Successful balloon angioplasty in a cat with unilateral left pulmonary artery branch stenosis.

A 9-month-old intact male Ragdoll cat was presented for evaluation of a left-sided systolic murmur that was first auscultated during examination for a newly developed cough. Transthoracic echocardiography revealed a narrowed left pulmonary artery and an increase in flow velocities at the level of the narrowing, consistent with left pulmonary artery branch stenosis. The right pulmonary artery appeared normal. Balloon angioplasty was performed and successfully reduced pressure gradient across the stenosis. The patient continues to do well 14 months after the procedure.

Ventricular systolic dysfunction in dogs diagnosed with hypoadrenocorticism.

In human patients with hypoadrenocorticism, a secondary dilated cardiomyopathy is noted that has been reported to resolve with replacement steroid therapy. A similar secondary dilated cardiomyopathy in dogs with hypoadrenocorticism has not been previously described. We present three dogs concurrently diagnosed with hypoadrenocorticism and ventricular dilation with systolic dysfunction. Two dogs were presented with clinical signs consistent with biventricular congestive heart failure and a third dog was presented with signs of acute hypoadrenocorticism without congestive heart failure. All dogs recovered to normal cardiac size and function with therapy. Hypoadrenocorticism should be considered as a differential diagnosis in dogs that present with ventricular dilation and systolic dysfunction if there are other indicators in the clinical and laboratory testing. Additionally, a thorough cardiac evaluation should be recommended for dogs that are found to have a heart murmur at the time of diagnosis of hypoadrenocorticism.

Immediate outcomes of low-pressure balloon valvuloplasty for severe pulmonary valve stenosis in 20 dogs: a retrospective, single-center case series.

INTRODUCTION: The primary objective of this study was to describe the immediate post-procedural outcomes in dogs with severe pulmonary stenosis that were treated with low-pressure balloon valvuloplasty (BV) at a single institution. ANIMALS, MATERIALS AND METHODS: Retrospective case series; medical records of dogs that underwent BV performed with a balloon dilation catheter >20 mm in diameter and a burst pressure of less than 4 atm (atm) were retrospectively reviewed. Twenty animals were identified fitting the criteria. Pre-procedural and post-procedural echocardiograms and peri-procedural angiograms were reviewed. Procedural success was defined as greater than 50% reduction in echocardiographically derived transpulmonary systolic pressure gradient (TPPG) or post-procedural TPPG of less than 50 mmHg. RESULTS: The median percent reduction from initial TPPG was 53% (range = 15-90%). Sixty percent of the dogs met the pre-specified criteria for a successful outcome. Post-procedural TPPG was not different based on valve types A or B (p=0.67), presence or absence of additional supravalvular (p=0.23) or subvalvular (p=0.83) obstructive components. DISCUSSION: The proportion of dogs that reach the successful outcome were not different based on valve type A or B. No relationship was noted between immediate outcomes and bodyweight or pulmonary annulus diameter. CONCLUSION: Dogs with severe pulmonic stenosis that underwent low-pressure BV had good immediate outcomes with no difference in outcome based on valve morphology. Further randomized controlled studies are needed to compare the outcomes of different strategies for BV in dogs with large-diameter pulmonary annulus.

Double-outlet right ventricle in a Vietnamese potbellied pig.

A 6-month-old, neutered male, Vietnamese potbellied pig presented for evaluation of exercise intolerance and intermittent episodes of exertional cyanosis. Initial diagnostic evaluation revealed arterial hypoxemia. Transthoracic echocardiogram revealed double-outlet right ventricle (DORV) and a subaortic ventricular septal defect. Agitated saline contrast study confirmed the entry of saline contrast from the right ventricle into both pulmonary artery and aorta. Due to deterioration of clinical status, the patient was euthanized 3 months later. Gross necropsy examination was performed confirming the congenital cardiac defects noted on the echocardiogram. To the authors knowledge, this is the first case report of DORV in a Vietnamese potbellied pig.

Periprocedural vascular access complications associated with percutaneous femoral arterial access using the modified Seldinger's technique in dogs during cardiac catheterization: a single-center experience.

BACKGROUND: The primary objective of this study is to evaluate the peri-procedural major and minor complications associated with percutaneous femoral arterial access using modified Seldinger's technique in dogs that underwent cardiac catheterization. METHODS: Medical records of 62 client owned dogs that underwent percutaneous femoral arterial access for interventional cardiac procedures were retrospectively evaluated. Post-procedural manual compression was used for hemostasis. Peri-procedural vascular access complications (that occurred from procedure time to discharge) were evaluated. Vascular access complications were divided into two groups: minor complications that did not require specific therapy and major complications that did require an intervention to address the complication associated with vascular access. RESULTS: The minor complication rate was 30.6% (19/62) with most dogs experiencing minor bruising and small hematomas. The major complication rate was 3.2% (2/62). Both major complications were associated with bleeding with one dog requiring blood transfusion and the other dog requiring fluid therapy. No peri-procedural mortality associated with vascular access was noted. CONCLUSION: This retrospective study suggests that percutaneous femoral arterial access using the modified Seldinger's technique with post-procedural manual compression for hemostasis is viable option for vascular access during cardiac catheterization and associated with no peri-procedural mortality in dogs. The lower rate of complications noted in this study may be related to operator experiences and as such complication rate at a single center may not reflect the experience at other centers.

Infective aortic valve endocarditis in a cat with patent ductus arteriosus and perimembranous ventricular septal defect.

A 3-year-old, male neutered, domestic short-haired cat presented for evaluation of respiratory distress. Transthoracic echocardiography revealed a left-to-right shunting ventricular septal defect, a left-to-right shunting patent ductus arteriosus, and a vegetative growth on the aortic valve leaflet consistent with aortic valve endocarditis. Because of poor response to therapy, the owner elected euthanasia, and a necropsy was performed. Gross necropsy examination confirmed the congenital cardiac defects, and aortic valve endocarditis was noted on the echocardiogram. Histopathological examination revealed diffuse interstitial pneumonia and evidence for systemic septic embolism including renal infarcts and brain microabscesses. To the authors' knowledge, this is the first case report of aortic valve endocarditis in a cat in association with congenital cardiac malformations.

Comparison of single- versus seven-day Holter analysis for the identification of dilated cardiomyopathy predictive criteria in apparently healthy Doberman Pinscher dogs.

INTRODUCTION: The primary objective of this study was to test whether seven-day Holter recording improves the sensitivity of detecting dilated cardiomyopathy (DCM) predictive criteria (DCMp) compared with 24-h Holter recording in asymptomatic Doberman Pinscher (DP) dogs. ANIMALS: Twenty-eight asymptomatic DP dogs with normal echocardiographic examinations. METHODS: Dogs with normal echocardiographic examinations underwent seven-day Holter monitoring. The presence of ≥50 ventricular premature complexes and or ≥ one couplet/one triplet/one episode of ventricular tachycardia per 24-h period was considered positive for DCMp. RESULTS: Five dogs were positive on the first day, and an additional six dogs tested positive from day two to seven of the Holter recording. The number of dogs positive for DCMp detected by four days was significantly different (p = 0.031) compared with the first-day Holter recording. CONCLUSIONS: Seven-day Holter recording detected significantly more dogs with DCMp compared with the first-day Holter recording. Follow-up studies are warranted to evaluate the long-term accuracy of multiple-day Holter analysis in predicting the development of DCM in DP dogs.

Pericardial Effusion in a Dog with Pericardial Hemangiosarcoma.

An adult Jack Russel terrier dog presented for evaluation of large-volume peritoneal and pleural effusion. Echocardiography revealed scant pericardial effusion and abnormally thickened pericardium. Electrocardiography revealed complete atrioventricular block with junctional and ventricular escape beats and occasional ventricular premature complexes. Computed tomography of the thorax confirmed diffuse abnormal thickening of the pericardium, and a tentative diagnosis of constrictive-effusive pericarditis was made. The dog underwent subtotal pericardiectomy to remove the parietal pericardium and permanent epicardial pacemaker implantation to manage bradycardia. Based on pericardial histopathology and immunohistochemistry, a diagnosis of pericardial hemangiosarcoma was made. Systemic chemotherapy was initiated with doxorubicin 1 month after surgery. Despite initial improvement with chemotherapy, the dog was euthanized 4 months after surgery because of development of recurrent pleural effusion. To the author's knowledge, this is the first case report in dogs to describe isolated pericardial location of hemangiosarcoma resulting in constrictive-effusive pericarditis.

Echocardiographic variables in healthy North American Salukis.

INTRODUCTION: To report normal echocardiographic variables from a population of healthy Salukis in North America. ANIMALS: The study included 83 healthy adult Salukis from North America with structurally normal hearts. METHODS: All animals underwent a full physical examination and two-dimensional, M-mode, and Doppler echocardiography using the right parasternal and left apical views with the left ventricular volumes calculated using the Simpson's method of discs. Echocardiographic variables were compared among sex, body surface area, and body weight (BW) using linear regression. The 95% predictive intervals were calculated for both unadjusted and BW-adjusted data. RESULTS: No relationship between sex and the echocardiographic variables was noted. Predictive intervals for echocardiographic variables are presented for 22 echocardiographic variables. Linear regression suggested that 16 of those variables were associated with BW. The 95% predictive intervals of echocardiographic variables adjusted for BW are reported. CONCLUSIONS: The data from this study provide breed-specific echocardiographic reference values for Salukis.

Sudden cardiac death in a dog during Holter recording-R on T phenomenon.

A 6-year-old castrated male Golden Retriever was diagnosed with severe subaortic stenosis with severe left atrial enlargement and high heart rate due to atrial fibrillation. Treatment with digoxin and diltiazem to control ventricular response rate was initiated. Ambulatory electrocardiographic monitoring (Holter monitoring) was performed at the beginning of treatment and was repeated to evaluate the patient's response to drug therapy. Drug dose adjustments were made based on response to therapy as assessed by Holter monitoring. The dog experienced sudden death at home 19 days after beginning treatment while wearing the Holter monitor. Analysis of the Holter recording revealed marked increase in number and complexity of ventricular arrhythmias. A ventricular premature complex occurring on a T wave (R on T) was noted preceding the polymorphic ventricular tachycardia. This arrhythmia immediately degenerated into ventricular fibrillation followed by asystole. This case report describes the arrhythmia that preceded cardiac arrest and reviews the risk factors that could have potentiated the fatal arrhythmia in this dog.

Alternative methods for the measurement of the minimal ductal diameter of a patent ductus arteriosus in a dog.

A two and half-year-old, 24 kg, spayed female German Shepherd was presented for evaluation of a suspected patent ductus arteriosus (PDA). Transthoracic echocardiographic examination confirmed a left to right shunting PDA. Closure of the PDA was recommended, and the owners elected to have minimally invasive transcatheter closure of the PDA performed. Standard ductal angiography failed to provide adequate measurements of the minimal ductal diameter (MDD). Alternative methods of measuring the MDD using an angiography catheter and a balloon catheter were performed. The PDA was occluded using an Amplatz® Canine Ductal Occluder without complication. Further evaluation of these techniques is needed to determine the accuracy, overall clinical efficacy, and safety of using alternative methods for the measurement of the MDD of a PDA.

Suppression of endogenous antioxidant enzymes by 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced oxidative stress in chicken liver during development.

Domestic chickens (Gallus gallus) are an excellent model in which to evaluate developmental toxicity and oxidative stress because of their high sensitivity to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). The goal of this study was to measure the effects of environmentally relevant doses of TCDD on endogenous hepatic antioxidant enzyme activity in hatchling chickens. The vehicle (sunflower oil) or 2, 20, or 200 pg/g TCDD was injected into chicken eggs before incubation. On hatching, livers were harvested and quickly frozen. The changes in activity of antioxidant enzymes, including glutathione peroxidase (GPx), glutathione reductase (GRx), copper zinc superoxide dismutase (SOD), and catalase (CAT) were determined as indicators of oxidative stress. TCDD exposure was associated with a significant suppression of the activities of the protective endogenous enzymes GPx, GRx, and SOD in the liver, even at the lowest dose. CAT activity was also suppressed, but not significantly. The measured decreases were 37% to 63% for GPx, 50% to 58% for GRx, 30% to 40% for SOD, and 16% to 24% for CAT. Noncomplex dose-response relationships were evident in GPx and GRx, whereas SOD and CAT curves were U-shaped. These results demonstrate that a decreased ability to scavenge reactive oxygen species may result from developmental TCDD exposure at very low doses, contributing to oxidative stress and thus to the embryotoxicity of TCDD.

Influence of treatment of diabetic rats with combinations of pycnogenol, beta-carotene, and alpha-lipoic acid on parameters of oxidative stress.

Treatment with antioxidants may act more effectively to alter markers of free radical damage in combinations than singly. This study has determined whether treatment with combinations of pycnogenol, beta-carotene, and alpha-lipoic acid was more effective at reducing oxidative stress in diabetic rats than treatment with these antioxidants alone. It is not feasible, based on this study, to assume that there are interactive effects that make combinations of these antioxidants more effective than any one alone to combat oxidative stress. Female Sprague-Dawley rats, normal and streptozotocin-induced diabetic, were treated (10 mg/kg/day ip for 14 days) with pycnogenol, beta-carotene, pycnogenol + beta-carotene, or pycnogenol + beta-carotene + alpha-lipoic acid; controls were untreated. Concentrations of thiobarbituric acid reactive substances, glutathione and glutathione disulfide, and activities of glutathione reductase, glutathione peroxidase, superoxide dismutase, and catalase were measured in liver, kidney, and heart. Four types of effects were observed: (1) treatment with beta-carotene alone either reversed (cardiac glutathione disulfide) or elevated (cardiac glutathione, hepatic glutathione peroxidase activity) levels seen in diabetic animals; (2) beta-carotene alone produced no effect, but pycnogenol both alone and in combinations elevated (renal glutathione peroxidase and glutathione reductase activities, hepatic glutathione reductase activity and glutathione disulfide) or depressed (cardiac glutathione disulfide) levels seen in untreated diabetic animals; (3) all treatments with antioxidants, either alone or in combination, either normalized (lipid peroxidation in all tissues), elevated (hepatic GSH, cardiac glutathione peroxidase activity), or had no effect on (activities of hepatic catalase and superoxide dismutase in all tissues) levels seen in diabetic animals; (4) in only one case (cardiac glutathione reductase activity) levels in diabetic animals treated with combinations of antioxidants were normal, but elevated in animals treated with either antioxidant alone. Antioxidant effects seem to be dependent on the nature of the antioxidant used and not on combination effects.

Effects of alpha-lipoic acid on biomarkers of oxidative stress in streptozotocin-induced diabetic rats.

Increased oxidative stress and impaired antioxidant defense mechanisms are important factors in the pathogenesis and progression of diabetes mellitus and other oxidant-related diseases. This study was designed to determine whether alpha-lipoic acid, which has been shown to have substantial antioxidant properties, when administered (10 mg/kg ip) once daily for 14 days to normal and diabetic female Sprague-Dawley rats would prevent diabetes-induced changes in biomarkers of oxidative stress in liver, kidney and heart. Serum glucose concentrations, aspartate aminotransferase activity, and glycated hemoglobin levels, which were increased in diabetes, were not significantly altered by alpha-lipoic acid treatment. Normal rats treated with a high dose of alpha-lipoic acid (50 mg/kg) survived but diabetic rats on similar treatment died during the course of the experiment. The activity of glutathione peroxidase was increased in livers of normal rats treated with alpha-lipoic acid, but decreased in diabetic rats after alpha-lipoic acid treatment. Hepatic catalase activity was decreased in both normal and diabetic rats after alpha-lipoic acid treatment. Concentrations of reduced glutathione and glutathione disulfide in liver were increased after alpha-lipoic acid treatment of normal rats, but were not altered in diabetics. In kidney, glutathione peroxidase activity was elevated in diabetic rats, and in both normal and diabetic animals after alpha-lipoic acid treatment. Superoxide dismutase activity in heart was decreased in diabetic rats but normalized after treatment with alpha-lipoic acid; other cardiac enzyme activities were not influenced by either diabetes or antioxidant treatment. These results suggest that after 14 days of treatment with an appropriate pharmacological dose, alpha-lipoic acid may reduce oxidative stress in STZ-induced diabetic rats, perhaps by modulating the thiol status of the cells.

Effects of pycnogenol treatment on oxidative stress in streptozotocin-induced diabetic rats.

Free radicals and oxidative stress have been implicated in the etiology of diabetes and its complications. This in vivo study has examined whether subacute administration of pycnogenol, a French pine bark extract containing procyanidins that have strong antioxidant potential, alters biomarkers of oxidative stress in normal and diabetic rats. Diabetes was induced in female Sprague-Dawley rats by a single injection of streptozotocin (90 mg/kg body weight, ip), resulting (after 30 days) in subnormal body weight, increased serum glucose concentrations, and an increase in liver weight, liver/body weight ratios, total and glycated hemoglobin, and serum aspartate aminotransferase activity. Normal and diabetic rats were treated with pycnogenol (10 mg/kg body weight/day, ip) for 14 days. Pycnogenol treatment significantly reduced blood glucose concentrations in diabetic rats. Biochemical markers for oxidative stress were assessed in the liver, kidney, and heart. Elevated hepatic catalase activity in diabetic rats was restored to normal levels after pycnogenol treatment. Additionally, diabetic rats treated with pycnogenol had significantly elevated levels of reduced glutathione and glutathione redox enzyme activities. The results demonstrate that pycnogenol alters intracellular antioxidant defense mechanisms in streptozotocin-induced diabetic rats.

Diabetes, oxidative stress, and antioxidants: a review.

Increasing evidence in both experimental and clinical studies suggests that oxidative stress plays a major role in the pathogenesis of both types of diabetes mellitus. Free radicals are formed disproportionately in diabetes by glucose oxidation, nonenzymatic glycation of proteins, and the subsequent oxidative degradation of glycated proteins. Abnormally high levels of free radicals and the simultaneous decline of antioxidant defense mechanisms can lead to damage of cellular organelles and enzymes, increased lipid peroxidation, and development of insulin resistance. These consequences of oxidative stress can promote the development of complications of diabetes mellitus. Changes in oxidative stress biomarkers, including superoxide dismutase, catalase, glutathione reductase, glutathione peroxidase, glutathione levels, vitamins, lipid peroxidation, nitrite concentration, nonenzymatic glycosylated proteins, and hyperglycemia in diabetes, and their consequences, are discussed in this review. In vivo studies of the effects of various conventional and alternative drugs on these biomarkers are surveyed. There is a need to continue to explore the relationship between free radicals, diabetes, and its complications, and to elucidate the mechanisms by which increased oxidative stress accelerates the development of diabetic complications, in an effort to expand treatment options.

Effects of quercetin on antioxidant defense in streptozotocin-induced diabetic rats.

In light of evidence that some complications of diabetes mellitus may be caused or exacerbated by oxidative damage, we investigated the effects of subacute treatment with the antioxidant quercetin on tissue antioxidant defense systems in streptozotocin-induced diabetic Sprague-Dawley rats (30 days after streptozotocin induction). Quercetin, 2-(3,4-dihydroxyphenyl)-3,5,7-trihydroxy-4H-1-benzopyran-4-one, was administered at a dose of 10mg/kg/day, ip for 14 days, after which liver, kidney, brain, and heart were assayed for degree of lipid peroxidation, reduced and oxidized glutathione content, and activities of the free-radical detoxifying enzymes catalase, superoxide dismutase, glutathione peroxidase, and glutathione reductase. Treatment of normal rats with quercetin increased serum AST and increased hepatic concentration of oxidized glutathione. All tissues from diabetic animals exhibited disturbances in antioxidant defense when compared with normal controls. Quercetin treatment of diabetic rats reversed only the diabetic effects on brain oxidized glutathione concentration and on hepatic glutathione peroxidase activity. By contrast, a 20% increase in hepatic lipid peroxidation, a 40% decline in hepatic glutathione concentration, an increase in renal (23%) and cardiac (40%) glutathione peroxidase activities, and a 65% increase in cardiac catalase activity reflect intensified diabetic effects after treatment with quercetin. These results call into question the ability of therapy with the antioxidant quercetin to reverse diabetic oxidative stress in an overall sense.

Effects of isoeugenol on oxidative stress pathways in normal and streptozotocin-induced diabetic rats.

Because some complications of diabetes mellitus may result from oxidative damage, we investigated the effects of subacute treatment (10mg/kg/day, intraperitoneal [ip], for 14 days) with the antioxidant isoeugenol on the oxidant defense system in normal and 30-day streptozotocin-induced diabetic Sprague-Dawley rats. Liver, kidney, brain, and heart were assayed for degree of lipid peroxidation, reduced and oxidized glutathione content, and activities of the free radical-detoxifying enzymes catalase, superoxide dismutase, glutathione peroxidase, and glutathione reductase. All tissues from diabetic animals exhibited disturbances in antioxidant defense when compared with normal controls. Treatment with isoeugenol reversed diabetic effects on hepatic glutathione peroxidase activity and on oxidized glutathione concentration in brain. Treatment with the lipophilic compound isoeugenol also decreased lipid peroxidation in both liver and heart of normal animals and decreased hepatic oxidized glutathione content in both normal and diabetic rats. Some effects of isoeugenol treatment, such as decreased activity of hepatic superoxide dismutase and glutathione reductase in diabetic rats, were unrelated to the oxidative effects of diabetes. In heart of diabetic animals, isoeugenol treatment resulted in an exacerbation of already elevated activities of catalase. These results indicate that isoeugenol therapy may not reverse diabetic oxidative stress in an overall sense.

Effects of coenzyme Q10 treatment on antioxidant pathways in normal and streptozotocin-induced diabetic rats.

Coenzyme Q10 is an endogenous lipid soluble antioxidant. Because oxidant stress may exacerbate some complications of diabetes mellitus, this study investigated the effects of subacute treatment with exogenous coenzyme Q10 (10 mg/kg/day, i.p. for 14 days) on tissue antioxidant defenses in 30-day streptozotocin-induced diabetic Sprague-Dawley rats. Liver, kidney, brain, and heart were assayed for degree of lipid peroxidation, reduced and oxidized glutathione contents, and activities of catalase, superoxide dismutase, glutathione peroxidase, and glutathione reductase. All tissues from diabetic animals exhibited increased oxidative stress and disturbances in antioxidant defense when compared with normal controls. Treatment with the lipophilic compound coenzyme Q10 reversed diabetic effects on hepatic glutathione peroxidase activity, on renal superoxide dismutase activity, on cardiac lipid peroxidation, and on oxidized glutathione concentration in brain. However, treatment with coenzyme Q10 also exacerbated the increase in cardiac catalase activity, which was already elevated by diabetes, further decreased hepatic glutathione reductase activity, augmented the increase in hepatic lipid peroxidation, and further increased glutathione peroxidase activity in the heart and brain of diabetic animals. Subacute dosing with coenzyme Q10 ameliorated some of the diabetes-induced changes in oxidative stress. However, exacerbation of several diabetes-related effects was also observed.

Characterization of oxidative stress in various tissues of diabetic and galactose-fed rats.

Rats fed a galactose-rich diet have been used for several years as a model for diabetes to study, particularly in the eye, the effects of excess blood hexoses. This study sought to determine the utility of galactosemia as a model for oxidative stress in extraocular tissues by examining biomarkers of oxidative stress in galactose-fed rats and experimentally-induced diabetic rats. Sprague-Dawley rats were divided into four groups: experimental control; streptozotocin-induced diabetic; insulin-treated diabetic; and galactose-fed. The rats were maintained on these regimens for 30 days, at which point the activities of catalase, glutathione peroxidase, glutathione reductase, and superoxide dismutase, as well as levels of lipid peroxidation and reduced and oxidized glutathione were determined in heart, liver, and kidney. This study indicates that while there are some similarities between galactosemic and diabetic rats in these measured indices of oxidative stress (hepatic catalase activity levels and hepatic and renal levels of oxidized glutathione in both diabetic and galactosemic rats were significantly decreased when compared to normal), overall the galactosemic rat model is not closely parallel to the diabetic rat model in extra-ocular tissues. In addition, several effects of diabetes (increased hepatic glutathione peroxidase activity, increased superoxide dismutase activity in kidney and heart, decreased renal and increased cardiac catalase activity) were not mimicked in galactosemic rats, and glutathione concentration in both liver and heart was affected in opposite ways in diabetic rats and galactose-fed rats. Insulin treatment reversed/prevented the activity changes in renal and cardiac superoxide dismutase, renal and cardiac catalase, and hepatic glutathione peroxidase as well as the hepatic changes in lipid peroxidation and reduced and oxidized glutathione, and the increase in cardiac glutathione. Thus, prudence should be exercised in the use of experimentally galactosemic rats as a model for diabetes until the correspondence of the models has been more fully characterized.