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- Author or Editor: David D. Sisson x
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Abstract
Objective—To evaluate the use of measuring plasma concentrations of atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP), and cardiac troponin-I (cTnI) to detect dogs with occult dilated cardiomyopathy (DCM).
Animals—118 client-owned dogs.
Procedures—Dogs were prospectively examined by use of ECG; echocardiography; and evaluation of concentrations of ANP, BNP, and cTnI. Occult DCM was diagnosed by evaluation of echocardiographic left ventricular dimensions and detection of ventricular arrhythmias on ECG. Sensitivity and specificity of assays for measurement of plasma concentrations of ANP, BNP, and cTnI to detect dogs with occult DCM were determined.
Results—Occult DCM was diagnosed in 21 dogs. A concentration of > 6.21 pg/mL for BNP had a sensitivity of 95.2% and specificity of 61.9% for identifying dogs with occult DCM. In contrast, concentrations of ANP and cTnI had relatively low predictive values.
Conclusions and Clinical Relevance—Blood-based screening for occult DCM in dogs can be accomplished by use of a BNP assay. Additional studies should be performed to optimize this method of screening dogs to detect occult DCM.
Abstract
Objective—To validate the use of a human enzyme immunoassay (EIA) kit for measurement of plasma antidiuretic hormone (ADH) concentration in dogs and evaluate plasma ADH concentrations in dogs with congestive heart failure (CHF) attributable to acquired cardiac disease, compared with findings in healthy dogs.
Animals—6 healthy dogs and 12 dogs with CHF as a result of chronic degenerative valve disease or dilated cardiomyopathy.
Procedures—Plasma samples from the 6 healthy dogs were pooled and used to validate the EIA kit for measurement of plasma ADH concentration in dogs by assessing intra-assay precision, dilutional linearity, and spiking recovery. Following validation, plasma ADH concentrations were measured in the 6 healthy dogs and in the 12 dogs with CHF for comparison.
Results—The EIA kit measured ADH concentrations in canine plasma samples with acceptable intra-assay precision, dilutional linearity, and spiking recovery. The intra-assay coefficient of variation was 11%. By use of this assay, the median plasma concentration of ADH in dogs with CHF was 6.15 pg/mL (SD, 3.2 pg/mL; range, 4.18 to 15.47 pg/mL), which was significantly higher than the median concentration in healthy dogs (3.67 pg/mL [SD, 0.93 pg/mL; range, 3.49 to 5.45 pg/mL]).
Conclusions and Clinical Relevance—Plasma ADH concentrations in dogs can be measured with the tested EIA kit. Plasma ADH concentrations were higher in dogs with CHF induced by acquired cardiac disease than in healthy dogs. This observation provides a basis for future studies evaluating circulating ADH concentrations in dogs with developing heart failure.
Abstract
OBJECTIVE To compare left ventricle (LV) volume and function variables obtained by use of 1-D, 2-D, and real-time 3-D echocardiography versus ECG-gated multidetector row CT (MDCT) angiography, which was considered the criterion-referenced standard.
ANIMALS 6 healthy, purpose-bred dogs.
PROCEDURES Dogs were anesthetized and administered a constant rate infusion of esmolol, and 1-D, 2-D, and 3-D echocardiography and ECG-gated, contrast-enhanced MDCT were performed. End-diastolic volume (EDV), end-systolic volume (ESV), stroke volume, and ejection fraction (EF) were calculated by use of the Teichholz method for 1-D echocardiography, single-plane and biplane modified Simpson method of disks (MOD) and area-length method for 2-D echocardiography, and real-time biplane echocardiography (RTBPE) and real-time 3-D echocardiography (RT3DE) for 3-D echocardiography. Volumes were indexed to body surface area and body weight. Median values, correlations, and limits of agreement were compared between echocardiographic modalities and MDCT.
RESULTS EDV and ESV measured by use of RTBPE and RT3DE had the strongest correlations with results for MDCT. Values obtained for EDV, ESV, stroke volume, and EF did not differ significantly between echocardiographic methods and MDCT. Use of RT3DE and RTBPE slightly underestimated EDV, ESV, and EF, compared with values for MDCT, as determined with Bland-Altman analysis.
CONCLUSIONS AND CLINICAL RELEVANCE Values for EDV and ESV obtained by use of 3-D echocardiography, including RTBPE and RT3DE, had the highest correlation with slight underestimation, compared with values obtained by use of MDCT. This was similar to results for 3-D echocardiography in human medicine.
Abstract
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.
Abstract
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.
Abstract
Objective—To evaluate the effects of medetomidine on dynamic left ventricular outflow tract (LVOT) obstruction in cats with left ventricular hypertrophy.
Design—Clinical trial.
Animals—6 domestic shorthair cats with echocardiographic evidence of dynamic LVOT obstruction.
Procedure—Cats were restrained in lateral recumbency, and baseline M-mode and Doppler echocardiographic examinations were performed. An ECG was recorded continuously, and blood pressure was measured indirectly with Doppler instrumentation. Medetomidine (20 µg/kg [9.1 µg/lb]) was then administered IM, and examinations were repeated 15 minutes later.
Results—Significant decreases in heart rate, LVOT velocity, and the LVOT pressure gradient were documented following medetomidine administration. After adjusting for the effects of heart rate by ANCOVA, there were no significant differences in any other systolic or diastolic indices of left ventricular function.
Conclusions and Clinical Relevance—Results suggest that administration of medetomidine to cats with dynamic LVOT obstruction may result in elimination of outflow tract obstruction; medetomidine may be a suitable sedative and analgesic agent in this subpopulation of cats. (J Am Vet Med Assoc 2002;221:1276–1281)
Abstract
Objective—To evaluate the cardiovascular effects of the α2-adrenergic receptor agonist medetomidine hydrochloride in clinically normal cats.
Animals—7 clinically normal cats.
Procedure—Cats were anesthetized with isoflurane, and thermodilution catheters were placed for measurement of central venous, pulmonary, and pulmonary capillary wedge pressures and for determination of cardiac output. The dorsal pedal artery was catheterized for measurement of arterial blood pressures and blood gas tensions. Baseline variables were recorded, and medetomidine (20 µg/kg of body weight, IM) was administered. Hemodynamic measurements were repeated 15 and 30 minutes after medetomidine administration.
Results—Heart rate, cardiac index, stroke index, ratepressure product, and right and left ventricular stroke work index significantly decreased from baseline after medetomidine administration, whereas systemic vascular resistance and central venous pressure increased. However, systolic, mean, and diastolic arterial pressures as well as arterial pH, and oxygen and carbon dioxide tensions were not significantly different from baseline values.
Conclusions and Clinical Relevance—When administered alone to clinically normal cats, medetomidine (20 µg/kg, IM) induced a significant decrease in cardiac output, stroke volume, and heart rate. Arterial blood pressures did not increase, which may reflect a predominant central α2-adrenergic effect over peripheral vascular effects. (Am J Vet Res 2001;62:1745–1762)
Abstract
Objective—To determine the nucleotide and amino acid sequence of atrial natriuretic peptide (ANP) in cats and its typical regions of cardiac expression.
Animals—5 healthy adult mixed-breed cats.
Procedure—Total RNA was extracted from samples obtained from the left and right atrium, left and right ventricle, and interventricular septum of each cat. The RNA was used to produce cDNA for sequencing and northern blot analysis. Genomic DNA was extracted from feline blood samples. Polymerase chain reaction primers designed from consensus sequences of other species were used to clone and sequence the feline ANP gene.
Results—The feline ANP gene consists of 1,072 nucleotides. It consists of 3 exons (123, 327, and 12 nucleotides) separated by 2 introns (101 and 509 nucleotides). It has several typical features of eukaryotic genes and a putative steroid-response element located within the second intron. Preprohormone ANP consists of 153 amino acids. The amino acid sequence of the active form of feline ANP (ANP-30) is identical to that of equine, bovine, and ovine ANP-30 and differs from that of human, canine, and porcine ANP-28 only by 2 carboxy-terminal arginine residues. The ANP mRNA was detected only in the left and right atria.
Conclusions and Clinical Relevance—The genetic and protein structure and principal regions of cardiac expression of feline ANP are similar to those of other species. Results of this study should be helpful in future studies on the natriuretic response in cats to diseases that affect cardiovascular function. (Am J Vet Res 2002;63:236–240)
