Hierarchical temporal processing deficit model of reality distortion and psychoses.

We posit in this article that hierarchical temporal processing deficit is the underlying basis of reality distortion and psychoses. Schizophrenia is a prototypical reality distortion disorder in which the patient manifests with auditory hallucinations, delusions, disorganized speech and thinking, cognitive impairment, avolition and social and occupational dysfunction. Reality distortion can be present in many other disorders including bipolar disorder, major depression and even dementia. Conceptually, schizophrenia is a heterogeneous entity likely to be because of numerous causes similar to dementia. Although no single symptom or set of symptoms is pathognomonic, a cardinal feature in all patients with schizophrenia is chronic distortion of reality. The model that we have proposed accounts for the varied manifestations of reality distortion including hallucinations and delusions. In this paper we consider the implications of this model for the underlying biology of psychoses and also for the neurobiology of schizophrenia and suggest potential targets to consider for the etiology and pathophysiology of reality distortion, especially in the context of schizophrenia.

Quiet timer blanking in a dog with sick sinus syndrome and a permanent transvenous pacemaker.

A 14-year-old, 5.8 kg (12.7 lb) male castrated Jack Russell Terrier was referred for investigation of syncope and an arrhythmia. Electrocardiogram showed pronounced variation in the sinus rate including long periods of sinus arrest and an inconsistent escape rhythm. Sick sinus syndrome was the presumptive diagnosis. A single lead permanent transvenous pacemaker was implanted and was programmed to perform ventricular-demand pacing. Postoperative pacemaker interrogation revealed undersensing and asynchronous pacing during episodes of supraventricular tachycardia (SVT). This intermittent pacemaker malfunction was attributed to a specific pacemaker programming feature called quiet timer blanking. Adjustment of pacemaker parameters did not restore normal function. Treatment with sotalol (5 mg per os q 12 h) was used to medically treat the SVT, and asynchronous pacing was not observed during follow-up visits. To the authors' knowledge, this is the first documented case of quiet timer blanking causing paroxysmal undersensing and asynchronous pacing in a dog with a permanent pacemaker.

The influence of high-intensity moderate duration exercise on cardiac troponin I and C-reactive protein in sled dogs.

BACKGROUND: C-reactive protein (CRP) and cardiac troponin I (cTnI) are biomarkers of systemic inflammation and cardiac damage, respectively. OBJECTIVE: To investigate the effects of short-duration high-intensity exercise on plasma cTnI and serum CRP concentrations in sprint racing sled dogs. ANIMALS: Twenty-two Alaskan sled dogs of 2 different teams participating in a 2-day racing event. METHODS: In this prospective field study, cephalic venipuncture was performed on all dogs before racing and immediately after racing on 2 consecutive days. Plasma cTnI and serum CRP concentrations were evaluated at each time point. RESULTS: There was a mild, significant rise (P<.01) in median cTnI concentrations from resting (0.02 ng/mL; 0.0-0.12 ng/mL) on both days after racing (day 1=0.06, 0.02-0.2 ng/mL; day 2=0.07, 0.02-0.21 ng/mL). Serum CRP concentrations showed a mild significant increase (P<.01) on day 2 after racing mean (9.2±4.6 µg/mL) as compared with resting (6.5+4.3 µg/mL) and day 1 after racing (5.0+2.9 µg/mL). Neither cTnI or CRP concentrations exceeded the upper reference range for healthy dogs. CONCLUSIONS AND CLINICAL RELEVANCE: Strenuous exercise of short duration did not result in cTnI concentrations above the reference range for healthy dogs. Although increased after 2 days of short-duration strenuous exercise, CRP did not reach concentrations suggestive of inflammation, as reported previously in the endurance sled dogs. Therefore, we surmise that moderate exercise does not present a confounding variable in the interpretation of cTnI and CRP concentrations in normal dogs.

Reproducibility of geometric and flow-based echocardiographic measurements used for quantification of left ventricular total and forward stroke volume in healthy dogs.

BACKGROUND: Cardiac structure and function in dogs are commonly assessed using echocardiography. A variety of linear, area, and flow-based measurements can be used to calculate left ventricular (LV) total stroke volume (TSV) and forward stroke volume (FSV), but the reproducibility of many of these measurements has not been fully studied. We hypothesized that survey of echocardiographic variables would identify those with high reproducibility and inform future investigation of different methods to measure LV TSV and FSV. METHODS: The reproducibility of 25 geometric and flow-based echocardiographic measurements was prospectively evaluated in 23 healthy dogs by two experienced observers. Reproducibility (i.e., interobserver agreement) was described using intraclass correlation coefficients. The reproducibility of various methods to calculate LV TSV and FSV was explored. RESULTS: Reproducibility was generally good to excellent. Variables of LV width, length, and area and aortic and sinotubular junction diameter and velocity time integral were among measures with the highest reproducibility. Measurements of mitral annular diameter and mitral inflow velocity time integral possessed lower reproducibility. Calculation of LV TSV using measurements involved in the cube and bullet formulas demonstrated higher reproducibility than the Simpson's method of disks or mitral inflow methods. Calculation of LV FSV using LV outflow tract and aortic diameters from the right parasternal view generally demonstrated higher reproducibility compared with the left-sided view. CONCLUSIONS: The reproducibility of many simple geometric and flow-based echocardiographic measurements is high. Comparison of the reliability of different measurement informs future investigation of echocardiographic methods to determine LV TSV and FSV in dogs.

Toxicity in Doberman Pinchers with ventricular arrhythmias treated with amiodarone (1996-2005).

BACKGROUND: Asymptomatic Doberman Pinschers with dilated cardiomyopathy (DCM) often die suddenly owing to ventricular tachycardia that degenerates into ventricular fibrillation. A safe and effective antiarrhythmic drug treatment is needed. This will require a large, well-controlled, prospective study. HYPOTHESIS: Amiodarone toxicity is common in Dobermans with occult DCM and ventricular tachyarrhythmias refractory to antiarrhythmia therapy. Infrequent monitoring of hepatic function is inadequate. Frequent monitoring may be useful to determine dogs in which the dosage should be decreased or the drug withdrawn. METHODS: Medical records from the University of Georgia and Cornell University were searched for Doberman Pinschers diagnosed with preclinical DCM that received amiodarone for severe ventricular arrhythmias refractory to other antiarrhythmic agents. Echocardiographic data, Holter recording data, hepatic enzyme serum activity, and serum amiodarone concentrations were recorded. The presence of clinical signs of toxicity was recorded. Serum amiodarone concentrations were obtained in some dogs. RESULTS: Reversible toxicity was identified in 10 of 22 (45%) dogs. CONCLUSION AND CLINICAL IMPORTANCE: Adverse effects from amiodarone were common and were, in part, dosage related. Patients should be monitored for signs of toxicity and liver enzyme activity should be measured at least monthly.

Combination therapy with digoxin and diltiazem controls ventricular rate in chronic atrial fibrillation in dogs better than digoxin or diltiazem monotherapy: a randomized crossover study in 18 dogs.

BACKGROUND: Atrial fibrillation (AF) with excessively high ventricular rates (VR) occurs in dogs with advanced heart disease. Rate control improves clinical signs in these patients. Optimal drug therapy and target VR remain poorly defined. HYPOTHESIS: Digoxin-diltiazem combination therapy reduces VR more than either drug alone in dogs with high VR AF. ANIMALS: Eighteen client-owned dogs (>15 kg) with advanced heart disease, AF, and average VR on 24-hour Holter > 140 beats per minute (bpm). METHODS: After baseline Holter recording, dogs were randomized to digoxin or diltiazem monotherapy, or combination therapy. Repeat Holter evaluation was obtained after 2 weeks; dogs were then crossed over to the other arm (monotherapy or combination therapy) for 2 weeks and a third Holter was acquired. Twenty-four hour average VR, absolute and relative VR changes from baseline, and percent time spent within prespecified VR ranges (>140, 100-140, and <100 bpm) were compared. Correlations between serum drug concentrations and VR were examined. RESULTS: Digoxin (median, 164 bpm) and diltiazem (median, 158 bpm) decreased VR from baseline (median, 194 bpm) less than the digoxin-diltiazem combination (median, 126 bpm) (P < .008 for each comparison). With digoxin-diltiazem, VR remained <140 bpm for 85% of the recording period, but remained >140 bpm for 88% of the recording period with either monotherapy. Serum drug concentrations did not correlate with VR. CONCLUSIONS AND CLINICAL IMPORTANCE: At the dosages used in this study, digoxin-diltiazem combination therapy provided a greater rate control than either drug alone in dogs with AF.

Effect of transvenous electrical cardioversion on plasma cardiac troponin I concentrations in horses with atrial fibrillation.

BACKGROUND: Whether electrical cardioversion of cardiac arrhythmias results in cardiomyocyte damage is unknown. OBJECTIVE: To describe effect of transvenous electrical cardioversion (TVEC) on plasma cardiac troponin I (cTnI) concentration in horses. ANIMALS: All horses presented to the Cornell University Hospital for Animals for cardioversion of atrial fibrillation between May 2006 and October 2008 were eligible for inclusion in the study. Owners of 14 horses elected for TVEC and each horse was then enrolled (16 procedures). METHODS: Prospective observational study measuring concentrations of plasma cTnI before and after TVEC. RESULTS: Median cTnI concentration increased from 0.045 ng/mL at baseline (range 0.0-0.20 ng/mL) to 0.11 ng/mL after TVEC (range 0.0-3.73 ng/mL) (P= .036). This increase was not associated with the number of shocks delivered, maximal energy delivered, cumulative energy delivered, chronicity of atrial fibrillation before cardioversion, or positioning of the pulmonary artery catheter. CONCLUSIONS: The increase in cTnI is unlikely to be clinically important. The increase might be correlated with persistent atrial dysfunction after TVEC, suggesting that a longer convalescent period after the procedure could be warranted.

Bradycardia-associated syncope in 7 Boxers with ventricular tachycardia (2002-2005).

BACKGROUND: Syncope is a recognized problem in Boxers and often is the result of rapid ventricular tachycardia (VT). Affected dogs may have echocardiographic evidence of dilated cardiomyopathy, but frequently have normal echocardiograms. Although VT is probably the most common cause of syncope in Boxers, neurocardiogenic bradycardia can also occur. OBJECTIVE: We describe 7 Boxers with comorbid VT and neurocardiogenic bradycardia, wherein the syncope was secondary to bradycardia rather than VT. ANIMALS: Seven Boxers were selected from a larger population of Boxers with Holter-documented VT because these dogs had documented bradycardia at the time of syncope. METHODS: Retrospective study. RESULTS: Although all dogs had Holter-documented VT, the etiology of the syncopal episodes was consistent with neurocardiogenic bradycardia. CLINICAL IMPORTANCE: Neurocardiogenic bradycardia or VT can occur as isolated problems in Boxers. In some Boxers, VT and potential or manifest neurocardiogenic bradycardia coexist. The administration of a beta-blocker or sotalol to such dogs can aggravate or precipitate neurocardiogenic bradycardia-related syncope.

Lidocaine converts acute vagally associated atrial fibrillation to sinus rhythm in German Shepherd dogs with inherited arrhythmias.

BACKGROUND: Lidocaine is most frequently used to treat ventricular arrhythmias. However, lidocaine may have an antiarrhythmic effect for certain supraventricular arrhythmias. HYPOTHESIS: We hypothesized that lidocaine would be effective in converting experimentally induced atrial fibrillation (AF) to sinus rhythm and that a decrease in the dominant frequency (DF) and an increase in the organization as judged by the spectral entropy (SE) would occur over the course of the conversion. ANIMALS: Seven German Shepherd (GS) Dogs. METHODS: Dogs were anesthetized with fentanyl and pentobarbital. AF was induced with standard pacing protocols while left and right atrial monophasic action potentials (MAP) were recorded. The power spectra from the MAP recordings were analyzed to determine DF and SE during treatment with boluses of 2 mg/kg lidocaine. RESULTS: Lidocaine converted AF to sinus rhythm in all dogs and all episodes (n = 19). Conversion time was 27-87 seconds. After atropine, sustained AF was not induced; however, 5 episodes of atrial tachycardia resulted, and 3 were converted with lidocaine. Frequency domain analysis of 12 conversion sequences showed that left and right DF of the MAP signals decreased from the time of injection to conversion to sinus rhythm (P < .001). Mean SE indicated a gradient between the left and right atria (P = .003) that did not change during conversion. CONCLUSIONS AND CLINICAL IMPORTANCE: Vagally associated AF in GS dogs is terminated with lidocaine. Lidocaine is likely an effective treatment in clinical dogs with vagally associated AF.

Hypercoagulability in cats with cardiomyopathy.

BACKGROUND: Arterial thromboembolism (ATE) is a common complication of feline cardiomyopathy; however, the pathogenesis of ATE is unknown. HYPOTHESIS: Systemic activation of the coagulation cascade (hypercoagulability) and endothelial injury promote ATE in cardiomyopathic cats. ANIMALS: Healthy cats (n = 30) and 3 groups of cardiomyopathic cats: Group (1) left atrial enlargement only (LAE [n = 11]), ie, left atrial to aortic ratio >1.4; Group (2) LAE with spontaneous echocardiographic contrast, atrial thrombi or both (SEC-T [n = 16]); and Group (3) acute ATE with LAE (n = 16). METHODS: Hypercoagulability was defined by 2 or more laboratory abnormalities reflecting coagulation factor excess (high fibrinogen concentration or Factor VIII coagulant activity), inhibitor deficiency (low antithrombin activity), or thrombin generation (high thrombin-antithrombin complex [TAT] and d-dimer concentrations). High von Willebrand factor antigen concentration (vWF : Ag) was considered a marker of endothelial injury. Data were analyzed using nonparametric statistics. RESULTS: The 3 groups of cats with cardiac disease had higher median fibrinogen concentrations than did the healthy cats. Criteria of hypercoagulability were found exclusively in cats with SEC-T (50%) and ATE (56%). Hypercoagulability was not associated with left atrial size or congestive heart failure (CHF). ATE cats had significantly higher median vWF : Ag concentration than did the other groups. CONCLUSION AND CLINICAL IMPORTANCE: Systemic hypercoagulability is evident in many cardiomyopathic cats, often without concurrent CHF or overt ATE. Hypercoagulabilty may represent a risk factor for ATE. High vWF : Ag in ATE cats was attributed to downstream endothelial injury from the occlusive thrombus.

Retrospective Evaluation of the Effect of Heart Rate on Survival in Dogs with Atrial Fibrillation.

BACKGROUND: Atrial fibrillation (AF) usually is associated with a rapid ventricular rate. The optimal heart rate (HR) during AF is unknown. HYPOTHESIS/OBJECTIVES: Heart rate affects survival in dogs with chronic AF. ANIMALS: Forty-six dogs with AF and 24-hour ambulatory recordings were evaluated. METHODS: Retrospective study. Holter-derived HR variables were analyzed as follows: mean HR (meanHR, 24-hour average), minimum HR (minHR, 1-minute average), maximum HR (maxHR, 1-minute average). Survival times were recorded from the time of presumed adequate rate control. The primary endpoint was all-cause mortality. Cox proportional hazards analysis identified variables independently associated with survival; Kaplan-Meier survival analysis estimated the median survival time of dogs with meanHR <125 bpm versus ≥125 bpm. RESULTS: All 46 dogs had structural heart disease; 31 of 46 had congestive heart failure (CHF), 44 of 46 received antiarrhythmic drugs. Of 15 dogs with cardiac death, 14 had CHF. Median time to all-cause death was 524 days (Interquartile range (IQR), 76-1,037 days). MeanHR was 125 bpm (range, 62-203 bpm), minHR was 82 bpm (range, 37-163 bpm), maxHR was 217 bpm (range, 126-307 bpm). These were significantly correlated with all-cause and cardiac-related mortality. For every 10 bpm increase in meanHR, the risk of all-cause mortality increased by 35% (hazard ratio, 1.35; 95% CI, 1.17-1.55; P < 0.001). Median survival time of dogs with meanHR<125 bpm (n = 23) was significantly longer (1,037 days; range, 524-open) than meanHR ≥125 bpm (n = 23; 105 days; range, 67-267 days; P = 0.0012). Mean HR was independently associated with all-cause and cardiovascular mortality (P < 0.003). CONCLUSIONS AND CLINICAL IMPORTANCE: Holter-derived meanHR affects survival in dogs with AF. Dogs with meanHR <125 bpm lived longer than those with meanHR ≥ 125 bpm.

Third-Degree Atrioventricular Block and Collapse Associated with Eosinophilic Myocarditis in a Horse.

Third-degree atrioventricular block (AVB) and primary inflammatory myocarditis are uncommon findings in horses. The horse of this report presented for collapse at rest and was found to have multiple cardiac arrhythmias, most notably 3rd-degree AVB. The horse was subsequently diagnosed with eosinophilic myocarditis on necropsy, a rare form of myocarditis not previously reported in horses. Despite extensive testing, an etiologic agent could not be identified, illustrating the difficulty in identifying a specific cause of myocarditis in horses.

Anodal stimulation in two dogs with transvenous permanent bipolar pacemakers.

Management of symptomatic bradyarrhythmias such as complete atrioventricular block often involves permanent implantation of a transvenous pacemaker. Both during and after implantation, the operator can telemetrically assess and adjust a variety of electrical parameters associated with the pacemaker function in order to optimize the sensitivity, reliability, and power consumption of the device. Herein, we report an unexpected change in the paced electrocardiographic QRS complex morphology in two dogs undergoing bipolar pacing associated with changes in the pacemaker output amplitude settings first detected during threshold testing. The exclusivity of the electrocardiographic changes solely on pacemaker output settings, consistency between the surface electrocardiogram and ventricular endocardial electrogram, and resolution of this phenomenon when dogs were re-programmed to unipolar pacing is consistent with depolarization of the ventricular myocardium by the anodal electrode of the pacing lead at high pacemaker amplitudes. Anodal stimulation is a potential cause of varying QRS complex morphology witnessed during pacemaker evaluation and interrogation.

Evaluation of in-hospital electrocardiography versus 24-hour Holter for rate control in dogs with atrial fibrillation.

OBJECTIVES: To determine if the in-clinic ECG-derived heart rate could predict the at-home Holter-derived 24-hour average heart rate (Holter24h ), and whether it is useful to identify slow versus fast atrial fibrillation in dogs. MATERIALS AND METHODS: 82 pairs of 1-minute ECGs and 24-hour Holter recordings were acquired in 34 dogs with atrial fibrillation. The initial 24-hour Holter was used to test if the ECG heart rate can identify dogs with "slow" versus "fast" atrial fibrillation based on a Holter24h threshold value of 140 bpm. RESULTS: ECG heart rate overestimated Holter24h by 26 bpm (95% CI: 3 bpm, 48 bpm; P < 0 · 015) with a 95% limit of agreement of -21 to 83 bpm. The in-clinic ECG-derived heart rate Ä155 bpm had a sensitivity of 73% and a specificity of 100% for identifying a Holter24h HR Ä140 bpm; an in-clinic ECG-derived HR <160 bpm had a sensitivity and specificity of 91% each. CLINICAL SIGNIFICANCE: In-clinic ECG assessment of heart rate in dogs with atrial fibrillation does not reliably predict the heart rate in their home environment. However, an in-clinic heart rate greater than 155 bpm is useful in identifying "fast" atrial fibrillation, allowing clinicians to stratify which case may benefit from antiarrhythmic therapy.

Failure of spectro-temporal mapping to detect ventricular late potentials in dogs.

OBJECTIVE: To determine whether ventricular late potentials (LP) identified by time-domain analysis (TDA) of the signal-averaged ECG could be identified by three-dimensional frequency-domain analysis (FDA). ANIMALS: 11 dogs (9 of which subsequently died suddenly) with ventricular tachyarrhythmias (10 with ventricular tachycardia) and abnormal TDA of the signal-averaged ECG. PROCEDURE: Signal-averaged ECG that were abnormal when analyzed in the time domain subsequently were processed further in the frequency domain. Correlation ratios were calculated, and spectro-temporal maps were plotted, which were then compared with control data. RESULTS: Three-dimensional FDA did not detect LP. CONCLUSIONS AND CLINICAL RELEVANCE: LP may be detectable by TDA of the signal-averaged ECG and may be a specific marker for VT and sudden death in some dogs. However, FDA by use of the method applied in this study is invalid.

Relation of vitamin D status to congestive heart failure and cardiovascular events in dogs.

BACKGROUND: Vitamin D plays a pivotal role in cardiac function, and there is increasing evidence that vitamin D deficiency is associated with the development of congestive heart failure (CHF) in people. HYPOTHESIS: Serum vitamin D concentration is lower in dogs with CHF compared with unaffected controls and serum vitamin D concentration is associated with clinical outcome in dogs with CHF. ANIMALS: Eighty-two client-owned dogs. METHODS: In this cross-sectional study, we examined the association between circulating 25-hydroxyvitamin D [25(OH)D], a measure of vitamin D status, and CHF in dogs. In the prospective cohort study, we examined whether 25(OH)D serum concentration was associated with clinical outcome in dogs with CHF. RESULTS: Mean 25(OH)D concentration (100 ± 44 nmol/L) in 31 dogs with CHF was significantly lower than that of 51 unaffected dogs (123 ± 42 nmol/L; P = .023). The mean calculated vitamin D intake per kg of metabolic body weight in dogs with CHF was no different from that of unaffected dogs (1.37 ± 0.90 µg/kg metabolic body weight versus 0.98 ± 0.59 µg/kg body weight, respectively, P = .097). There was a significant association of serum 25(OH)D concentration on time to clinical manifestation of CHF or sudden death (P = .02). CONCLUSION AND CLINICAL RELEVANCE: These findings suggest that low concentrations of 25(OH)D may be a risk factor for CHF in dogs. Low serum 25(OH)D concentration was associated with poor outcome in dogs with CHF. Strategies to improve vitamin D status in some dogs with CHF may prove beneficial without causing toxicity.

Elimination half-life of intravenously administered equine cardiac troponin I in healthy ponies.

REASONS FOR PERFORMING STUDY: To date, no information is available on the true biological elimination half-life (T(1/2) ) of cardiac troponin I (cTnI) in the equine species. Such data are required to better evaluate the optimal time to acquire the cTnI sample following acute myocardial injury. OBJECTIVE: To determine the T(1/2) of equine cTnI. METHODS: Four healthy ponies received i.v. injections of recombinant equine cTnI. Plasma cTnI concentrations were measured with a point-of-care cTnI analyser at multiple time points after injection. Standard pharmacokinetic analysis was performed to establish the T(1/2) of cTnI. RESULTS: The average T(1/2) of cTnI was determined to be 0.47 h using a single rate elimination model. CONCLUSION: The elimination of recombinant equine cTnI following i.v. administration is very rapid. Establishing the T(1/2 ) of troponin provides critical information in understanding the clinical application of this cardiac biomarker in equine practice.

Association of metabolic risk factors with cartilage degradation assessed by T2 relaxation time at the knee: data from the osteoarthritis initiative.

OBJECTIVE: To evaluate the association of metabolic risk factors with severity and 2-year progression of early degenerative cartilage changes at the knee, measured with T2 relaxation times in middle-aged subjects from the Osteoarthritis Initiative. METHODS: Cartilage segmentation and T2 map generation were performed in knee 3T magnetic resonance images from 403 subjects ages 45-60 years without radiographic osteoarthritis (OA). The influence of risk factors on baseline T2 and longitudinal progression of T2 was analyzed using linear regression, adjusting for age, sex, and other OA risk factors. RESULTS: Four metabolic risk factors, i.e., high abdominal circumference (P < 0.001), hypertension (P = 0.041), high fat consumption (P = 0.023), and self-reported diabetes mellitus (P = 0.010), were individually associated with higher baseline T2. When the 4 metabolic risk factors were considered in a multivariate regression model, higher T2 remained significantly associated with abdominal circumference (P < 0.001) and diabetes mellitus (P = 0.026), and there was a trend for high fat consumption (P = 0.096). For the individual risk factors, only diabetes mellitus remained associated with higher baseline T2 after adjustment for body mass index (BMI). After adjustment for BMI, baseline T2 increased in a dose-response manner with the number of metabolic risk factors present (P = 0.032 for linear trend), and subjects with ≥3 metabolic factors (versus <3) had significantly higher baseline T2 (mean difference 1.2 msec [95% confidence interval 0.3, 2.1]; P = 0.011). Metabolic risk factors were not significantly associated with increases in T2 during followup. CONCLUSION: Metabolic risk factors are associated with higher T2, suggesting that increased cartilage degeneration may be caused by modifiable metabolic disorders.

Hypertrophic cardiomyopathy in a litter of five mixed-breed cats.

A litter of five, 18-month-old, mixed-breed cats were determined to have hypertrophic cardiomyopathy (HCM). Although no overt clinical signs were present in any cat, systolic heart murmurs were present in each. Electrocardiograms were normal, while subjective interpretations of heart enlargement on radiographs were made on four cats. Echocardiographic analyses indicated abnormalities consistent with HCM. Overt clinical signs are absent two years following diagnosis.

Feline diabetes mellitus: a retrospective mortality study of 55 cats (1982-1994).

Signalment, concomitant diseases, prognostic factors, and mortality were evaluated, retrospectively, in 55 diabetic cats (mean age, 11 years; range, five to 18 years). Sixty-seven percent of the cats were between 7.5 and 15 years of age. One-year mortality (n = 23) was high; most early deaths were due to comorbid disease, and the rate of death diminished in cats surviving beyond one year. The median survival time for all cats was 29 months; among cats that died, the median survival time was 11 months. Of the cats surviving more than one year, 16 were alive at a mean of 41 months. Only 13 of 37 cats died due to diabetes mellitus; the majority died due to concomitant diseases, with renal failure (n = 8) and hepatopathies (n = 6) being the most common causes. No clinical data was identified as being of prognostic significance.