Preliminary evaluation of the efficacy of intravenous magnesium sulfate for the treatment of ventricular arrhythmias in 16 dogs.

OBJECTIVE: To evaluate the efficacy of IV magnesium sulfate in decreasing the number of ventricular ectopic beats or convert ventricular tachyarrhythmia to sinus rhythm in dogs. DESIGN: Prospective, observational feasibility study. SETTING: Private referral center. ANIMALS: Sixteen client-owned dogs exhibiting 1 or more of the following: (1) sustained or paroxysmal ventricular tachycardia (heart rate > 180/min), (2) single or multiform ventricular complexes at > 60 ectopies/min. INTERVENTIONS: Pretreatment (T1) blood creatinine and electrolyte concentrations were measured. A 60-second lead II ECG strip and systolic arterial blood pressure (SABP) were recorded. Magnesium sulfate 0.1 mmol/kg (0.2 mEq/kg) was administered IV over 5 minutes. Five minutes after completion of the magnesium sulfate injection (T2), electrolyte concentrations were measured again. A second 60-second lead II ECG strip and SABP were recorded. The number of ectopic ventricular and supraventricular beats (sinus beats) that occurred in 60 seconds during the T1 and T2 ECG recordings was compared. T1 and T2 electrolytes and SABP were also compared. RESULTS: There was an increase in the ionized magnesium concentration, a decrease in the heart rate and the number of ventricular ectopic beats, and an increase in the number of supraventricular beats at T2. Two dogs converted to a sinus rhythm at T2 that was not sustained. CONCLUSIONS: Intravenous administration of 0.1 mmol/kg (0.2 mEq/kg) magnesium sulfate in dogs with ventricular ectopy decreased the number of ventricular beats and heart rate. However, a specific conclusion regarding the use of magnesium sulfate as a first-line therapy for dogs with ventricular tachyarrhythmias at the investigated dose cannot be made.

Taurine deficiency and dilated cardiomyopathy in golden retrievers fed commercial diets.

INTRODUCTION: Golden retrievers are over-represented in cases of taurine-deficient dilated cardiomyopathy and recently a surge in cases has prompted further investigation. OBJECTIVE: To describe the clinical, dietary, and echocardiographic features in golden retrievers diagnosed with taurine deficiency and dilated cardiomyopathy, and to determine specific dietary associations. A second aim was to determine the whole blood taurine concentrations in a representative sample of healthy golden retrievers. ANIMALS: Twenty-four client-owned golden retrievers with documented taurine deficiency and dilated cardiomyopathy and 52 healthy client-owned golden retrievers. METHODS: In this multicenter prospective observational study, baseline and follow-up echocardiographic data, complete diet and medical histories, and whole blood, plasma, or serum taurine concentrations were obtained. Baseline and follow-up echocardiographic data were compared. Associations were evaluated between specific diets and taurine deficiency or congestive heart failure. The prevalence of low whole blood taurine concentrations in the healthy golden retrievers was calculated. RESULTS: Twenty-three of 24 dogs diagnosed with taurine deficiency and dilated cardiomyopathy were fed diets that were either grain-free, legume-rich, or a combination of these factors. None of these diets were feeding trial tested using Association of American Feed Control Officials (AAFCO) procedures. Twenty-three of 24 dogs had significant improvement in their echocardiographic parameters and normalization of taurine concentrations following diet change and taurine supplementation. Nine of 11 dogs diagnosed with congestive heart failure (CHF) had resolution of their congestion at follow-up with five no longer requiring diuretic therapy and four tolerating diuretic dose reduction by >50%. CONCLUSIONS: Certain diets and diet characteristics were associated with the development of taurine deficiency. Taurine deficiency and dilated cardiomyopathy in golden retrievers is likely multifactorial, including a combination of dietary, metabolic, and genetic factors.

Correction: Taurine deficiency and dilated cardiomyopathy in golden retrievers fed commercial diets.

[This corrects the article DOI: 10.1371/journal.pone.0209112.].

Evaluation of coagulation status in dogs with naturally occurring canine hyperadrenocorticism.

OBJECTIVE: To determine whether or not there are differences in coagulation parameters (eg, thrombelastography [TEG], activated partial thromboplastin time [aPTT], prothrombin time [PT], and fibrinogen) among dogs with naturally occurring hyperadrenocorticism (HAC), dogs with HAC undergoing medical management, and dogs without HAC. DESIGN: Prospective, observational study. SETTING: Veterinary teaching hospital. ANIMALS: Forty-six client-owned dogs undergoing adrenal function testing. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Nine dogs were diagnosed with HAC de novo, 19 dogs were presented for therapeutic monitoring of previously diagnosed HAC, and 18 dogs did not have HAC. Variables compared between groups were age, body weight, platelet count, mean platelet volume, serum concentrations of cholesterol, triglycerides, antithrombin, PT, aPTT, fibrinogen, and TEG parameters (eg, alpha angle, R, K, and maximum amplitude [MA]). Dogs with HAC and dogs treated for HAC had higher serum cholesterol than dogs without HAC (P < 0.05). All groups had mean MA greater than the institutional reference interval. There was a weak, positive correlation between hematocrit and MA that was independent of diagnosis (r(2) = 0.266, P = 0.004). CONCLUSIONS: The results of this study do not support the supposition that a significant difference exists in coagulation tendencies between dogs with HAC prior to treatment, dogs with HAC during treatment, and dogs without HAC. This disagreement with the classically accepted notion that HAC leads to a hypercoagulable state could be due to a couple of possibilities. Namely, the link between HAC and hypercoagulability may be relatively weak, or our findings may be the result of a type II error either as a result of a small sample size or the use of coagulation assays that are insensitive to the effects of HAC on the hemostatic system.

Prevalence of select infectious agents in inflammatory aural and nasopharyngeal polyps from client-owned cats.

Benign, inflammatory polyps may affect the nasopharynx and auditory canal of cats. It has been proposed that inflammation induced by infectious disease agents could trigger polyp formation. The objective of this pilot study was to determine the prevalence of feline herpesvirus-1 (FHV-1), feline calicivirus (FCV), Mycoplasma species, Bartonella species and Chlamydophila felis nucleic acids in polyp tissues collected from 30 clinically affected cats. Samples collected from the tympanic bulla from 12 clinically normal cats were also assayed. DNA or RNA of some of the target agents were amplified from samples from 25% of normal cats and 33% of affected cats; however, statistical associations were not detected for individual agent results or grouped results. The study documents that common oropharyngeal or blood borne agents can be detected in the tympanic bullae of normal cats. Failure to consistently amplify RNA or DNA of the select agents from polyp tissues suggests the agents studied were not directly associated with the pathogenesis of this syndrome in the cats tested. Alternately, the inflammatory response may have cleared microbial nucleic acids to undetectable levels by the time of sample collection.

Incidence of and risk factors for diabetes mellitus in cats that have undergone renal transplantation: 187 cases (1986-2005).

OBJECTIVE: To compare incidence of diabetes mellitus in cats that had undergone renal transplantation with incidence in cats with chronic renal failure, compare mortality rates in cats that underwent renal transplantation and did or did not develop diabetes mellitus, and identify potential risk factors for development of posttransplantation diabetes mellitus (PTDM) in cats. DESIGN: Retrospective case series. ANIMALS: 187 cats that underwent renal transplantation. PROCEDURES: Medical records were reviewed. RESULTS: 26 of the 187 (13.9%) cats developed PTDM, with the incidence of PTDM being 66 cases/1,000 cat years at risk. By contrast, the incidence of diabetes mellitus among a comparison population of 178 cats with chronic renal failure that did not undergo renal transplantation was 17.9 cases/1,000 cat years at risk, and cats that underwent renal trans-plantation were 5.45 times as likely to develop diabetes mellitus as were control cats with chronic renal failure. The mortality rate among cats with PTDM was 2.38 times the rate among cats that underwent renal transplantation but did not develop PTDM. Age, sex, body weight, and percentage change in body weight were not found to be significantly associated with development of PTDM. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that cats that undergo renal transplantation have an increased risk of developing diabetes mellitus, compared with cats with chronic renal failure, and that mortality rate is higher for cats that develop PTDM than for cats that do not.

The effect of ramipril on left ventricular mass, myocardial fibrosis, diastolic function, and plasma neurohormones in Maine Coon cats with familial hypertrophic cardiomyopathy without heart failure.

BACKGROUND: Hypertrophic cardiomyopathy (HCM) is the most common heart disease of cats, resulting in left ventricular (LV) hypertrophy, myocardial fibrosis, and diastolic dysfunction. HYPOTHESIS: Ramipril will reduce LV mass, improve diastolic function, and reduce myocardial fibrosis in cats with HCM without congestive heart failure (CHF). ANIMALS: This prospective, blinded, placebo-controlled study included 26 Maine Coon and Maine Coon cross-bred cats with familial HCM but without CHF. METHODS: Cats were matched for LV mass index (LVMI) and were randomized to receive ramipril (0.5 mg/kg) or placebo q24h for 1 year, with investigators blinded. Plasma brain natriuretic peptide (BNP) concentration, plasma aldosterone concentration, Doppler tissue imaging (DTI), and systolic blood pressure were measured at baseline and every 3 months for 1 year. Cardiac magnetic resonance imaging (cMRI) was performed to quantify LV mass and myocardial fibrosis by delayed enhancement (DE) cMRI at baseline and 6 and 12 months. Plasma angiotensin-converting enzyme (ACE) activity was measured on 16 cats 1 hour after PO administration. RESULTS: Plasma ACE activity was adequately suppressed (97%) in cats treated with ramipril. LV mass, LVMI, DTI, DE, blood pressure, plasma BNP, and plasma aldosterone were not different in cats treated with ramipril compared with placebo (P = .85, P = .94, P = .91, P = .89, P = .28, P = .18, and P = .25, respectively). CONCLUSION: Treatment of Maine Coon cats with HCM without CHF with ramipril did not change LV mass, improve diastolic function, alter DE, or alter plasma BNP or aldosterone concentrations in a relevant manner.

Comparison of myocardial contrast enhancement via cardiac magnetic resonance imaging in healthy cats and cats with hypertrophic cardiomyopathy.

OBJECTIVE: To quantify myocardial contrast enhancement (MCE) of the left ventricle (LV) by use of cardiac magnetic resonance imaging (CMRI) in healthy cats and cats with hypertrophic cardiomyopathy (HCM) and to compare MCE between the 2 groups. ANIMALS: 10 healthy cats and 26 Maine Coon cats with moderate to severe HCM but without clinical evidence of congestive heart failure. PROCEDURE: Anesthetized cats underwent gradient echo CMRI examination. Short-axis images of the LV were acquired before and 7 minutes after IV administration of gadolinium dimeglumine. Regions of interest were manually traced in the quadrants of 5 mid-LV slices acquired at end systole, and the MCE percentage was calculated from summed weight-averaged data from all slices. Doppler tissue imaging echocardiography was performed to measure the early diastolic myocardial velocity (Em) as an index of diastolic function. Three-way repeated-measures ANOVA was used to determine differences in MCE between cats with HCM and healthy cats. Simple linear regression was used to assess whether MCE was correlated with LV mass, LV mass index (LVMI), or Em. A Student t test was used to compare the SDs of the postcontrast myocardial signal intensity between the 2 groups. RESULTS: There was no difference in MCE between cats with HCM and healthy cats. There was no correlation of MCE with LV mass, LVMI, or Em. There was no difference in heterogeneity of signal intensities of LV myocardium between the 2 groups. CONCLUSIONS AND CLINICAL RELEVANCE: Contrast-enhancement CMRI was not useful in detecting diffuse myocardial fibrosis in cats with HCM.