Search

BACKGROUND: Hypertrophic cardiomyopathy is the most prevalent heart disorder in cats and principal cause of cardiovascular morbidity and mortality. Yet, the impact of preclinical disease is unresolved.HYPOTHESIS/OBJECTIVES: Observational study to characterize cardiovascular morbidity and survival in cats with preclinical nonobstructive (HCM) and obstructive (HOCM) hypertrophic cardiomyopathy and in apparently healthy cats (AH).ANIMALS: One thousand seven hundred and thirty client-owned cats (430 preclinical HCM; 578 preclinical HOCM; 722 AH).METHODS: Retrospective multicenter, longitudinal, cohort study. Cats from 21 countries were followed through medical record review and owner or referring veterinarian interviews. Data were analyzed to compare long-term outcomes, incidence, and risk for congestive heart failure (CHF), arterial thromboembolism (ATE), and cardiovascular death.RESULTS: During the study period, CHF, ATE, or both occurred in 30.5% and cardiovascular death in 27.9% of 1008 HCM/HOCM cats. Risk assessed at 1, 5, and 10 years after study entry was 7.0%/3.5%, 19.9%/9.7%, and 23.9%/11.3% for CHF/ATE, and 6.7%, 22.8%, and 28.3% for cardiovascular death, respectively. There were no statistically significant differences between HOCM compared with HCM for cardiovascular morbidity or mortality, time from diagnosis to development of morbidity, or cardiovascular survival. Cats that developed cardiovascular morbidity had short survival (mean ± standard deviation, 1.3 ± 1.7 years). Overall, prolonged longevity was recorded in a minority of preclinical HCM/HOCM cats with 10% reaching 9-15 years.CONCLUSIONS AND CLINICAL IMPORTANCE: Preclinical HCM/HOCM is a global health problem of cats that carries substantial risk for CHF, ATE, and cardiovascular death. This finding underscores the need to identify therapies and monitoring strategies that decrease morbidity and mortality.

The objectives of this study were to determine a breed-specific vertebral heart scale (VHS) range for the dachshund and compare results to the established reference range of 9.7 ± 0.5, calculate inter-observer variability, and correlate VHS with echocardiography. Fifty-one normal dachshunds had radiographs and an echocardiogram performed. Five observers measured VHS to the nearest 0.25 vertebra. The data was analyzed using one-way analysis of variance, Wilcoxon Rank Sum test, Mann-Whitney rank sum test, calculation of reference and confidence intervals, Spearman rank-order correlations, and generation of intra-class correlations and confidence intervals. P < .05 was considered significant. The median for right lateral VHS was significantly larger than left (10.3 [range 9.25–11.55] versus 10.1 [range, 8.7–11.31], p < .0001). VHS for females was significantly larger than for males (left: 10.56 [9.2–11.31] versus 9.74 [8.7–10.88] and right: 10.8 [9.5–11.55] versus 9.99 [9.25–10.8], p = .0002). Observer consistency was high with an intra-class correlation coefficient of 0.95. No significant correlation was found between left atrial echocardiographic parameters and VHS. Results indicate normal dachshunds have a median VHS above the published generic canine reference range, and VHS can be reliably performed by observers with varying degrees of clinical experience.

Background Epidemiologic knowledge regarding noncardiovascular and all‐cause mortality in apparently healthy cats (AH) and cats with preclinical hypertrophic cardiomyopathy (pHCM) is limited, hindering development of evidence‐based healthcare guidelines. Objectives To characterize/compare incidence rates, risk, and survival associated with noncardiovascular and all‐cause mortality in AH and pHCM cats. Animals A total of 1730 client‐owned cats (722 AH, 1008 pHCM) from 21 countries. Methods Retrospective, multicenter, longitudinal, cohort study. Long‐term health data were extracted by medical record review and owner/referring veterinarian interviews. Results Noncardiovascular death occurred in 534 (30.9%) of 1730 cats observed up to 15.2 years. Proportion of noncardiovascular death did not differ significantly between cats that at study enrollment were AH or had pHCM (P = .48). Cancer, chronic kidney disease, and conditions characterized by chronic weight‐loss‐vomiting‐diarrhea‐anorexia were the most frequently recorded noncardiovascular causes of death. Incidence rates/risk of noncardiac death increased with age in AH and pHCM. All‐cause death proportions were greater in pHCM than AH (65% versus 40%, respectively; P

Development of new vaccines, diagnostics, and therapeutics for biodefense or other relatively rare infectious diseases is hindered by the lack of naturally occurring human disease on which to conduct clinical trials of efficacy. To overcome this experimental gap, the U.S. Food and Drug Administration established the Animal Rule, in which efficacy testing in two well-characterized animal models that closely resemble human disease may be accepted in lieu of large-scale clinical trials for diseases with limited natural human incidence. In this report, we evaluated the Brown Norway rat as a model for pneumonic plague and describe the natural history of clinical disease following inhalation exposure to Yersinia pestis. In high-capacity, high-containment housing, we monitored temperature, activity, heart rate, and rhythm by capturing electronic impulses transmitted from abdominal telemeter implants. Using this system, we show that reduced activity and development of fever are sensitive indications of disease progression. Furthermore, we identified heart arrhythmias as contributing factors to the rapid progression to lethality following the fever response. Together, these data validate the Brown Norway rat as an experimental model for human pneumonic plague and provide new insight that may ultimately lead to novel approaches in postexposure treatment of this devastating infection.

Background Doxorubicin is a common antineoplastic agent with dose-dependent cardiotoxic adverse effects, and pre-existing myocardial dysfunction is a contraindication to its use. Objectives To systematically define the hemodynamic and biochemical alterations in dogs undergoing chemotherapy for newly diagnosed lymphoma and assess the reversibility of these alterations with fluid administration. Animals Twenty-one client-owned dogs with newly diagnosed lymphoma were evaluated 1 week after induction of chemotherapy. Underlying degenerative valve disease was exclusionary. Eighteen healthy age- and weight-matched dogs were used as controls. Methods Physical examination, blood pressure by Doppler, echocardiography, and biochemical evaluation (routine serum biochemistry, plasma renin activity and aldosterone concentrations, plasma and urine osmolalities, and urine electrolyte concentrations) were measured in dogs with lymphoma and compared to controls. Dogs with lymphoma received crystalloids IV at 6 mL/kg/h for 24 hours. All variables were reassessed at 4 and 24 hours. Deuterium oxide dilution and bromide dilution were used to determine total body water and extracellular water space, respectively. Results Baseline echocardiograms showed significantly smaller chamber dimensions in dogs with lymphoma compared to controls. These changes were reversed by fluid administration. Systolic blood pressure and urine sodium concentration were significantly increased, and bromide dilution space, PCV, urine specific gravity, and urine potassium concentration were significantly decreased compared to controls. Conclusion and Clinical Importance Echocardiographic and biochemical abnormalities in dogs with lymphoma appear consistent with volume depletion, and may be the result of systemic hypertension and subsequent pressure natriuresis.

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.

An 8-year-old, castrated male Basset Hound was evaluated for congestive heart failure and atrial fibrillation. Echocardiography and angiography demonstrated a left-to-right shunting aorticopulmonary fistula. Coil embolization of the fistula was initially successful in reducing the volume of blood flow through the vascular network. The dog was medically managed for congestive heart failure until it was euthanized 6 months after initial presentation. The physiology and treatment of centrally located arteriovenous fistulae are discussed.

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.

Background: Hydration status is important to the cardiovascular system because of its effects on preload. Decreased preload can alter echocardiographic measurements of systolic and diastolic function, potentially confounding interpretation of results. Hypothesis/Objectives: Mild fluid deficits are associated with measurable echocardiographic changes that are validated by physical and biochemical markers of decreased intravascular volume. Animals: Twenty-five healthy staff/student-owned dogs with no evidence of cardiac or renal disease. Methods: Prospective, interventional laboratory study. Dogs were randomly assigned to water deprivation (WD) alone for 8 hours (n = 13) or to furosemide treatment (FTx, 2.5 mg/kg IV) followed by WD for 8 hours (n = 12). Echocardiograms, biochemical sampling, and physical parameters were measured at baseline, and after 4 and 8 hours. Results: Both protocols induced fluid deficit as indicated by significant (P < .00001) decreases in weight at 4 hours (WD, 1.1%; FTx, 3.7%) and 8 hours (WD, 2.7%; FTx, 4.5%). Furosemide significantly decreased left ventricular end-diastolic volume (54.3 ± 19.3–42.1 ± 17.3 mL, P < .0001), cardiac index (4.2 ± 1.1–2.9 ± 0.9 L/min/M2, P < .0001), and mitral valve E wave velocity (0.79 ± 0.2–0.66 ± 0.2 m/s, P= .0004). These changes were accompanied by significant increases in blood urea nitrogen concentration (13.8 ± 2.6–14.8 ± 2.7 mg/dL, P= .04), vasopressin concentration (1.4 ± 1.2–3.3 ± 1.9 pg/mL, P= .045), and PCV (49.8 ± 4.5–53.2 ± 6.5%, P= .006). Effects of water deprivation alone were similar, but less pronounced. Conclusions and Clinical Importance: Mild fluid deficits have measurable hemodynamic effects in dogs. Hydration status should be considered when evaluating cardiac function by echocardiogram.

Background: Pimobendan is a positive inotrope and vasodilator that may be useful in the treatment of pulmonary hypertension (PHT) secondary to degenerative mitral valve disease. Hypothesis: Pimobendan decreases the severity of PHT measured echocardiographically and improves quality-of-life scores. Changes in N-terminal probrain natriuretic peptide (NT-proBNP) concentrations will reflect improvement in severity of PHT. Animals: Ten client-owned dogs with peak tricuspid regurgitant flow velocity (TRFV) ≥3.5 m/s. Methods: Prospective short-term, double-blinded, crossover design, with a long-term, open-label component. Short term, dogs were randomly allocated to receive either placebo or pimobendan (0.18–0.3 mg/kg PO q12 h) for 14 days. After a 1-week washout, they received the alternative treatment for 14 days, followed by pimobendan open-label for 8 weeks. Results: Short-term comparison: peak TRFV decreased in all dogs on pimobendan compared with placebo from a median of 4.40 (range, 3.2–5.6) to 3.75 (range, 2.4–4.8) m/s (P < .0001). NT-proBNP concentration decreased after treatment with pimobendan from a median of 2,143 (range, 450–3,981) to 1,329 (range, 123–2,411) pmol/L (P= .0009). All dogs improved their quality-of-life score (P= .006). In the long-term comparisons, peak TRFV decreased in all dogs from a median of 4.28 (range, 3.5–5.7) to 3.52 (range, 2.4–5.0) m/s (P < .0001). No significant changes in NT-proBNP or quality-of-life scores were detected. Conclusions and Clinical Importance: Pimobendan lowered severity of measurable PHT, improved quality-of-life scores, and decreased NT-proBNP concentrations short-term. Long term, only the reduction in TRFV was maintained.

Duchenne muscular dystrophy (DMD) affects both skeletal and cardiac muscle. It is currently unclear whether the strategies developed for skeletal muscle can ameliorate cardiomyopathy. Synthetic mini-/micro-dystrophin genes have yielded impressive skeletal muscle protection in animal models. The 6-kb DeltaH2-R19 minigene is particularly promising because it completely restores skeletal muscle force to wild-type levels. Here, we examined whether expressing this minigene in the heart, but not skeletal muscle, could normalize cardiac function in the mdx model of DMD cardiomyopathy. Transgenic mdx mice were generated to express the DeltaH2-R19 minigene under the control of the alpha-myosin heavy-chain promoter. Heart structure and function were examined in adult and very old mice. The DeltaH2-R19 minigene enhanced cardiomyocyte sarcolemmal strength and prevented myocardial fibrosis. It also restored the dobutamine response and enhanced treadmill performance. Surprisingly, heart-restricted DeltaH2-R19 minigene expression did not completely normalize electrocardiogram and hemodynamic abnormalities. Overall, systolic function and ejection fraction were restored to normal levels but stroke volume and cardiac output remained suboptimal. Our results demonstrate that the skeletal muscle-proven DeltaH2-R19 minigene can correct cardiac histopathology but cannot fully normalize heart function. Novel strategies must be developed to completely restore heart function in DMD.

Objective: To describe successful treatment of third-degree atrioventricular (AV) block using temporary noninvasive transthoracic pacing and placement of a permanent transvenous pacemaker in a case of suspected lily-of-the-valley (Convallaria majalis) intoxication in a dog. Case summary: A 2-year-old neutered male Beagle weighing 17.8 kg was presented to the emergency service for treatment of bradycardia, vomiting, and lethargy. An electrocardiogram revealed third-degree AV block that was nonresponsive to atropine. Ten hours after admission, the dog became obtunded. Treatment initially consisted of temporary noninvasive transthoracic pacing and eventually placement of a permanent transvenous pacemaker. The initial history did not suggest that the dog had access to any known cardiotoxins. However, C. majalis, which contains cardiac glycosides, was identified within the dog's environment and the dog's serum did contain digoxin or an immunologically cross-reactive compound. New or unique information provided: This is the first reported successful management of C. majalis toxicosis in a dog. Temporary noninvasive transthoracic pacing was used in the management of this case as a safe and effective bridge to permanent pacemaker implantation.

Angiotensin-II (Ang-II) contributes to cardiac remodeling and left ventricular dysfunction. In contrast, exercise may have beneficial effects on left ventricular structure and function.We investigated the effects of low-intensity exercise training (ET) on in vivo cardiac function in hypertensive TG (mREN-2)27 rats (Ren-2) which develop left ventricular hypertrophy and dysfunction. Ren-2 rats and Sprague Dawley (SD) controls (4-5 weeks) began treadmill exercise every day for 5-6 weeks. Cardiac function was evaluated by echocardiography. Cardiac output and stroke volume were increased by ET in both 8-wk-old SD and Ren-2. Slope of mitral deceleration time, a non-invasive measure of diastolic function, was lower in the Ren-2 rats, but not changed by ET. LV collagen deposition, as assessed by hydroxyproline assay, was not affected by rat strain or ET at 10-11 weeks of age. Left ventricular B-type natriuretic peptide mRNA levels were higher in the Ren-2 rats (100%), but not affected by ET. Both alpha (~14.5 fold) and beta (~2.5 fold) myosin heavy chain mRNA were higher in the LV of Ren-2 rats (p0.05), but were not changed by ET.Low-intensity exercise training in Ren-2 rats, a model of Ang-II-mediated hypertension, maintains cardiac index and stroke volume in the presence of impaired diastolic function at 8 wks of age.

Object The object of this study was to determine whether the combination of cyclosporine and simvastatin could ameliorate cerebral vasospasm after subarachnoid hemorrhage (SAH) in a canine model to a greater extent than simvastatin alone. Methods Animals were assigned to one of three groups: control (five dogs), simvastatin alone (four), or simvastatin and cyclosporine (four). A double SAH model was used. Baseline basilar artery (BA) angiograms were obtained. These were repeated at Days 3, 7, and 10. Measurement of the BA diameter was performed. Decreased BA diameter was seen on Day 3 in the control and simvastatin/cyclosporine group. A return to baseline diameters was seen by Day 7. An increase from baseline diameter was seen in the simvastatin group at Day 10. Conclusions Cyclosporine may interfere with the vasodilatory effects of simvastatin. Vasodilation greater than baseline is seen at Day 10 in the simvastatin group. The combination of simvastatin and cyclosporine does not ameliorate cerebral vasospasm in a canine model to a greater extent than simvastatin alone.

The present study was conducted to test the hypothesis that salt-dependent hypertension, in rats with an unresponsive renin-angiotensin system, is characterized by a “whole body autoregulation” hemodynamic profile. To test this hypothesis, rats were chronically instrumented to continuously measure cardiac output (CO) and arterial pressure (AP). A venous catheter was implanted for infusion of saline vehicle (Veh; n = 8) or treatment [enalapril (2 mg · kg–1 · day–1) plus ANG II: ANG-NORM (5 ng · kg–1 · min–1 ANG II, n = 8) or ANG-HI (10 ng · kg–1 · min–1 ANG II, n = 9)] to pharmacologically clamp plasma ANG II. After a 10-day recovery period on a 0.1% NaCl diet, AP and CO were measured continuously for 5 days of control (0.1% NaCl), 7 days of high salt (4.0% NaCl), and 5 days of recovery (0.1% NaCl). Hemodynamics did not change in the Veh group at any time. AP increased by ∼20 mmHg in the ANG-NORM and ANG-HI groups when NaCl was increased. Hypertension was mediated by an increase in CO of ∼12% at steady state, with no change in total peripheral resistance (TPR) during the high salt period. AP returned to control levels when dietary sodium was decreased, mediated by a ∼10% decrease in TPR, with CO remaining elevated. There was no difference in the hemodynamic responses to increased salt between the ANG-HI and ANG-NORM groups. We conclude that the whole body autoregulation hypothesis does not explain the hemodynamic profile of salt-dependent hypertension in rats with an unresponsive renin-angiotensin system.

Pericardial effusion (PE) resulting from neoplasia usually is associated with a poor prognosis, whereas idiopathic PE frequently has a good prognosis. This study examined the utility of pH measurement to distinguish between these 2 etiologies. Dogs were classified as having idiopathic PE (n = 12) if pericarditis was diagnosed on histopathology (n = 4) or if no historical, physical, or echocardiographic evidence of recurrent PE was present for at least 6 months after pericardiocentesis (n = 8). Dogs were classified as having neoplastic PE (n = 25) if pericardial or myocardial neoplasia was detected on histopathology (n = 11) or a discrete mass associated with the right atrium, right ventricle, or the aorta was visualized on echocardiography (n = 14). Samples of PE were centrifuged and the supernatant pH was measured with a portable pH meter. The lowest pH (6.40) was found in a dog with idiopathic PE and the highest pH (7.85) was found in a dog with neoplastic PE. However, data from the 2 groups overlapped in 33 out of 37 (89%) instances, and median pH from the idiopathic and neoplastic groups was not significantly different (7.40 and 7.47, respectively; P = 0.28; difference in medians = -0.7; 95% CI, -0.26-0.06). Because of the degree of overlap, our data provide little justification for the use of pH measurement as a diagnostic test in cases of PE.

The absence of dystrophin in the heart leads to Duchenne cardiomyopathy. Dystrophin-deficient dogs represent a critical model to translate novel therapies developed in mice to humans. Unfortunately, little is known about cardiophysiology changes in these dogs. We performed prospective electrocardiographic and echocardiographic examinations at 3, 6 and 12 months of age in four normal and three affected dogs obtained from the same litter. Affected dogs showed growth retardation and serum creatine kinase elevation. Necropsy confirmed cardiac dystrophin deficiency and histopathology. Q/R ratio elevation and diastolic left ventricular (LV) internal diameter reduction were the most consistent findings in affected dogs at all ages. At 6 and 12 months, dystrophic dogs also showed significant reduction of PR intervals, LV end diastolic/systolic volumes and systolic LV internal diameters. Epicardial and endocardial slope times were significantly reduced in affected dogs at 12 months. These results establish the baseline for evaluating experimental therapies in the future.

TEA domain transcription factor-1 (TEAD-1) is essential for proper heart development and is implicated in cardiac specific gene expression and the hypertrophic response of primary cardiomyocytes to hormonal and mechanical stimuli, and its activity increases in the pressure-overloaded hypertrophied rat heart. To investigate whether TEAD-1 is an in vivo modulator of cardiac specific gene expression and hypertrophy, we developed transgenic mice expressing hemagglutinin-tagged TEAD-1 under the control of the muscle creatine kinase promoter. We show that a sustained increase in TEAD-1 protein leads to an age-dependent dysfunction. Magnetic resonance imaging revealed decreases in cardiac output, stroke volume, ejection fraction, and fractional shortening. Isolated TEAD-1 hearts revealed decreased left ventricular power output that correlated with increased betaMyHC protein. Histological analysis showed altered alignment of cardiomyocytes, septal wall thickening, and fibrosis, although electrocardiography displayed a left axis shift of mean electrical axis. Transcripts representing most members of the fetal heart gene program remained elevated from fetal to adult life. Western blot analyses revealed decreases in p-phospholamban, SERCA2a, p-CX43, p-GSK-3alpha/beta, nuclear beta-catenin, GATA4, NFATc3/c4, and increased NCX1, nuclear DYKR1A, and Pur alpha/beta protein. TEAD-1 mice did not display cardiac hypertrophy. TEAD-1 mice do not tolerate stress as they die over a 4-day period after surgical induction of pressure overload. These data provide the first in vivo evidence that increased TEAD-1 can induce characteristics of cardiac remodeling associated with cardiomyopathy and heart failure.

Duchenne cardiomyopathy is a heart disease resulting from the loss of cardiac dystrophin. It significantly reduces the life quality and shortens lifespan in Duchenne muscular dystrophy (DMD), Becker muscular dystrophy (BMD) and X-linked dilated cardiomyopathy patients and carriers. Gene replacement therapy with adeno-associated viral vector (AAV) and gene repair therapy with exon skipping hold great promise for restoring dystrophin expression and ameliorating cardiomyopathy. The last few years have witnessed tremendous advances towards Duchenne cardiomyopathy gene therapy. The infrastructure (animal models and functional assays) is now available for comprehensive preclinical studies. Essential parameters, such as the therapeutic threshold, have also been defined. Together with the recent developments in novel AAV vectors and modified antisense oligonucleotides, clinical application of Duchenne cardiomyopathy gene therapy may become a reality in the near future.

Objective—To evaluate assessment of circulating amino terminal-pro-B-type natriuretic peptide (NT-proBNP) concentration as a means to discriminate between congestive heart failure and primary pulmonary disease in dogs. Design—Prospective case series. Animals—46 dogs with signs of respiratory distress or coughing. Procedures—All dogs underwent physical and thoracic radiographic examinations. Dogs with evidence of heart disease (eg, murmur, arrhythmia, or large cardiac silhouette detected by radiography) also underwent echocardiography. Dogs with no evidence of heart disease or failure were included if they underwent bronchoalveolar lavage (with cytologic examination and bacterial culture of the lavage fluid). Blood samples for NT-proBNP assay were obtained within 12 hours of the diagnosis of heart failure or prior to bronchoalveolar lavage in dogs with primary pulmonary disease. Circulating concentrations of NT-proBNP were compared between groups and correlated with radiographic and echocardiographic measures of cardiac size. Results—Congestive heart failure and primary pulmonary disease were diagnosed in 25 and 21 dogs, respectively. Dogs with congestive heart failure had significantly higher median serum or plasma NT-proBNP concentration (2,554 pmol/L; interquartile [25% to 75%] range, 1,651.5 to 3,475.5 pmol/L) than dogs with primary pulmonary disease (357 pmol/L; interquartile range, 192.5 to 565.5 pmol/L). Radiographic vertebral heart score and echocardiographic left atrial-to-aortic diameter ratio were not correlated with NT-proBNP concentration. Left ventricular end-diastolic diameter (measured echocardiographically) and NT-proBNP concentration were weakly correlated. Conclusions and Clinical Relevance—Serum or plasma NT-proBNP concentration assessment may be useful for discrimination of congestive heart failure from primary pulmonary disease in dogs with respiratory distress or cough.

Infection is an infrequent but major complication of cardiovascular device implantation.Treatment of patients with cardiovascular implant infection with antibiotic therapy and removal of the device is superior to antibiotic therapy alone.Medical records were reviewed for dogs that received a cardiovascular device from June 2001 to August 2006 at the University of Minnesota Veterinary Medical Center and the University of Missouri Veterinary Medical Teaching Hospital.Six of 63 (9.5%) pacemaker systems and 2 of 47 (4.3%) patent ductus arteriosus (PDA) occlusion devices became infected. Median time from procedure to diagnosis of implant infection was 62 days (range, 5 to 419). Median age of dogs with pacemaker infections was 8.5 years (range, 6.2 to 11.9). Pseudomonas aeruginosa and Staphylococcus spp were the most commonly cultured isolates. Four dogs were treated with antibiotics and pacemaker replacement. All 4 recovered completely from their infections. One was alive at the end of the study period, and 3 had been euthanized. However, the reasons for euthanasia were unrelated to pacemaker infection. In contrast, both dogs with infected pacemakers that were treated with antibiotics alone were euthanized because of complications attributable to infection. Infection of PDA occlusion devices occurred in puppies16 weeks of age, and Pasteurella spp were isolated from both. One was successfully treated with a combination of antibiotics and surgery, and the other was euthanized without treatment.Antibiotic therapy alone is associated with chronic complications in patients with cardiovascular implants and is unlikely to effect a cure.

Case Description—A 13-year-old llama was examined because of lethargy, inappetence, and syncope. Clinical Findings—Physical examination revealed muffled heart and lung sounds and peripheral edema. Clinicopathologic abnormalities included lymphopenia, hyperglycemia, prerenal azotemia, mild hyponatremia, mild hypoalbuminemia, and high γ-glutamyltransferase and creatine kinase activities. On ultrasonography, the liver appeared hyperechoic and ascites and pleural effusion were seen. Echocardiography revealed severe dilatation of the right atrium, right ventricle, and pulmonary artery; severe tricuspid regurgitation; and high right ventricular systolic pressure consistent with right-sided heart failure secondary to pulmonary hypertension. Treatment and Outcome—Treatment with furosemide was attempted, but because of failing health, the llama was euthanized 4 weeks later. Macronodular cirrhosis of the liver, glomerulonephritis, and intimal fibrosis and medial hypertrophy of muscular pulmonary arteries were seen on histologic examination of postmortem specimens. Clinical Relevance—Findings in this case were similar to those reported for human patients with portopulmonary hypertension secondary to hepatic cirrhosis. Pulmonary hypertension secondary to hepatic disease should be considered in the differential diagnosis of right-sided heart failure.

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.

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 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.