Septic pericarditis caused by a migrating grass awn in a cat.

Septic pericarditis and cardiac tamponade associated with migrating grass awn foreign bodies is reported rarely in companion animals. We report such a case in a previously healthy, 9-year-old, neutered female, indoor-outdoor, domestic long-hair cat who presented for acute tachypnea. Large volume pericardial effusion and pericardial tamponade was identified by thoracic-focused assessment with sonography. Following removal of 108 mL of purulent pericardial effusion by pericardiocentesis, the cat improved. Cytologic examination of pericardial fluid demonstrated septic, suppurative inflammation, Pasteurella sp. was cultured from pericardial effusion, and antibiotics were administered. Subsequent echocardiographic examination revealed large volume pericardial effusion, pericardial thickening, and a linear foreign body within the pericardial space. Whole-body computed tomography confirmed pericardial thickening, pericardial, and pleural effusion. A 16-mm long grass awn was identified within the pericardial space during thoracic exploratory surgery performed through a median sternotomy. Successful foreign body removal and subtotal pericardiectomy was accomplished. Histopathology of pericardial tissue disclosed chronic pericarditis with lymphoplasmacytic-to-pyogranulomatous inflammation, and transmural presence of grass awn foreign body. The cat responded to supportive therapy and was discharged 4 days postoperatively. When examined 3 weeks later, the cat appeared healthy with normal appetite. The cat remained healthy as of this writing, 487 days following surgery. To the author's knowledge, this is the first report in the cat of septic pericarditis and cardiac tamponade resulting from a migrating grass awn foreign body.

B-cell lymphoma invading and compressing the heart base and pericardium in a cat.

A 3-year-old, 3.5-kg, neutered male, domestic shorthair cat presented with progressive lethargy, anorexia, coughing, and acute respiratory distress of two-week duration. Auscultation detected diffuse pulmonary crackles. Lung sounds were absent over the left cranial thorax. Sinus tachycardia was recorded. Thoracic radiographs revealed cardiac silhouette enlargement, dorsal displacement of the carina, and uniform, soft tissue opacity in the left cranial hemithorax. Transthoracic two-dimensional echocardiography revealed a large mass within and external to the pericardial space, effacing the pericardium, and compressing basal cardiac structures. The point-of-care feline immunodeficiency virus and feline leukemia virus test was negative. Euthanasia was elected, and permission for necropsy granted. Gross postmortem evaluation revealed a prominent mediastinal mass that effaced the left cranial lung lobe and invaded the heart base and pericardium. The mass was confirmed as B-cell lymphoma by histopathology and immunohistochemistry.

Perceptions of quality of life and priorities of owners of cats with heart disease.

BACKGROUND: Owners' perceptions and priorities regarding quality of life (QoL) are important considerations given the unknown efficacy of many commonly administered medications, stress of hospital visits, difficulties providing home care, and personal choices including euthanasia. OBJECTIVE: To describe the relative importance of quality versus quantity of life to owners of cats with heart disease. ANIMALS: Two hundred and thirty-nine cats with heart disease. METHODS: Prospective questionnaire-based clinical study. Cat owners completed a questionnaire to identify important parameters when assessing their cat's QoL, the relative importance of quality versus quantity of life, and willingness to trade survival time for QoL. Variables associated with these parameters were evaluated with multivariate analyses. RESULTS: Appetite, owner interaction, sleep patterns, and litterbox habits were deemed important to QoL. Concern over pet suffering was significantly greater than concern over life expectancy. Ninety-three percent of owners were willing to trade survival time for good QoL; 57% of these were willing to trade up to 6 months. On multivariate analysis, the only factor significantly (P=.002) associated with willingness to trade 6 months was study site. Owner concern regarding stress of administering medications at home increased with number and frequency of medications. CONCLUSIONS AND CLINICAL RELEVANCE: These results indicated that QoL is more important to owners of cats with heart disease than longevity. The various priorities and concerns of cat owners should be taken into account in order to provide optimal care.

Sudden death in a dog with aortic coarctation.

A previously healthy, one-year-old, intact female Vizsla dog collapsed and experienced cardiopulmonary arrest after a stressful event. Postmortem examination identified juxtaductal aortic coarctation (AoCo) with complex morphology. Located in the isthmus aorta adjacent to the ligamentum arteriosum, the AoCo comprised a shelf-like structure caused by invagination of the aortic wall into the lumen. Just distally, a second region of aortic occlusion resulted from an obstructing aortic membrane that restricted blood flow into the descending aorta through a small, eccentric ostium. Plausibly, the AoCo contributed to high afterload which led to reduction of coronary blood flow, myocardial hypoxia, and sudden death during physical stress. Although AoCo is a well-recognized congenital defect in humans, it has been reported only rarely in animals. The present case details the gross and histologic features of a complex, juxtaductal AoCo in a dog who died suddenly after stress. These morphologic findings may be informative when contemplating diagnosis of this anomaly.

Giant pericardial-occupying compressive primary cardiac hemangiosarcoma in a cat.

Hemangioarcoma in the cat is an infrequently diagnosed tumor, and cardiac involvement is rare. We report a previously healthy, 8-year-old, domestic shorthair cat with acute collapse associated with pericardial effusion and cardiac tamponade. Following pericardiocentesis and removal of 15 mL of fluid, the cat improved rapidly. A massive, space-occupying, intrapericardial tumor adhered to and compressing the right atrium and ventricle was detected by echocardiography. Approximately 5 weeks following initial presentation, bicavitary effusion and tachypnea developed, and the cat was euthanized. Necropsy revealed a giant intrapericardial mass adhered to and impinging upon the right heart. Histologic and immunohistochemical examination confirmed hemangiosarcoma with no gross or histologic evidence of metastasis. To the authors' knowledge, this is the first account of a pericardial-occupying, primary feline cardiac hemangiosarcoma resulting in compression of the right heart and cardiac tamponade, Further, this report describes novel clinicopathological relationships between radiographic and echocardiographic findings and gross and microscopic pathology.

Irish wolfhounds with subclinical atrial fibrillation: progression of disease and causes of death.

INTRODUCTION: To evaluate the frequency of dilated cardiomyopathy (DCM) and cardiac death (CD) in Irish wolfhounds (IW) with subclinical atrial fibrillation (AF) and to compare cardiac and all-cause mortality to those of a contemporaneous control group of apparently healthy IW with sinus rhythm. ANIMALS: Fifty-two IW with AF, but without echocardiographic evidence of DCM or other cardiac disease, and an age- and gender-matched control cohort of 52 apparently healthy IW. METHODS: Data from 1552 IW were retrospectively evaluated. Fifty-two dogs with subclinical AF were compared with 52 IW controls. Time from initial diagnosis to development of DCM was recorded, and survival data were analyzed using cumulative incidence functions. RESULTS: 26/52 AF dogs developed DCM. At study end, in the AF and control group each, 49/52 AF dogs had died, three remained alive. Death in the AF cohort was attributed to CD in 22/49 dogs (12 congestive heart failure [CHF], 10 sudden cardiac deaths [SCD]), while 27 dogs died from non-CD. In the control group, significantly fewer dogs developed DCM (11/52 dogs, p=0.004), even fewer died from CD (5/49; three CHF, two SCD; p=0.001). The odd ratios (95% confidence interval) for dogs with AF vs. controls to develop DCM was 3.7 (1.6-8.8) and to die from CD was 7.2 (2.4-21.2). Median all-cause survival for AF IWs (CD, 36.3 months; non-CD, 33.2 months) did not differ significantly from the control group (CD, 28.6 months, p=0.377; non-CD, 45.3 months, p=0.631). CONCLUSION: IW with subclinical AF commonly develop DCM and die from cardiac death.

Dilated cardiomyopathy in 151 Irish Wolfhounds: Characteristic clinical findings, life expectancy and causes of death.

Dilated cardiomyopathy (DCM) is an important cause of morbidity in Irish Wolfhounds (IW), a breed also predisposed to neoplastic and orthopedic diseases that shorten life expectancy. The objective of this study was to investigate survival and causes of death in IW with DCM and to characterise the clinical findings of DCM over time. Data from cardiovascular examinations performed in 1591 IW, including echocardiography and electrocardiography, were retrospectively evaluated. IW with DCM on medical therapy with long term longitudinal follow-up were included in this study (n=151; 95 males, 56 females). Based on their clinical status at initial diagnosis, IW were classified into one of three groups: preclinical DCM with sinus rhythm (PC-DCM-SR, n=35), preclinical DCM with atrial fibrillation (PC-DCM-AF, n=87), and congestive heart failure with DCM and AF (CHF-DCM-AF, n=29). Survival data were analyzed using cumulative incidence functions, Kaplan-Meier and Cox regression. CHF was predominantly characterized by chylous pleural and mild pericardial effusions. Causes of death were cardiac (CD) in 73/151 and non-cardiac (non-CD) in 62/151; 16 dogs remained alive at study end. The majority of deaths in both preclinical DCM groups were non-CD (PC-DCM-AF=51.9% non-CD, 48.1% CD; PC-DCM-SR, 65.5% non-CD, 34.5% CD). In the CHF-DCM-AF group most dogs (89.6%) experienced a CD. Median survival of the CHF-DCM-AF group (7.3 months) was significantly shorter than in the PC-DCM-AF group (21.9 months) or PC-DCM-SR group (29.1 months, P=0.001). CHF-DCM-AF in IW was associated with reduced life expectancy and CD, while most IW with preclinical DCM died from non-cardiac causes.

Bartonella spp. as a Possible Cause or Cofactor of Feline Endomyocarditis-Left Ventricular Endocardial Fibrosis Complex.

Endomyocarditis is a commonly detected post-mortem finding in domestic cats presenting for sudden onset cardiovascular death, yet the aetiology remains unresolved. Cats are documented reservoir hosts for Bartonella henselae, the infectious cause of cat scratch disease in man. Various Bartonella spp. have been associated with culture-negative endocarditis, myocarditis and sudden death in man and animals. We hypothesized that Bartonella spp. DNA could be amplified more often from the hearts of cats with feline endomyocarditis-left ventricular endocardial fibrosis (FEMC-LVEF) complex compared with cats with hypertrophic cardiomyopathy (HCM) or cats with grossly and microscopically unremarkable hearts (designated non-cardiac disease controls). Formalin-fixed and paraffin wax-embedded, cardiac tissues from 60 domestic and purebred cats aged 3 months to 18 years were examined, and histological features were recorded. Cardiac tissue sections were tested for Bartonella DNA using multiple 16-23S intergenic transcribed spacer region polymerase chain reaction (PCR) primer sets, including two Bartonella genera, a Bartonella koehlerae species-specific and a Bartonella vinsonii subsp. berkhoffii-specific assay, followed by DNA sequence confirmation of the species or genotype. Special precautions were taken to avoid DNA cross-contamination between tissues. Bartonella spp. DNA was amplified by PCR and sequenced from 18 of 36 cats (50%) with FEMC-LVEF and 1/12 (8.3%) cats with HCM. Bartonella spp. DNA was not amplified from any non-cardiac disease control hearts. Based on PCR/DNA sequencing, one Bartonella spp. was amplified from 10 cats, while the remaining eight were coinfected with more than one Bartonella spp. To our knowledge, this study represents the first documentation of B. vinsonii subsp. berkhoffii genotype I infection in cats (n = 11). Fluorescence in-situ hybridization testing facilitated visualization of Bartonella bacteria within the myocardium of four of seven PCR-positive FEMC-LVEF hearts. Collectively, these findings support the hypothesis that Bartonella spp. may play a primary role or act as a cofactor in the pathogenesis of FEMC-LVEF. Studies involving cats from other geographical regions and definitive demonstration of Bartonella spp. within regions of inflammation are needed to confirm an association between Bartonella spp. and FEMC-LVEF induced morbidity and mortality in cats.

Longitudinal Analysis of Quality of Life, Clinical, Radiographic, Echocardiographic, and Laboratory Variables in Dogs with Preclinical Myxomatous Mitral Valve Disease Receiving Pimobendan or Placebo: The EPIC Study.

BACKGROUND: Changes in clinical variables associated with the administration of pimobendan to dogs with preclinical myxomatous mitral valve disease (MMVD) and cardiomegaly have not been described. OBJECTIVES: To investigate the effect of pimobendan on clinical variables and the relationship between a change in heart size and the time to congestive heart failure (CHF) or cardiac-related death (CRD) in dogs with MMVD and cardiomegaly. To determine whether pimobendan-treated dogs differ from dogs receiving placebo at onset of CHF. ANIMALS: Three hundred and fifty-four dogs with MMVD and cardiomegaly. MATERIALS AND METHODS: Prospective, blinded study with dogs randomized (ratio 1:1) to pimobendan (0.4-0.6 mg/kg/d) or placebo. Clinical, laboratory, and heart-size variables in both groups were measured and compared at different time points (day 35 and onset of CHF) and over the study duration. Relationships between short-term changes in echocardiographic variables and time to CHF or CRD were explored. RESULTS: At day 35, heart size had reduced in the pimobendan group: median change in (Δ) LVIDDN -0.06 (IQR: -0.15 to +0.02), P < 0.0001, and LA:Ao -0.08 (IQR: -0.23 to +0.03), P < 0.0001. Reduction in heart size was associated with increased time to CHF or CRD. Hazard ratio for a 0.1 increase in ΔLVIDDN was 1.26, P = 0.0003. Hazard ratio for a 0.1 increase in ΔLA:Ao was 1.14, P = 0.0002. At onset of CHF, groups were similar. CONCLUSIONS AND CLINICAL IMPORTANCE: Pimobendan treatment reduces heart size. Reduced heart size is associated with improved outcome. At the onset of CHF, dogs treated with pimobendan were indistinguishable from those receiving placebo.

Naturally Occurring Biventricular Noncompaction in an Adult Domestic Cat.

A definitively diagnosed case of left ventricular noncompaction (LVNC) has not been previously reported in a non-human species. We describe a Maine Coon cross cat with echocardiographically and pathologically documented LVNC. The cat was from a research colony and was heterozygous for the cardiac myosin binding protein C mutation associated with hypertrophic cardiomyopathy (HCM) in Maine Coon cats (A31P). The cat had had echocardiographic examinations performed every 6 months until 6 years of age at which time the cat died of an unrelated cause. Echocardiographic findings consistent with LVNC (moth-eaten appearance to the inner wall of the mid- to apical region of the left ventricle (LV) in cross section and trabeculations of the inner LV wall that communicated with the LV chamber) first were identified at 2 years of age. At necropsy, pathologic findings of LVNC were verified and included the presence of noncompacted myocardium that consisted of endothelial-lined trabeculations and sinusoids that constituted more than half of the inner part of the LV wall. The right ventricular (RV) wall also was affected. Histopathology identified myofiber disarray, which is characteristic of HCM, although heart weight was normal and LV wall thickness was not increased.

Structural and molecular pathology of the atrium in boxer arrhythmogenic right ventricular cardiomyopathy.

OBJECTIVE: To investigate the expression and distribution of desmosomal and gap junction proteins of the intercalated disc in the atria of boxers with arrhythmogenic right ventricular cardiomyopathy (ARVC). ANIMALS: Nineteen control dogs and 13 boxers with histopathologically confirmed ARVC. METHODS: Right and left atrial samples were examined using immunofluorescence and Western blots. The intercalated disc proteins investigated included total and phosphorylated connexin43 (Cx43 and pCx43), connexin45, connexin40, plakoglobin, plakophilin-2, desmoplakin, and N-cadherin. RESULTS: Histopathological changes characteristic of ARVC were present in the left or right atrium of 12 out of 13 boxers and were absent in all control dogs. When compared to the 19 control dogs, immunofluorescence analysis revealed a decrease in signal intensity for pCx43 and plakoglobin in the left (p = 0.03 and p = 0.014, respectively) and right atrium (p = 0.015 and p = 0.002, respectively) of affected boxers. Connexin43 and pCx43 Western blot band density was significantly decreased in the left (p = 0.025 and p = 0.027, respectively) and right atrium (p = 0.001 and p = 0.044, respectively) of affected boxers. CONCLUSION: Altered intercalated disc and gap junction proteins were identified in atrial myocardium of ARVC boxers, supporting atrial involvement as part of this disorder. Reduction in pCx43 in conjunction with histological changes could represent the substrate for atrial arrhythmias associated with ARVC. Furthermore, these findings detected in boxer dogs, lend support for the broader term, arrhythmogenic cardiomyopathy, as preferred nomenclature used to describe this disease in humans.

Long-term Outcome of Irish Wolfhound Dogs with Preclinical Cardiomyopathy, Atrial Fibrillation, or Both Treated with Pimobendan, Benazepril Hydrochloride, or Methyldigoxin Monotherapy.

BACKGROUND: Dilated cardiomyopathy (DCM) is a common cause of morbidity and mortality in the Irish Wolfhound (IW). However, the benefit of medical treatment in IW dogs with preclinical DCM, atrial fibrillation (AF), or both has not been demonstrated. OBJECTIVES: Compare the time to develop congestive heart failure (CHF) or sudden death in IW dogs with preclinical DCM, AF, or both receiving monotherapy with pimobendan, methyldigoxin, or benazepril hydrochloride. ANIMALS: Seventy-five client-owned IW dogs. METHODS: Irish Wolfhound dogs were prospectively randomized to receive pimobendan (Vetmedin®), benazepril HCl (Fortekor®), or methyldigoxin (Lanitop®) monotherapy in a 1:1:1 ratio in a blinded clinical trial. The prospectively defined composite primary endpoint was onset of CHF or sudden death. To assure stringent evaluation of treatment effect, data from dogs complying with the study protocol were analyzed. RESULTS: Sixty-six IW fulfilling the study protocol included 39 males, 27 females; median (interquartile range) age, 4.0 years (3.0-5.0 years) and weight, 70.0 kg (63.0-75.0 kg). Primary endpoint was reached in 5 of 23 (21.7%) IW receiving pimobendan, 11 of 22 (50.0%) receiving benazepril HCl, and 9 of 21 (42.9%) receiving methyldigoxin. Median time to primary endpoint was significantly longer for pimobendan (1,991 days; 65.4 months) compared to methyldigoxin (1,263 days; 41.5 months; P = .031) or benazepril HCl-(997 days; 32.8 months; P = .008) treated dogs. CONCLUSIONS AND CLINICAL IMPORTANCE: In IW dogs with preclinical DCM, AF or both, pimobendan monotherapy significantly prolonged time to onset of CHF or sudden death than did monotherapy with benazepril HCl or methyldigoxin.

Effect of Pimobendan in Dogs with Preclinical Myxomatous Mitral Valve Disease and Cardiomegaly: The EPIC Study-A Randomized Clinical Trial.

BACKGROUND: Pimobendan is effective in treatment of dogs with congestive heart failure (CHF) secondary to myxomatous mitral valve disease (MMVD). Its effect on dogs before the onset of CHF is unknown. HYPOTHESIS/OBJECTIVES: Administration of pimobendan (0.4-0.6 mg/kg/d in divided doses) to dogs with increased heart size secondary to preclinical MMVD, not receiving other cardiovascular medications, will delay the onset of signs of CHF, cardiac-related death, or euthanasia. ANIMALS: 360 client-owned dogs with MMVD with left atrial-to-aortic ratio ≥1.6, normalized left ventricular internal diameter in diastole ≥1.7, and vertebral heart sum >10.5. METHODS: Prospective, randomized, placebo-controlled, blinded, multicenter clinical trial. Primary outcome variable was time to a composite of the onset of CHF, cardiac-related death, or euthanasia. RESULTS: Median time to primary endpoint was 1228 days (95% CI: 856-NA) in the pimobendan group and 766 days (95% CI: 667-875) in the placebo group (P = .0038). Hazard ratio for the pimobendan group was 0.64 (95% CI: 0.47-0.87) compared with the placebo group. The benefit persisted after adjustment for other variables. Adverse events were not different between treatment groups. Dogs in the pimobendan group lived longer (median survival time was 1059 days (95% CI: 952-NA) in the pimobendan group and 902 days (95% CI: 747-1061) in the placebo group) (P = .012). CONCLUSIONS AND CLINICAL IMPORTANCE: Administration of pimobendan to dogs with MMVD and echocardiographic and radiographic evidence of cardiomegaly results in prolongation of preclinical period and is safe and well tolerated. Prolongation of preclinical period by approximately 15 months represents substantial clinical benefit.

Spontaneously occurring arrhythmogenic right ventricular cardiomyopathy in the domestic cat: A new animal model similar to the human disease.

BACKGROUND: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a primary myocardial disease of incompletely resolved pathogenesis and is a largely unappreciated cause of sudden death in the young. METHODS AND RESULTS: Clinical features of 12 domestic cats with ARVC (7 male; 1 to 20 years old, mean 7.3+/-5.2 years) were right-sided congestive heart failure (n=8), supraventricular tachyarrhythmias (n=5), ventricular tachycardia (n=3), polymorphic ventricular arrhythmias (n=6), and right bundle-branch block (n=5). ARVC was suspected in all 8 cats examined with echocardiography by marked enlargement of the right ventricle (RV) and right atrium and tricuspid regurgitation. Eight died of cardiovascular disease and 4 died of noncardiac conditions. At autopsy, hearts of ARVC cats were characterized grossly by moderate-to-severe RV cavity enlargement and wall thinning (n=12) and apical aneurysm formation (n=6). Histology demonstrated pronounced RV lesions in all 12 ARVC cats, including marked myocardial injury (myocyte death and atrophy) and repair (fibrous and/or fatty replacement). Injury and repair were also evident in the left ventricle (LV) in 10 cats, and 2 had involvement of both atria. Myocarditis was present in 10 of the 12 ARVC cats. Apoptosis was detected in 9 ARVC cats (mean apoptotic index, 28+/-23% RV, 21+/-19% LV, and 17+/-15% ventricular septum) but not in controls. CONCLUSIONS: In the common domestic cat, we identified a clinically relevant cardiomyopathy that closely mimics ARVC in humans. This unique feline model of human disease will be relevant to defining pathogenesis and investigating mechanisms responsible for disease progression in ARVC.

Clinical Features and Outcome of Dogs with Epiglottic Retroversion With or Without Surgical Treatment: 24 Cases.

BACKGROUND: Published information describing the clinical features and outcome for dogs with epiglottic retroversion (ER) is limited. HYPOTHESIS/OBJECTIVES: To describe clinical features, comorbidities, outcome of surgical versus medical treatment and long-term follow-up for dogs with ER. We hypothesized that dogs with ER would have upper airway comorbidities and that surgical management (epiglottopexy or subtotal epiglottectomy) would improve long-term outcome compared to medical management alone. ANIMALS: Twenty-four client-owned dogs. METHODS: Retrospective review of medical records to identify dogs with ER that underwent surgical or medical management of ER. RESULTS: Dogs with ER commonly were middle-aged to older, small breed, spayed females with body condition score (BCS) ≥6/9. Stridor and dyspnea were the most common presenting signs. Concurrent or historical upper airway disorders were documented in 79.1% of cases. At last evaluation, 52.6% of dogs that underwent surgical management, and 60% of dogs that received medical management alone, had decreased severity of presenting clinical signs. In dogs that underwent surgical management for ER, the incidence of respiratory crisis decreased from 62.5% before surgery to 25% after surgical treatment. The overall calculated Kaplan-Meier median survival time was 875 days. CONCLUSION AND CLINICAL IMPORTANCE: Our study indicated that a long-term survival of at least 2 years can be expected in dogs diagnosed with epiglottic retroversion. The necessity of surgical management cannot be determined based on this data, but dogs with no concurrent upper airway disorders may benefit from a permanent epiglottopexy to alleviate negative inspiratory pressures.

Relationship of plasma N-terminal pro-brain natriuretic peptide concentrations to heart failure classification and cause of respiratory distress in dogs using a 2nd generation ELISA assay.

BACKGROUND: Cardiac biomarkers provide objective data that augments clinical assessment of heart disease (HD). HYPOTHESIS/OBJECTIVES: Determine the utility of plasma N-terminal pro-brain natriuretic peptide concentration [NT-proBNP] measured by a 2nd generation canine ELISA assay to discriminate cardiac from noncardiac respiratory distress and evaluate HD severity. ANIMALS: Client-owned dogs (n = 291). METHODS: Multicenter, cross-sectional, prospective investigation. Medical history, physical examination, echocardiography, and thoracic radiography classified 113 asymptomatic dogs (group 1, n = 39 without HD; group 2, n = 74 with HD), and 178 with respiratory distress (group 3, n = 104 respiratory disease, either with or without concurrent HD; group 4, n = 74 with congestive heart failure [CHF]). HD severity was graded using International Small Animal Cardiac Health Council (ISACHC) and ACVIM Consensus (ACVIM-HD) schemes without knowledge of [NT-proBNP] results. Receiver-operating characteristic curve analysis assessed the capacity of [NT-proBNP] to discriminate between dogs with cardiac and noncardiac respiratory distress. Multivariate general linear models containing key clinical variables tested associations between [NT-proBNP] and HD severity. RESULTS: Plasma [NT-proBNP] (median; IQR) was higher in CHF dogs (5,110; 2,769-8,466 pmol/L) compared to those with noncardiac respiratory distress (1,287; 672-2,704 pmol/L; P < .0001). A cut-off >2,447 pmol/L discriminated CHF from noncardiac respiratory distress (81.1% sensitivity; 73.1% specificity; area under curve, 0.84). A multivariate model comprising left atrial to aortic ratio, heart rate, left ventricular diameter, end-systole, and ACVIM-HD scheme most accurately associated average plasma [NT-proBNP] with HD severity. CONCLUSIONS AND CLINICAL IMPORTANCE: Plasma [NT-proBNP] was useful for discriminating CHF from noncardiac respiratory distress. Average plasma [NT-BNP] increased significantly as a function of HD severity using the ACVIM-HD classification scheme.

Molecular screening by polymerase chain reaction detects panleukopenia virus DNA in formalin-fixed hearts from cats with idiopathic cardiomyopathy and myocarditis.

Viral myocarditis has been suggested as an etiology for cardiomyopathy in several mammalian species. Myocarditis and idiopathic cardiomyopathy have been reported in the domestic cat, although a viral etiology has not been demonstrated. Because of the continuing interest in the potential relationship between viral myocarditis and cardiomyopathy, we evaluated hearts from cats with spontaneous, idiopathic cardiomyopathy for viral genomic material within myocytes by polymerase chain reaction, and for the presence of myocarditis by light microscopy. Thirty-one (31) formalin-fixed hearts from domestic cats who died of idiopathic cardiomyopathy were randomly selected from pathology archives. Seventeen (17) formalin-fixed hearts from healthy cats were similarly selected as normal controls. The polymerase chain reaction (PCR) was used to evaluate myocardial tissue for the presence of viral genome from feline panleukopenia virus, herpes virus, calici virus, and corona virus. Hearts were examined using light microscopy for histologic evidence of myocarditis according to the Dallas criteria. Panleukopenia virus was identified by PCR in 10 of 31 cats with cardiomyopathy but in none of the controls. Neither cardiomyopathic or control cats tested positive by PCR for herpes virus, calici virus, and corona virus. Myocarditis was detected by histologic examination in 18 of 31 cardiomyopathic cats and in none of 17 control cats. Myocarditis and or feline panleukopenia virus genome was detected in felines with idiopathic hypertrophic, dilated, and restrictive cardiomyopathy, suggesting a possible role of viral infection and inflammation in the pathogenesis of cardiomyopathy in this species.

Hypertrophic cardiomyopathy in pigs: quantitative pathologic features in 55 cases.

naturally occurring hypertrophic cardiomyopathy (HCM) was diagnosed in 55 purebred pigs 6 to 12 months of age. Ten (18%) of the pigs died suddenly during auction or shipment or were found dead by their keepers. The other 45 pigs failed to meet the criteria for brediing stock. Forty-six purebred and 64 hybrid pigs were studied for control. Heart weights were significantly heavier (p < 0.001) in the pigs with HCM (473.5 ± 31.8 g; heart weight [HW]/body weight [BW] ratio 4.6 ± 0.7) than in the purebred (334.4 ± 29.7 g; HW/BW 3.4 ± 0.3) and hybrid (344.3 ± 28.9 g; HW/BW 3.4 ± 0.1) pigs without HCM. The ventricular septum (VS) in the 55 pigs with HCM was significantly thicker (26.0 ± 3.1 mm; p < 0.001) than in the purebred (19.6 ± 2.6 mm) and hybrid (14.1 ± 0.5 mm) pigs without HCM. The left ventricular free wall (LV) was significantly thicker (p < 0.001) in the pigs with HCM (20.0 ± 2.7 mm) than in the purebred (18.1 ± 2.1 mm) and hybrid (15.6 ± 0.3 mm) pigs without HCM. Asymmetric septal hypertrophy was evident because the ratio of VS to LV was significantly greater (p < 0.001) in the pigs with HCM (1.3 ± 0.2) than in the purebred (1.0 ± 0.2) and hybrid (0.9 ± 0.01) pigs without HCM. The anterior portion of the VS appeared to bulge into and impinge upon the left ventricular outflow tract, in which a fibrotic endocardial plaque was often seen. Histologic features included marked muscle cell disorganization in the VS, LV, right ventricular free wall. Abnormal intramural coronary arteries and myocardial fibrosis were seen in most pigs with HCM. Silver impregnation stains showed that there were marked increases in perimysial coils, pericellular weaves, and cell-to-cell struts. Matrix disorientation was evident in the hearts with HCM. Quantitation revealed that the collagen protein in the hearts with HCM (23.8 ± 2.8 µg/mg protein) was significantly higher (p < 0.001) than in the hearts of purebred (15.7 ± 1.8 µg/mg protein) and hybrid (13.9 ± 4.2 µg/m pprotein) pigs without HCM. Total muscle protein in the hearts of the purebred pigs with (51.6 ± 3.3 mg) and without (51.9 ± 3.0 mg) HCM was not different; however, in hearts with HCM (51.6 ± 3.3 mg) it was significantly higher (p < 0.001) than in those of hybrid pigs (47.6 ± 4.4 mg) without HCM. There was 47% to 52% more stainable collagen in the heart with HCM (44.7 ± 5.2 µg collagen/mg protein) than in the purebred (30.3 ± 4.0 µg collagen/mg protein) and hybrid (28.3 ± 8.1 µg collagen/mg protein) hearts without HCM. Gross and histologic features and connective tissue abnormalities in the pigs with HCM were strikingly similar to those in humans, cats, and dogs with HCM. Thus we conclude that spontaneous porcine HCM presents a new and important model for the cardiovascular investigator.

Plasma taurine concentrations in normal dogs and in dogs with heart disease.

Plasma taurine concentrations were determined in 76 dogs with dilated cardiomyopathy (DCM), 28 dogs with acquired valvular disease (AVD), and 47 normal (control) dogs. The data were collected at 2 referral centers, The Animal Medical Center, New York, NY (AMC), and the University of California, Davis (UCD), and the studies were conducted independently. Different anticoagulants (sodium citrate at AMC and lithium heparin at UCD) were used to collect the plasma samples. Paired analysis of samples showed a significant difference in plasma taurine concentrations, depending on the anticoagulant used. Consequently, results from each clinic were analyzed separately. Plasma taurine concentrations were significantly higher in dogs with AVD (median, 133 nmol/mL; range, 25 to 229 nmol/mL) than in control dogs (median, 63 nmol/mL; range 44 to 224 nmol/mL) and dogs with DCM (median, 72 nmol/mL; range, 1 to 247 nmol/mL) at AMC (P < .001). The number of dogs with AVD at UCD was too small to draw meaningful conclusions. At UCD, the median plasma taurine concentration was 98 nmol/mL (range, 28-169 nmol/mL) in dogs with AVD, 75 nmol/mL (range, 0.1-184 nmol/mL) in dogs with DCM, and 88 nmol/mL (range 52-180 nmol/mL) in control dogs. There were no significant differences in plasma taurine concentrations between dogs with DCM and the control dogs at either hospital. Congestive heart failure and administration of cardiac medication had no significant effect on plasma taurine concentrations. Plasma taurine concentration was low (< 25 nmol/mL) in 17% (13/76) of the dogs with DCM. Seven of the 13 dogs with low plasma taurine concentrations were Cocker Spaniels or Golden Retrievers.(ABSTRACT TRUNCATED AT 250 WORDS)

Doxorubicin-induced cardiotoxicosis. Clinical features in 32 dogs.

Clinical cardiac abnormalities developed in 32 of 175 dogs that had various malignancies and were treated with doxorubicin: 31 dogs had electrocardiographic abnormalities including arrhythmias and nonspecific alterations in the R wave, ST segment, or QRS duration and 7 dogs had congestive heart failure. All seven dogs that had congestive heart failure died within 90 days. At necropsy, 13 of 32 affected dogs had noninflammatory myocardial degeneration, myocytolysis, vacuolation, and/or fibrosis and there was intramural coronary arteriosclerosis in all 13. Five dogs with lymphosarcoma were in complete clinical remission when they died of doxorubicin-induced cardiomyopathy, but the overall survival times of the lymphosarcoma subset was nevertheless longer than in previous studies. The clinical use of doxorubicin in the dog can cause cardiotoxicosis but the therapeutic benefit appears to outweigh risks in most dogs.