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Biomedical subjects

V B Reef

Publications and source records attributed to V B Reef.

70 records · Page 4Linked to original sources
PubMed1987

Echocardiographic detection of tricuspid atresia in two foals.

M-mode, 2-dimensional, and contrast echocardiographic studies were used to detect tricuspid atresia in 2 foals. M-mode echocardiographic findings included a small right ventricle, large left ventricle, large mitral valve excursion, large left atrium (foal 2), dropout of the cranial aspect of the aortic root, and a thick band of echoes in the tricuspid valve region. These findings were confirmed by 2-dimensional echocardiography. In addition, a large right atrium, persistent foramen ovale, ventricular septal defect, and large mitral valve apparatus were imaged. One foal also had a thick right atrial wall. Contrast echocardiography confirmed the intracardiac flow of blood from right to left atrium and then to the left ventricle, followed by simultaneous opacification of the right ventricle and aorta. The use of these echocardiographic techniques enables accurate antemortem diagnosis and prognosis of tricuspid atresia in the foal.

Animals↗
PubMed1987

Use of ultrasonography for the detection of aortic-iliac thrombosis in horses.

Two dimensional ultrasonographic evaluation of the iliac arteries and terminal portion of the aorta was utilized in 18 horses with histories of exercise intolerance or hindlimb lameness. A plaque or thrombus was imaged in one or more of these vessels in 5 horses. In 2 horses, the initial rectal examination findings were normal and the thrombus may have been missed without the use of diagnostic ultrasonography.

Animals↗
PubMed1987

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.

Animals↗
PubMed1986

Implantation of a permanent transvenous pacing catheter in a horse with complete heart block and syncope.

A permanent, transvenous, atrioventricular, sequential pacing system was implanted successfully in a 7-year-old Quarter Horse gelding with complete heart block. The transvenous atrial and ventricular electrodes were placed in their respective positions in the heart, using real-time, 2-dimensional echocardiography. The horse was able to return successfully to competition as a show horse.

Animals↗
PubMed1986

Rupture of an aortic sinus aneurysm in a 15-year-old broodmare.

A 15-year-old, Standardbred broodmare with an aortic sinus aneurysm developed rupture of the aneurysm with subsequent rupture of a tricuspid valve chorda tendinae, tricuspid regurgitation, acute right-sided congestive heart failure, and pulmonary thromboembolism. Shunting of blood from the aorta through the ruptured aneurysm into the right ventricle resulted in decreased renal perfusion and acute renal failure. Initially, treatment of the mare with analgesics, fluids, and digoxin resulted in clinical improvement, but the mare's condition deteriorated after 8 days and the mare was euthanatized due to unrelenting pain and a poor prognosis. Echocardiography was useful in diagnosis of the cardiac disease in the broodmare.

Animals↗
PubMed1985

Evaluation of the equine cardiovascular system.

A thorough examination of the cardiovascular system is an integral part of a physical examination in the horse. The normal equine cardiovascular parameters are discussed, with an emphasis on auscultatory findings. The availability and application of other diagnostic techniques are discussed based upon findings of the physical examination.

Angiocardiography↗
PubMed1985

Cardiovascular disease in the equine neonate.

Cardiac disease in the equine neonate occurs infrequently. Murmurs are often heard in foals and are not considered significant unless they persist beyond 4 days of age. Congenital cardiac defects are the most common form of primary cardiac disease in the foal, with ventricular septal defects occurring most frequently. Other neonatal foal diseases such as ruptured bladders, white muscle disease, neonatal respiratory distress syndrome, and septicemia have secondary cardiac involvement.

Animals↗
PubMed1984

Lymphosarcoma and associated immune-mediated hemolytic anemia and thrombocytopenia in horses.

Three horses with equine lymphosarcoma were examined because of clinical signs including chronic weight loss, respiratory distress, peripheral edema, and chronic colic. Clinicopathologic findings included evidence of an immune-mediated hemolytic anemia. Immune-mediated thrombocytopenia also was diagnosed in 1 of the horses and suspected in another. One horse died in spite of treatment, 1 died 5 hours after surgical removal of a tumor encircling the jejunum, and 1 was euthanatized because of deteriorating condition. Necropsy of each horse revealed extensive neoplastic infiltration of peripheral lymph nodes and abdominal or thoracic viscera with neoplastic lymphocytes.

Anemia, Hemolytic, Autoimmune↗
PubMed1984

Echocardiographic detection of tetralogy of Fallot and myocardial abscesses in a calf.

A 4-month-old Holstein bull was examined because of a loud heart murmur and recurring fever. The calf was polycythemic and became cyanotic following and mild exercise. A tetralogy of Fallot was diagnosed echocardiographically. Echo-free spaces were delineated in the left ventricle and interventricular septum. These fluid filled spaces were documented as myocardial abscesses on post-mortem examination.

Abscess↗
PubMed1983

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.

Anemia, Hemolytic, Autoimmune↗
PubMedDate not supplied

Aorto-cardiac fistulas in seven horses.

This report describes the history, clinical, electrocardiographic and echocardiographic findings, treatment, outcome and post-mortem findings in seven horses with aorto-cardiac fistula. Affected horses included 5 stallions, one gelding and one mare; 2 each of the Thoroughbred, Arabian and Standardbred breeds and one Thoroughbred-cross with a mean +/- s.d. age of 12 +/- 4 years, range 6-18 years. The presenting signs were acute distress (four horses), exercise intolerance (two horses) and the lesion was detected during a routine examination in one horse. Five horses had monomorphic ventricular tachycardia on admission and one other had a history of this arrhythmia. Five horses had a characteristic continuous murmur loudest in the right fourth intercostal space. Echocardiography (six horses) and/or post-mortem examination (four horses) revealed the horses had aorto-cardiac fistulas arising from the right aortic sinus in all five horses in which the site was recorded. Two horses had ruptured aneurysmal dilatations of the aortic wall at this site. Fistulas extended into the right ventricle in four horses; the right atrium in two horses, the left ventricle in one horse, and five horses had dissecting tracts in the septal myocardium. Horses survived for periods ranging from 24 h to 4 years. Aorto-cardiac fistula should be considered in the differential diagnosis for horses presenting with acute distress, bounding arterial pulse, a right-sided continuous murmur and/or monomorphic ventricular tachycardia, particularly in middle-aged or older stallions. Echocardiography is the technique of choice for confirming the diagnosis and demonstrating accompanying cardiac changes.

Age Factors↗
PubMedDate not supplied

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.

Animals↗
PubMedDate not supplied

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.

Animals↗
PubMedDate not supplied

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.

Animals↗