echocardiography was performed on 30 clinically normal 1- to 6-year-old racing Standardbreds. There were 13 females, 13 geldings, and 4 stallions. Cardiac disease was not detected with M-mode, 2-dimensional real-time or pulsed-wave Doppler echocardiography. Normal flow velocities for right and left atrial outflow, right and left ventricular outflow, the aorta, and pulmonary artery were determined. Peak flow velocities for right and left atrial outflow occurred during the rapid filling phase and were higher toward the mitral valve (mean, 0.70 +/- 0.24 m/s) than toward the tricuspid valve (mean, 0.49 +/- 0.17 m/s). Peak flow velocities in the right and left ventricular outflow tracts were similar (means, 0.81 +/- 0.10 m/s and 0.75 +/- 0.39 m/s, respectively). Peak flow velocities in the pulmonary artery (mean, 1.09 +/- 0.42 m/s) and aorta (mean, 1.01 +/- 0.29 m/s) were similar, although flow peaked earlier in systole in the aorta than in the pulmonary artery.

Mitral valvular insufficiency associated with ruptured chordae tendineae in three foals.

Mitral valvular insufficiency associated with ruptured chordae tendineae was diagnosed in 3 foals with signs of congestive heart failure, which were believed to be secondary to the development of pulmonary hypertension associated with the valvular insufficiency. The septal leaflet of the mitral valve was affected in all 3 foals, and foal 2 also had ruptured chordae tendineae associated with the caudal mitral valve leaflet. Bacterial endocarditis and myocardial necrosis were associated with the ruptured chordae tendineae in foals 3 and 2, respectively. Idiopathic rupture was considered in foal 1. Two-dimensional echocardiography demonstrated a flail mitral valve leaflet in foals 2 and 3 and a ruptured chorda tendineae in foal 3. The ruptured chorda tendineae in foal 1 was not visualized with M-mode echocardiography.

Clostridium perfringens cellulitis and immune-mediated hemolytic anemia in a horse.

A 10-year-old Quarter Horse mare was referred for evaluation and treatment of a large pectoral skin slough and hemoglobinuria. The skin slough was secondary to Clostridium perfringens cellulitis and associated gas gangrene. Cold hemagglutinin disease was diagnosed and was suspected to be secondary to C perfringens septicemia. The autoimmune hemolytic anemia, severe intravascular hemolysis, and hemoglobinuria were treated with dexamethasone and hydrocortisone. The infection was treated with 20 X 10(6) units of sodium penicillin, IV, 4 times daily, and the wound was debrided. When the mare relapsed, treatment was changed to 6 g of chloramphenicol sodium succinate, IV, 4 times daily. The mare died on day 11 of hospitalization, despite intensive therapy.