Clinical signs associated with severe ST segment elevation in three cats with a hypertrophic cardiomyopathy phenotype.

Three cats were presented for unusual collapsing episodes. Echocardiography revealed a hypertrophic cardiomyopathy (HCM) phenotype in each cat. Continuous electrocardiographic monitoring showed that the clinical signs coincided with periods of severe ST-segment elevation in each cat. The first cat was treated with amlodipine and diltiazem but did not improve and was euthanized due to poor quality of life. Postmortem examination revealed cardiac lymphoma without obstructive coronary disease. The second cat was thought to have cardiac lymphoma, based on pericardial effusion cytology, and was euthanized before starting therapy. The third cat was diagnosed with HCM and left ventricular outflow tract obstruction and was treated with atenolol and diltiazem. This treatment reduced the frequency of episodic clinical signs, but the cat subsequently developed congestive heart failure and was euthanized. This case series describes clinical signs associated with severe ST elevation in cats with an HCM phenotype, and their outcomes. Continuous electrocardiographic monitoring was necessary to detect transient ST elevation in each case.

Two- and three-dimensional transesophageal echocardiographic assessment and successful occlusion of a window-like patent ductus arteriosus in two dogs.

A 16-month-old Labrador-Poodle cross (case 1) and a 3-month-old German shorthaired pointer (case 2) were referred for patent ductus arteriosus (PDA) occlusion. Two-dimensional transthoracic and two- and three-dimensional transesophageal echocardiography revealed a window-like PDA characterized by a wide and short ductus. Due to the atypical PDA morphology with no ampulla in case 1, ductal occlusion was attempted with non-canine-specific Amplatzer occluder devices. However, these were too small and failed to remain stable. Amplatz Canine Duct Occluder (ACDO) devices were used with success in both cases. Due to the defects' morphology, the proximal ACDO disc protruded into the aorta but there were no signs of obstruction to aortic blood flow 16 months (case 1) and 1 month (case 2) post-occlusion. We describe two cases of a window-like type PDA that were successfully occluded with an ACDO.

Hypertrophic cardiomyopathy in a dog: a systematic diagnostic approach.

A seven-year-old female neutered Parson Russel terrier was referred for syncopal episodes. An electrocardiogram revealed paroxysmal atrial flutter followed by periods of sinus arrest, suggesting sick sinus syndrome. Echocardiography showed severe biventricular wall thickening (hypertrophic cardiomyopathy (HCM) phenotype) with no signs of fixed or dynamic left ventricular outflow tract obstruction. Blood pressure, abdominal ultrasound, serum total thyroxin and thyroid-stimulating hormone, and insulin-like growth factor-1 were all within normal limits. Cardiac troponin I was elevated (1.7 ng/mL, ref<0.07). Serological tests for common infectious diseases were negative. A 24-h Holter confirmed that the syncopal episodes were associated with asystolic pauses (sinus arrest after runs of atrial flutter) ranging between 8.5 and 9.6 s. Right ventricular endomyocardial biopsies (EMB) were performed at the time of pacemaker implantation to assess for storage or infiltrative diseases that mimic HCM in people. Histological analysis of the EMB revealed plurifocal inflammatory infiltrates with macrophages and lymphocytes (CD3+ > 7/mm2) associated with myocyte necrosis, but no evidence of myocyte vacuolisation or infiltrative myocardial disorders. These findings were compatible with myocardial ischaemic injury or acute lymphocytic myocarditis. Molecular analysis of canine cardiotropic viruses were negative. The dog developed refractory congestive heart failure and was euthanised 16 months later. Cardiac post-mortem examination revealed cardiomyocyte hypertrophy and disarray with diffuse interstitial and patchy replacement fibrosis, and small vessel disease, confirming HCM. We described a systemic diagnostic approach to an HCM phenotype in a dog, where a diagnosis of HCM was reached by excluding HCM phenocopies.

Isolated discrete upper septal thickening in a non-referral cat population of senior and young cats.

INTRODUCTION/OBJECTIVES: Discrete upper septal thickening (DUST) is a phenotype of elderly people. The cardiac phenotype in senior cats has been incompletely described. We aimed to characterize the echocardiographic phenotype of senior cats, specifically to determine prevalence of DUST and hypertrophic cardiomyopathy (HCM). ANIMALS: One hundred and forty-nine healthy, normotensive cats. MATERIALS AND METHODS: Prospective cross-sectional study. Senior (≥9 years) and young (<6 years) cats were recruited from non-referral population. We defined DUST as an isolated basilar septal bulge, and HCM as left ventricular wall thickness ≥6 mm. An interventricular septum ratio (basal-to-mid septal thickness ratio) was calculated. We assessed for associations between clinical and echocardiographic variables and DUST. Data are presented as mean (±SD), median (range), or frequency (percentage). RESULTS: One-hundred and two senior and 47 young cats were enrolled. Aortoseptal angle (AoSA) was steeper in senior cats (137° (±14.5) vs. 145° (±12.3) in young cats, P=0.002). Eighteen cats had DUST (18/149, 12%), fourteen senior, and four young cats (P=0.4). Cats with DUST had steeper AoSA (125° (±8.3) vs. 142° (±13.7), P<0.0001) and higher interventricular septum ratio (1.4 (1.2-2.0) vs. 1.0 (0.7-1.8)). Univariable analysis showed decreased odds of DUST with greater AoSA (OR 0.9, P<0.0001), age was not associated with DUST. Twenty-nine senior cats had HCM (28.4%). DISCUSSION/CONCLUSIONS: Prevalence of DUST was 12%. There was no association between age and DUST. Smaller/steeper AoSA was the main factor associated with DUST. There was a high prevalence of HCM in this senior population.

Ventricular pre-excitation in cats: 17 cases.

OBJECTIVES: Atrioventricular accessory pathways are abnormal electrical connections between the atria and ventricles that predispose to ventricular pre-excitation (VPE) and tachycardias. ANIMALS: Seventeen cats with VPE and 15 healthy matched-control cats. MATERIAL AND METHODS: Multicenter case-control retrospective study. Clinical records were searched for cats with VPE, defined as preserved atrioventricular synchrony, reduced PQ interval, and increased QRS complex duration with a delta wave. Clinical, electrocardiography, echocardiographic, and outcome data were collated. RESULTS: Most cats with VPE were male (16/17 cats), non-pedigree cats (11/17 cats). Median age and mean body weight were 5.4 years (0.3-11.9 years) and 4.6 ± 0.8 kg, respectively. Clinical signs at presentation included lethargy (10/17 cats), tachypnea (6/17 cats), and/or syncope (3/17 cats). In two cats, VPE was an incidental finding. Congestive heart failure was uncommon (3/17 cats). Nine (9/17) cats had tachyarrhythmias: 7/9 cats had narrow QRS complex tachycardia and 2/9 cats had wide QRS complex tachycardia. Four cats had ventricular arrhythmias. Cats with VPE had larger left (P < 0.001) and right (P < 0.001) atria and thicker interventricular septum (P = 0.019) and left ventricular free wall (P = 0.028) than controls. Three cats had hypertrophic cardiomyopathy. Treatment included different combinations of sotalol (5/17 cats), diltiazem (5/17 cats), atenolol (4/17 cats), furosemide (4/17 cats), and platelet inhibitors (4/17 cats). Five cats died, all from cardiac death (median survival time 1882 days [2-1882 days]). CONCLUSIONS: Cats with VPE had a relatively long survival, albeit showing larger atria and thicker left ventricular walls than healthy cats.

Thin and hypokinetic myocardial segments in cats with cardiomyopathy.

INTRODUCTION/OBJECTIVES: Thin and hypokinetic myocardial segments (THyMS) represent adverse ventricular (LV) remodeling in human hypertrophic cardiomyopathy. We describe the echocardiographic features and outcome in cats with THyMS, and in a subpopulation, the echocardiographic phenotype before LV wall thinning was detected (pre-THyMS). ANIMALS: Eighty client-owned cats. MATERIALS AND METHODS: Retrospective multicenter study. Clinical records were searched for cats with THyMS, defined as LV segment(s) with end-diastolic wall thickness (LVWT) <3 mm and hypokinesis in the presence of ≥one LV segment(s) with LVWT >4 mm and normal wall motion. When available, echocardiograms pre-THyMS were assessed. Survival time was defined as time from first presentation with THyMS to death. RESULTS: Mean thickest LV wall segment (MaxLVWT) was 6.1 mm (95% CI 5.8-6.4 mm) and thinnest (MinLVWT) was 1.7 mm (95% CI 1.6-1.9 mm). The LV free wall was affected in 74%, apex in 13% and septum in 5%. Most cats (85%) presented with heart failure and/or arterial thromboembolism. Median circulating troponin I concentration was 1.4 ng/mL ([range 0.07-180 ng/mL]). Prior echocardiography results were available for 13/80 cats, a mean of 2.5 years pre-THyMS. In segments subsequently undergoing thinning, initial MaxLVWT measured 6.7 mm (95% CI 5.8-7.7 mm) vs. 1.9 mm (95% CI 1.5-2.4 mm) at last echocardiogram (P<0.0001). Survival data were available for 56/80 cats, median survival time after diagnosing THyMS was 153 days (95% CI 83-223 days). Cardiac histopathology in one cat revealed that THyMS was associated with severe transmural scarring. CONCLUSIONS: Cats with THyMS had advanced cardiomyopathy and a poor prognosis.

Spontaneous closure of a traumatic acquired Gerbode defect in a dog.

A one-year-old female English Springer Spaniel with no previous history of cardiac disease presented to the Queen's Veterinary School Hospital following a blunt traumatic incident with an acquired, direct Gerbode defect and associated third-degree atrioventricular block. Two months after the initial incident, follow-up echocardiography showed a nearly closed Gerbode defect with just trivial residual flow. A 24-h Holter monitor indicated second-degree atrioventricular block with occasional junctional tachycardia. A reassessment 22 months later confirmed spontaneous closure of the previously acquired traumatic Gerbode defect, with 2:1 second-degree atrioventricular block. The dog remained clinically asymptomatic, and free of treatment. To our knowledge, this is the first reported case of spontaneous closure of a previously acquired traumatic Gerbode defect in a dog.

Unilateral external jugular vein aneurysm in a dog.

An 11-month-old Staffordshire Bull Terrier was referred with a two-month history of fluctuating unilateral jugular groove swelling, which appeared to enlarge after exercise. There was no history of trauma. Multimodal imaging findings (using transdermal and transesophageal ultrasound and dual phase computed tomography angiography) were consistent with large, saccular, left jugular vein aneurysm, running parallel to the left carotid artery. There did not appear to be any arteriovenous communication present. There were no cardiac abnormalities found on echocardiography. Following surgical excision, histopathological analysis supported the clinical suspicion of a congenital external jugular venous aneurysm.

Echocardiographic assessment of right ventricular systolic function in healthy Beagle dogs compared to high field cardiac magnetic resonance imaging.

Ten healthy Beagle dogs were used to compare selected echocardiographic parameters of right ventricular (RV) systolic function with high field cardiac magnetic resonance imaging (MRI). All dogs underwent complete transthoracic echocardiography before and during anesthesia, as well as cardiac MRI with determination of morphology-based ejection fraction, and phase contrast angiography-derived stroke volume. A correlation analysis was carried out between echocardiographic and MRI parameters. The values of fractional area change, tricuspid annular plane systolic excursion, tissue Doppler imaging derived peak velocity of the isovolumic contraction wave and systolic wave of the lateral tricuspid valve annulus showed lower values under general anesthesia. Of all echocardiographic parameters of RV systolic function, only fractional area change (r = 0.671, P = 0.034) and tissue Doppler imaging derived peak velocity of the systolic wave of the lateral tricuspid valve annulus (r = 0.768; P = 0.01), showed a significant correlation with MRI derived stroke volume. None of the echocardiographic parameters correlated with MRI derived ejection fraction. When evaluating the RV echocardiographically, fractional area change and peak velocity of the systolic wave of the lateral tricuspid valve annulus appear to be the most reliable predictors of RV systolic function when compared to MRI under anesthesia.

Holter monitoring demonstrates that ventricular arrhythmias are common in cats with decompensated and compensated hypertrophic cardiomyopathy.

Arrhythmias can complicate cardiac disease in cats and are a potential cause of sudden death. The aim of this study was to evaluate the presence and nature of cardiac arrhythmias, and the potential correlation between plasma serum troponin I (cTnI) concentrations and the presence or severity of arrhythmias in cats with decompensated (dHCM) and compensated hypertrophic cardiomyopathy (cHCM). Forty one client-owned cats were studied: 16 with cHCM, 15 with dHCM and 10 healthy control cats. Physical examination, echocardiography, cTnI and 24-h Holter recordings were obtained in all cats and thoracic radiographs in cats with dHCM. Cats in both HCM groups were followed for 1 year after their initial Holter examination. The median (range) number of ventricular premature complexes (VPCs) over 24h was 867 (1-35,160) in cats with dHCM, 431 (0-18,919) in cats with cHCM and 2 (0-13) in healthy control cats. The median number of episodes of ventricular tachycardia (VTach) was 0 (0-1497) in dHCM and 0.5 (0-91) in cats with cHCM. The number of VPCs, VTach episodes and heart rate was not different between the HCM groups. Plasma serum troponin I was highest in the cats with dHCM, but there was no correlation between cTnI concentration and the number of arrhythmias. Thirteen of 31 cats with HCM died, but an association with the presence and complexity of ventricular arrhythmias was not observed. Compared to healthy cats, ventricular arrhythmias were common in cats with cHCM and dHCM, but neither presence nor complexity of arrhythmias could be linked to prognosis.

Transient Myocardial Thickening in Cats Associated with Heart Failure.

BACKGROUND: Cats with hypertrophic cardiomyopathy (HCM) and congestive heart failure (CHF) can have resolution of both left ventricular hypertrophy and CHF. OBJECTIVES: To describe the clinical characteristics of cats with transient myocardial thickening (TMT) and CHF compared with a control population of cats without resolution of HCM. ANIMALS: A total of 21 cats with TMT, 21 cats with HCM. METHODS: Retrospective study. Clinical records at 4 veterinary centers were searched for TMT cases and a control group of cats with HCM and CHF. TMT was defined as initial maximal left ventricular wall thickness (LVWT) ≥6 mm with left-sided CHF, with subsequent resolution of CHF, reduction in left atrium/aorta (LA/Ao), and LVWT<5.5 mm. HCM was defined as persistent LVWT ≥6 mm. RESULTS: Cats with TMT were younger (2 [0.4-11.4] years) than cats with HCM (8 [1.6-14] years) (P < 0.0001), and antecedent events were more common (15/21 versus 6/21, respectively) (P = 0.01). In cats with TMT, LVWT normalized from 6.8 [6.0-9.7] mm to 4.8 [2.8-5.3] mm and LA/Ao decreased from 1.8 [1.6-2.3] to 1.45 [1.2-1.7] after a mean interval of 3.3 (95% CI: 1.8-4.7) months. CHF recurred in 1 of 21 TMT and 15 of 21 cats with HCM. Cardiac treatment was discontinued in 20 of 21 cats with TMT and 0 of 21 HCM cats. All cats with TMT survived, whereas 8 of 19 cats with HCM died during the study period. CONCLUSIONS AND CLINICAL IMPORTANCE: TMT occurs in younger cats, and antecedent events are common. The prognosis is better in cats with CHF associated with TMT than HCM.

Cats with diabetes mellitus have diastolic dysfunction in the absence of structural heart disease.

Diabetes mellitus (DM) can result in cardiovascular dysfunction and heart failure characterized by diastolic dysfunction with or without the presence of systolic dysfunction in people and laboratory animals. The objective of this prospective study was to determine if cats with newly diagnosed DM had myocardial dysfunction and, if present, whether it would progress if appropriate antidiabetic therapy was commenced. Thirty-two diabetic cats were enrolled and received baseline echocardiographic examination; of these, 15 cats were re-examined after 6 months. Ten healthy age- and weight-matched cats served as controls. Diabetic cats at diagnosis showed decreased diastolic, but not systolic function, when compared to healthy controls, with lower mitral inflow E wave (E) and E/E' than controls. After 6 months, E and E/IVRT' decreased further in diabetic cats compared to the baseline evaluation. After excluding cats whose DM was in remission at 6 months, insulin-dependent diabetic cats had lower E, E/A and E' than controls. When classifying diastolic function according to E/A and E'/A', there was shift towards impaired relaxation patterns at 6 months. All insulin-dependent diabetic cats at 6 months had abnormal diastolic function. These results indicate that DM has similar effects on diastolic function in feline and human diabetics. The dysfunction seemed to progress rather than to normalize after 6 months, despite antidiabetic therapy. In cats with pre-existing heart disease, the development of DM could represent an important additional health risk.

Unexplained bleeding as primary clinical complaint in dogs infected with Angiostrongylus vasorum.

INTRODUCTION: Unexplained bleeding was the primary clinical complaint in 15 dogs diagnosed with A. vasorum and was observed in the mouth, as external bleeding, as large subcutaneous hematoma, as hemoptysis, in the brain, post ovariectomy, as epistaxis, in the anterior ocular chamber and on a tracheal intubation tube. In 8 dogs the cause of bleeding initially was suspected to be a minor trauma or a surgical complication, and various surgical approaches had been undertaken to eliminate the problem. In only 3 dogs respiratory signs were observed before the bleeding prompted referral. The median time elapsed between the first recognized clinical signs attributed to A. vasorum until diagnosis was 2 weeks (range1 day to 4 months). Four dogs died, 3 on the day of admission and 1 dog 4 days after admission. Suspected causes of death were respiratory failure and cerebral hemorrhage in 2 dogs each. Four dogs had been pre-treated with NSAIDs; of these, 2 dogs developed severe hemoptysis (1 died), 1 dog developed brain hemorrhage (and died), and 1 dog developed a large subcutaneous hematoma with marked anemia. Bleeding at various sites may be the only recognized abnormality in A. vasorum infection. Without a high index of suspicion, the diagnosis and appropriate therapy may be delayed to the point of a fatal outcome. Tests of coagulation were quite variable and the cause of bleeding likely multifactorial.

INTRODUCTION: Un saignement inexplicable a été le symptôme clinique primaire chez 15 chiens chez lesquels une infestation à A. vasorum a été diagnostiquée par la suite. Ces saignements ont été observés sous forme d'hémorragies dans la gueule, de saignements externes, de gros hématomes sous-cutanés, d'hémoptysie, de saignements cérébraux, de saignements abdominaux après ovariectomie, de saignements dans la chambre antérieure de l'oeil ou sur le trachéotube lors d'intubations. Chez 8 chiens, on a supposé que le saignement était initialement dû à un petit traumatisme ou à une complication opératoire et diverses mesures chirurgicales ont été prises pour résoudre le problème. Chez trois chiens, des symptômes respiratoires ont été observés avant que le saignement n'amène à l'envoi dans un centre de référence. Le temps moyen écoulé entre les premiers symptômes causés par A. vasorum et le diagnostic était de 2 semaines (1 jour à 4 mois). Quatre chiens sont décédés, 3 le jour de leur arrivée et un 4 jours plus tard. Les causes probables de la mort étaient dans deux cas une déficience respiratoire et dans deux une hémorragie cérébrale. Quatre chiens avaient été traités précédemment avec des AINS; deux d'entre eux ont développé une hémoptysie massive et un en est mort, un chien a présenté une hémorragie cérébrale fatale et le dernier a développé un volumineux hématome sous-cutané avec une anémie massive. Un saignement à un endroit quelconque peut être la seule anomalie constatée lors d'une infestation par A. vasorum. Si on n'a pas d'importants soupçons de cette affection, le diagnostic et le traitement adéquat peuvent être tellement retardés qu'une issue fatale survient. La cause pathophysiologique des hémorragies est vraisemblablement multifactorielle.

Hypovolemia induced systolic anterior motion of the mitral valve in two dogs.

Systolic anterior (septal) motion of the mitral valve (SAM) is a common secondary phenomenon in hypertrophic cardiomyopathy (HCM) in people and cats. In humans, it is increasingly recognized that SAM may be found in other cardiac and non-cardiac disease states. In small animal cardiology, SAM unassociated with HCM has been described in dogs with mitral valve dysplasia and right ventricular pressure overload. In this report, we describe two cases of dogs where transient SAM was caused by hypovolemia. When SAM was present both dogs showed pseudohypertrophy and tachycardia. Important factors in the genesis of SAM in this scenario are probably hypovolemia induced changes in left ventricular geometry affecting the orientation of the mitral valve apparatus combined with elevated catecholamine levels. SAM associated with increased wall thickness is not pathognomonic of HCM; this observation is of particular clinical importance when extrapolated to species where HCM is highly prevalent, e.g., cats. An echocardiographic diagnosis should always be evaluated together with full clinical assessment of history and physical examination.

Intrapulmonary arteriovenous anastomoses in dogs with severe Angiostrongylus vasorum infection: clinical, radiographic, and echocardiographic evaluation.

BACKGROUND: In both humans and dogs the pulmonary vasculature is able to recruit large-diameter anatomical intrapulmonary arteriovenous anastomoses (IPAVAs). In healthy people the opening of these anastomoses affects the degree of exercise-induced increase in pulmonary arterial pressure. The presence of these IPAVAs can be demonstrated using saline contrast echocardiography. OBJECTIVES: The aims of the present study were to characterize severely affected, naturally infected dogs with Angiostrongylus vasorum, to evaluate if these dogs can open IPAVAs, and to assess if the recruitment of such anastomoses affects the severity of pulmonary hypertension (PH). ANIMALS: Eight client-owned dogs with severe A. vasorum infection were recruited. METHODS: Dogs with A. vasorum infection that presented with severe dyspnea and/or syncope were prospectively screened by echocardiography for the presence of PH and IPAVAs. Only severely affected dogs, based on a combination of clinical, radiographic and echocardiographic abnormalities, were enrolled. RESULTS: Opening of IPAVAs could be demonstrated in three dogs with no to moderate PH, and could not be demonstrated in five dogs with severe PH. In two dogs thoracic radiographs showed only mild interstitial changes, while computer tomography and postmortem examination revealed severe pulmonary interstitial and vascular disease. CONCLUSIONS: These results suggest that dogs may open IPAVAs and that opening of such anastomoses may play a regulatory role in the development of PH. There may be a marked discrepancy between radiographic changes and disease severity in A. vasorum.