Case Description—2 spayed female (8 and 9 years old) and 1 sexually intact male (6.5 years old) Boxers were treated because of sustained ventricular tachycardia by electrical cardioversion.
Clinical Findings—Physical examination of the 8-year-old female Boxer revealed tachycardia (heart rate, 250 beats/min), weak femoral pulses, pale mucous membranes, panting, and lethargy. The 6.5-year-old male Boxer had similar physical examination findings, with the addition of a syncopal event. Analysis of the ECG rhythm strips for the 8- and 6.5-year-old dogs indicated a right ventricular origin of the ventricular tachycardia. The 9-year-old female Boxer was being treated with an IV constant rate infusion of lidocaine hydrochloride because of ventricular arrhythmias during the initial examination; physical examination re-vealed weakness, pale mucous membranes, prolonged capillary refill time, weak femoral pulses, and tachycardia (heart rate, 265 beats/min). Analysis of the ECG rhythm strip for the 9-year-old Boxer indicated a left ventricular origin of the ventricular tachycardia.
Treatment and Outcome—Pharmacological cardioversion treatment was unsuccessful in all 3 Boxers; however, electrical cardioversion by use of a biphasic defibrillator synchronized to conduct 30 J of energy during the peak of the QRS complex was successful in each dog. The electrical cardioversion procedure was performed 2 times (5-day interval between procedures) in the 9-year-old female as a result of relapse of the ventricular tachycardia condition.
Clinical Relevance—Results and follow-up monitoring suggested electrical cardioversion of sustained ventricular tachycardia may be a safe and effective treatment in Boxers that are unresponsive to medical treatment.
Objective—To determine the prevalence of systemic
hypertension in cats with diabetes mellitus and establish
ranges for echocardiographic variables in diabetic
Animals—14 cats with diabetes mellitus and 19
healthy control cats.
Procedure—Systolic blood pressure was measured
indirectly with a noninvasive Doppler technique.
Ophthalmic and echocardiographic examinations
were performed, and urine protein concentration was
measured. Cats were considered to have hypertension
if they had systolic blood pressure > 180 mm Hg
and at least 1 other clinical abnormality typically associated
with hypertension (eg, hypertensive retinopathy,
left ventricular hypertrophy, or proteinuria).
Results—None of the diabetic or control cats had
systolic blood pressure > 180 mm Hg. One diabetic
cat had left ventricular hypertrophy, but systolic blood
pressure was 174 mm Hg. None of the cats had evidence
of hypertensive retinopathy or proteinuria.
Mean values for echocardiographic variables for the
diabetic cats were not significantly different from published
values for healthy cats.
Conclusions and Clinical Relevance—Results suggest
that hypertension does not occur or occurs in
only a small percentage of cats with diabetes mellitus.
(J Am Vet Med Assoc 2003;223:198–201)
Objective—To determine ECG and echocardiographic measurements in healthy anesthetized Grevy's zebras (Equus grevyi).
Animals—20 healthy zebras.
Procedures—Auscultation, base-apex ECG, and echocardiography were performed on anesthetized zebras.
Results—Low-grade systolic murmurs were detected in the left basilar region in 4 of 20 zebras. Evaluation of ECGs from 19 zebras revealed sinus rhythm with a predominantly negative QRS complex and a mean ± SD heart rate of 67 ± 10 beats/min. Echocardiograms of sufficient image quality were obtained for 16 zebras. Interventricular septal thickness in diastole, left ventricular chamber in diastole and systole, left atrial diameter, and left ventricular mass were significantly and moderately correlated with estimated body weight (r values ranged from 0.650 to 0.884). Detectable swirling of blood in the right and sometimes the left ventricles was detected in 9 of 16 zebras, whereas physiologic regurgitation of blood was detected for the aortic valve in 3 zebras, pulmonary valve in 2 zebras, mitral valve in 2 zebras, and tricuspid valve in 1 zebra.
Conclusions and Clinical Relevance—Results of this study provide reference information for use in the cardiac evaluation of anesthetized Grevy's zebras.
Objective—To compare the acute effects of cardiac pacing from various transvenous pacing sites on left ventricular (LV) function and synchrony in clinically normal dogs.
Animals—10 healthy adult mixed-breed dogs.
Procedures—Dogs were anesthetized, and dual-chamber transvenous biventricular pacing systems were implanted. Dogs were paced in single-chamber mode from the right atrial appendage (RAA) alone and in dual-chamber mode from the right ventricular apex (RVA), from the left ventricular free wall (LVFW), and simultaneously from the RVA and LVFW (BiV). Standard ECG and echocardiographic measurements, cardiac output measured with the lithium dilution method (LiDCO), and tissue Doppler–derived measurements of LV synchrony were obtained during each of the pacing configurations.
Results—Placement of the biventricular pacing systems was possible in 8 of the 10 dogs. The QRS duration was significantly different among all pacing sites, and the order of increasing duration was RAA, BiV, LVFW, and RVA. Pacing sites did not differ with respect to fractional shortening; however, pacing from the RVA resulted in a significantly lower ejection fraction than pacing from all other sites. During RVA and LVFW pacing, LiDCO was significantly lower than that at other sites; there was no significant difference between RAA and BiV pacing with respect to LiDCO. Although the degree of dyssynchrony was significantly lower during pacing from the RAA versus other ventricular pacing sites, it was not significantly different among sites.
Conclusions and Clinical Relevance—Ventricular activation by RAA pacing provided the best LV function and synchrony. Pacing from the RVA worsened LV function, and although pacing from the LVFW improved it, BiV pacing may provide additional improvement.
Objective—To map canine mitochondrial proteins and identify qualitative and quantitative differences in heart mitochondrial protein expression between healthy dogs and dogs with naturally occurring and induced dilated cardiomyopathy (DCM).
Sample Population—Left ventricle samples were obtained from 7 healthy dogs, 7 Doberman Pinschers with naturally occurring DCM, and 7 dogs with induced DCM.
Procedures—Fresh and frozen mitochondrial fractions were isolated from the left ventricular free wall and analyzed by 2-dimensional electrophoresis. Protein spots that increased or decreased in density by ≥ 2-fold between groups were analyzed by matrixassisted laser desorption/ionization time-of-flight mass spectrometry or quadrupole selecting, quadrupole collision cell, time-of-flight mass spectrometry.
Results—Within narrow pH gradients of control canine heart mitochondrial samples, a total of 1,528 protein spots were revealed. Forty subunits of heart mitochondrial proteins that differ significantly from control tissues were altered in tissue specimens from dogs with naturally occurring and induced forms of DCM. The most affected heart mitochondrial proteins in both groups were those of oxidative phosphorylation (55%). Upregulation of manganese superoxide dismutase was suggestive of heart oxidative injury in tissue specimens from dogs with both forms of DCM. Evidence of apoptosis was associated with overexpression of the heart mitochondrial voltage-dependent anion channel-2 protein and endonuclease G in tissue specimens from dogs with induced DCM.
Conclusions and Clinical Relevance—Alterations of heart mitochondrial proteins related to oxidative phosphorylation dysfunction were more prevalent in tissue specimens from dogs with induced or naturally occurring DCM, compared with those of control dogs.
Objective—To identify qualitative and quantitative differences in cardiac mitochondrial protein expression in complexes I to V between healthy dogs and dogs with natural or induced dilated cardiomyopathy (DCM).
Sample Population—Left ventricle samples were obtained from 7 healthy dogs, 7 Doberman Pinschers with naturally occurring DCM, and 7 dogs with DCM induced by rapid right ventricular pacing.
Procedures—Fresh and frozen mitochondrial fractions were isolated from the left ventricular free wall and analyzed by 2-dimensional electrophoresis. Protein spots that increased or decreased in density by 2-fold or greater between groups were analyzed by matrixassisted laser desorption/ionization time-of-flight mass spectrometry or quadrupole selecting, quadrupole collision cell, time-of-flight mass spectrometry.
Results—A total of 22 altered mitochondrial proteins were identified in complexes I to V. Ten and 12 were found in complex I and complexes II to V, respectively. Five were mitochondrial encoded, and 17 were nuclear encoded. Most altered mitochondrial proteins in tissue specimens from dogs with naturally occurring DCM were associated with complexes I and V, whereas in tissue specimens from dogs subjected to rapid ventricular pacing, complexes I and IV were more affected. In the experimentally induced form of DCM, only nuclear-encoded subunits were changed in complex I. In both disease groups, the 22-kd subunit was downregulated.
Conclusions and Clinical Relevance—Natural and induced forms of DCM resulted in altered mitochondrial protein expression in complexes I to V. However, subcellular differences between the experimental and naturally occurring forms of DCM may exist.
Objective—To determine whether serum N-terminal pro-B-type natriuretic peptide (NT-proBNP) concentration is useful in discriminating between cardiac and noncardiac (ie, primary respiratory tract disease) causes of respiratory signs (ie, coughing, stertor, stridor, excessive panting, increased respiratory effort, tachypnea, or overt respiratory distress) in dogs.
Design—Multicenter cross-sectional study.
Animals—115 dogs with respiratory signs.
Procedures—Dogs with respiratory signs were solicited for study. Physical examination, thoracic radiography, and echocardiography were used to determine whether respiratory signs were the result of cardiac (ie, congestive heart failure) or noncardiac (ie, primary respiratory tract disease) causes. Serum samples for NT-proBNP assay were obtained at time of admission for each dog. Receiver-operating characteristic curves were constructed to determine the ability of serum NT-proBNP concentration to discriminate between cardiac and noncardiac causes of respiratory signs.
Results—Serum NT-proBNP concentration was significantly higher in dogs with cardiac versus noncardiac causes of respiratory signs. In dogs with primary respiratory tract disease, serum NT-proBNP concentration was significantly higher in those with concurrent pulmonary hypertension than in those without. A serum NT-proBNP cutoff concentration > 1,158 pmol/L discriminated between dogs with congestive heart failure and dogs with primary respiratory tract disease with a sensitivity of 85.5% and a specificity of 81.3%.
Conclusions and Clinical Relevance—Measuring serum NT-proBNP concentration in dogs with respiratory signs helps to differentiate between congestive heart failure and primary respiratory tract disease as an underlying cause.