Anthony H. Tobias

Arterial Thromboembolism in Cats: Acute Crisis in 127 Cases (1992–2001) and Long-Term Management with Low-Dose Aspirin in 24 Cases

Records of 127 cats with arterial thromboembolism (ATE) were reviewed. Abyssinian, Birman, Ragdoll, and male cats were overrepresented. Tachypnea (91%), hypothermia (66%), and absent limb motor function (66%) were common. Of 90 cats with diagnostics performed, underlying diseases were hyperthyroidism (12), cardiomyopathy (dilated [8], unclassified [33], hypertrophic obstructive [5], hypertrophic [19]), neoplasia (6), other (4), and none (3). Common abnormalities were left atrial enlargement (93%), congestive heart failure (CHF, 44%), and arrhythmias (44%). Of cats without CHF, 89% were tachypneic. Common biochemical abnormalities were hyperglycemia, azotemia, and abnormally high serum concentrations of muscle enzymes. Of 87 cats treated for acute limb ATE, 39 (45%) survived to be discharged. Significant differences were found between survivors and nonsurvivors for temperature (P < .00001), heart rate (P = .038), serum phosphorus concentration (P = .024), motor function (P = .008), and number of limbs affected (P = .001). No significant difference was found between survivors and nonsurvivors when compared by age, respiratory rate, other biochemical analytes, or concurrent CHE A logistic regression model based on rectal temperature predicted a 50% probability of survival at 98.9 degrees F (37.2 degrees C). Median survival time (MST) for discharged cats was 117 days. Eleven cats had ATE recurrences, and 5 cats developed limb problems. Cats with CHF (MST: 77 days) had significantly shorter survival than cats without CHF (MST: 223 days; P = .016). No significant difference was found in survival or recurrence rate between cats receiving high-dose aspirin (> or = 40 mg/cat q72h) and cats receiving low-dose aspirin (5 mg/cat q72h). Adverse effects were less frequent and milder for the lower dosage.

Evaluation of serum cardiac troponin I concentration in dogs with renal failure

OBJECTIVE To determine whether dogs with renal failure have higher serum cardiac troponin I (cTnI) concentrations than healthy dogs. DESIGN Case-control study. ANIMALS 31 dogs with renal failure and 51 healthy dogs. PROCEDURES Serum concentrations of creatinine and cardiac troponin I, urine specific gravity, and systolic arterial blood pressure were measured for all dogs. Dogs underwent a standardized physical examination, and any dog with evidence of cardiovascular disease or other nonrenal disease was excluded from final analyses. Dogs were considered to be in renal failure when the serum creatinine concentration was >or= 3.0 mg/dL, urine specific gravity was between 1.007 and 1.030, and renal failure had been clinically diagnosed. RESULTS Dogs with renal failure had significantly higher serum cTnI concentrations (median, 0.35 ng/mL) than did healthy dogs (0.20 ng/mL). The renal failure group also had a significantly higher median systolic blood pressure (156 mm Hg) than did healthy dogs (138 mm Hg), although serum cTnI concentration was not correlated with systolic blood pressure in dogs with renal failure. There was no significant difference in age between dogs with renal failure and healthy dogs, but dogs with renal failure had significantly higher serum creatinine concentration and lower urine specific gravity. CONCLUSIONS AND CLINICAL RELEVANCE Although dogs with renal failure did not have overt clinical signs of cardiac disease, they had high serum cTnI concentrations, which may have been associated with subclinical cardiovascular disease. The cause of the high serum cTnI concentration in these dogs requires additional investigation.

Minimally Invasive Per‐Catheter Patent Ductus Arteriosus Occlusion in Dogs Using a Prototype Duct Occluder

BACKGROUND Per-catheter patent ductus arteriosus (PDA) occlusion in dogs with devices intended for humans is associated with technical difficulties, high rates of procedure abandonment, device migration, and residual ductal flow. HYPOTHESIS Use of a custom-made canine duct occluder (Amplatz Canine Duct Occluder, ACDO) would be feasible in dogs of varying weights and somatotypes and effective in occluding a wide range of PDA shapes and sizes. ANIMALS Eighteen client-owned dogs of various breeds with PDA. Weights ranged from 3.8 to 32.3 kg (median, 17.8 kg), and angiographic minimal ductal diameters ranged from 1.1 to 6.9 mm (median, 3.7 mm). Ductal morphologies included types IIA, IIB, and III. METHODS Per-catheter PDA occlusion with the ACDO was performed in all dogs. Persistent or recurrent ductal flow was assessed at the end of the procedure by angiography and at 1 day, 3 months, and >or=12 months after the procedure by echocardiography. RESULTS Successful ACDO placement was achieved in all 18 dogs. One dog required a 2nd procedure with a larger ACDO after the 1st device migrated to the pulmonary vasculature. Complete occlusion was confirmed in 17 of 18 dogs during the procedure, as well as at 1 day and 3 months after the procedure, and in 12 of 13 dogs evaluated at >or=12 months after the procedure. CONCLUSIONS AND CLINICAL IMPORTANCE Per-catheter PDA occlusion in dogs with the ACDO is feasible and effective in dogs of a wide range of weights and somatotypes and with PDAs of varying shapes and sizes.

Cardiopulmonary effects of intrathoracic insufflation in dogs.

This study was designed to quantify the effects of incremental positive insufflation of the intrathoracic space on cardiac output (CO), heart rate (HR), arterial pressure (AP), central venous pressure (CVP), and percent saturation of hemoglobin with oxygen (SPO2) in anesthetized dogs. Seven healthy, adult dogs from terminal teaching laboratories were maintained under anesthesia with isoflurane delivered with a mechanical ventilator. The experimental variables were recorded before introduction of an intrathoracic catheter, at intrathoracic pressures (IP) of 0 mm Hg, 3 mm Hg insufflation, and additional increments of 1 mm Hg insufflation thereafter until the SPO2 remained <85% despite increases in minute volume. Finally the variables were measured again at 0 mm Hg IP. The cardiac output and systolic and diastolic AP significantly (P < 0.05) decreased at 3 mm Hg IP. Significant decreases in SPO2 were seen at 10 mm Hg IP. Significant increase in CVP was noted at 6 mm Hg IP. Heart rate decreased significantly at 5 to 6 mm Hg IP but was not decreased above 6 mm Hg IP. Given the degree of CO decrease at low intrathoracic pressures, insufflation-aided thoracoscopy should be used with caution and at the lowest possible insufflation pressure. Standard anesthetic monitoring variables such as HR and AP measurements may not accurately reflect the animals cardiovascular status.

Differential cardiotoxicity in response to chronic doxorubicin treatment in male spontaneous hypertension-heart failure (SHHF), spontaneously hypertensive (SHR), and Wistar Kyoto (WKY) rats.

Life threatening complications from chemotherapy occur frequently in cancer survivors, however little is known about genetic risk factors. We treated male normotensive rats (WKY) and strains with hypertension (SHR) and hypertension with cardiomyopathy (SHHF) with 8 weekly doses of doxorubicin (DOX) followed by 12weeks of observation to test the hypothesis that genetic cardiovascular disease would worsen delayed cardiotoxicity. Compared with WKY, SHR demonstrated weight loss, decreased systolic blood pressure, increased kidney weights, greater cardiac and renal histopathologic lesions and greater mortality. SHHF showed growth restriction, increased kidney weights and renal histopathology but no effect on systolic blood pressure or mortality. SHHF had less severe cardiac lesions than SHR. We evaluated cardiac soluble epoxide hydrolase (sEH) content and arachidonic acid metabolites after acute DOX exposure as potential mediators of genetic risk. Before DOX, SHHF and SHR had significantly greater cardiac sEH and decreased epoxyeicosatrienoic acid (EET) (4 of 4 isomers in SHHF and 2 of 4 isomers in SHR) than WKY. After DOX, sEH was unchanged in all strains, but SHHF and SHR rats increased EETs to a level similar to WKY. Leukotriene D4 increased after treatment in SHR. Genetic predisposition to heart failure superimposed on genetic hypertension failed to generate greater toxicity compared with hypertension alone. The relative resistance of DOX-treated SHHF males to the cardiotoxic effects of DOX in the delayed phase despite progression of genetic disease was unexpected and a key finding. Strain differences in arachidonic acid metabolism may contribute to variation in response to DOX toxicity.

Supravalvular mitral stenosis in a cat.

A 3-year-old, 4-kg, castrated male domestic shorthair cat presented with signs of progressive respiratory distress. Thoracic radiographs showed pulmonary edema and pleural effusion. Echocardiography revealed a perforate membrane immediately above the mitral valve that divided the left atrium into proximal and distal chambers. The left auricle was proximal to the dividing membrane and connected to the markedly enlarged proximal left atrial chamber, consistent with the diagnosis of supravalvular mitral stenosis (SMS). Position of the obstructing membrane relative to the left auricle distinguishes SMS from cor triatriatum sinister (CTS). In CTS, the left auricle is distal to the dividing membrane and connects to the distal left atrial chamber.

Influence of Beta Blockers on Survival in Dogs with Severe Subaortic Stenosis

Background Subaortic stenosis (SAS) is one of the most common congenital cardiac defects in dogs. Severe SAS frequently is treated with a beta adrenergic receptor blocker (beta blocker), but this approach largely is empirical. Objective To determine the influence of beta blocker treatment on survival time in dogs with severe SAS. Methods Retrospective review of medical records of dogs diagnosed with severe, uncomplicated SAS (pressure gradient [PG] ≥80 mmHg) between 1999 and 2011. Results Fifty dogs met the inclusion criteria. Twenty‐seven dogs were treated with a beta blocker and 23 received no treatment. Median age at diagnosis was significantly greater in the untreated group (1.2 versus 0.6 years, respectively; P = .03). Median PG at diagnosis did not differ between the treated and untreated groups (127 versus 121 mmHg, respectively; P = .2). Cox proportional hazards regression was used to identify the influence of PG at diagnosis, age at diagnosis, and beta blocker treatment on survival. In the all‐cause multivariate mortality analysis, only age at diagnosis (P = .02) and PG at diagnosis (P = .03) affected survival time. In the cardiac mortality analysis, only PG influenced survival time (P = .03). Treatment with a beta blocker did not influence survival time in either the all‐cause (P = .93) or cardiac‐cause (P = .97) mortality analyses. Conclusions Beta blocker treatment did not influence survival in dogs with severe SAS in our study, and a higher PG at diagnosis was associated with increased risk of death.

Structural and functional cardiovascular changes and their consequences following interventional patent ductus arteriosus occlusion in dogs: 24 cases (2000–2006)

OBJECTIVE To investigate cardiovascular changes and survival times following complete interventional device occlusion of uncomplicated left-to-right shunting patent ductus arteriosus in dogs. DESIGN Retrospective cohort study. ANIMALS 24 dogs with uncomplicated patent ductus arteriosus that was fully occluded and reevaluated within 24 hours, approximately 3 months, and 1 year after the procedure. PROCEDURES Information on medical history, diagnostic imaging findings, treatment received, and survival times were obtained from medical records. Patients were allocated into 2 groups on the basis of age (< 1 year [n = 14] and ≥ 1 year [10]) at the time of the procedure. Additional follow-up information was obtained through interviews of owners and referral veterinarians. RESULTS Following ductal occlusion, decreases were detected in vertebral heart scale size, left ventricular chamber diameter in diastole and in systole, left atrial dimension, fractional shortening, aortic velocity, and ventricular wall thickness. There were no differences between age groups for postocclusion changes except vertebral heart scale size. Systolic dysfunction was detected in 14 (58%) patients on the final visit. Median survival time for all dogs after ductal occlusion was > 11.5 years. CONCLUSIONS AND CLINICAL RELEVANCE Complete ductal occlusion resulted in immediate removal of the volume overload state and eventual return of cardiac chamber dimensions to reference range, suggesting regression of eccentric hypertrophy. Systolic dysfunction persisted in some dogs but appeared to be clinically unimportant. Most cardiovascular changes were independent of patient age at the time of the procedure.

Caudal vena cava obstruction caused by redundant pacemaker lead in a dog.

Inferior vena cava obstruction, a rare but serious complication of transvenous pacemaker lead placement in humans, has not been reported in dogs. We describe this complication in a dog that developed ascites 8 months after pacemaker implantation. Radiography disclosed a loop of redundant lead within the caudal vena cava (CVC), and angiography demonstrated obstruction to blood flow. Withdrawal of the loop from the CVC did not restore blood flow. Persistent obstruction was suspected secondary to fibrosis resulting from vascular damage caused by the loop of lead. Angioplasty of the CVC obstruction restored blood flow and resolved the dogs clinical signs.

Cardiovascular manifestations of iatrogenic hyperthyroidism in two dogs

Two dogs were diagnosed with iatrogenic thyrotoxicosis (1 definitive, 1 presumptive). Both showed physical examination findings of agitation, tachypnea, and tachycardia. Sinus tachycardia with supraventricular ectopy was diagnosed in one case, and syncope and atrial flutter was present in the other. Both dogs had concurrent cardiac disease that might have contributed to the severity of their clinical signs. Excessive thyroid hormone supplementation in humans causes supraventricular arrhythmias including sinus tachycardia, supraventricular tachycardia, atrial fibrillation, and atrial flutter. Clinical signs and rhythm abnormalities resolved in both dogs with resolution of the thyrotoxicosis.