Feline arterial thromboembolism: an update.

ATE remains a devastating complication of cardiac disease. Despite some improvements in our understanding of the underlying causes and clinical features of this disease, short-term management remains a challenge, and mortality is high. Long-term mortality is primarily attributable to the severe underlying cardiac disease. Many questions remain to be answered regarding the ideal management approach for feline ATE. The authors' preferred diagnostic and therapeutic approaches for these difficult patients are detailed in Box. 1.     

Dilated cardiomyopathy: an update.

Despite many advances in he diagnosis and treatment of DCM, it continues to be an important cause of cardiovascular morbidity and mortality in large-breed dogs. In the coming years, it is hoped and anticipated tht further discoveries will be made in the areas of etiology, therapy, and assessment of prognosis, ultimately with a view to having a greater impact on the clinical management of these cases.     

Boxer dog cardiomyopathy: an update.

Boxer dog cardiomyopathy is an inheritable form of myocardial disease characterized most commonly by ventricular tachycardias, syncope, and, sometimes, systolic dysfunction and heart failure. Careful evaluation of boxer dog cardiomyopathy by several investigators has demonstrated that the disease may be best classified as arrhythmogenic right ventricular cardiomyopathy. Affected dogs have a variable prognosis; although some succumb to sudden cardiac death, many can remain asymptomatic or be successfully managed on antiarrhythmics for years.     

Feline endocrinology update.

This article highlights the advances in feline endocrinology, excluding diabetes mellitus and hyperadrenocorticism, which have recently been reviewed elsewhere. The goal will be to provide clinically relevant information regarding pathogenesis, diagnosis, and treatment options for these feline endocrine disorders.     

Canine hypertrophic cardiomyopathy.

Necropsy findings in 10 dogs with naturally occurring cardiac disease closely resembled hypertrophic cardiomyopathy in human beings and cats. Each dog had marked cardiac hypertrophy, and 8 dogs had disproportionate thickening of the ventricular septum with respect to the left ventricular free wall (compared with dogs with normal hearts or with cardiac hypertrophy due to acquired or congenital heart disease). Ratios of septum to free wall thickness in the 10 dogs ranged from 1.1 to 1.5, and 6 had ratios greater than or equal to 1.3. Marked cardiac muscle cell disorganization in the ventricular septum, characteristic of human patients with hypertrophic cardiomyopathy, was found in only 2 of the 10 dogs. Death occurred while the dogs were under anesthesia during the course of operative procedures (5 dogs) or unexpectedly in animals without previous manifestations of cardiac disease (3 dogs). Four dogs had clinical signs of congestive heart failure, including 2 with marked cardiac decompensation. Two of these 4 dogs with heart failure and 1 dog that died during unrelated surgery, but without prior signs of heart disease, had electrocardiographic evidence of complete heart block.     

Feline heart disease: An update

Heart disease is relatively common in cats and our understanding of feline cardiomyopathy has improved considerably over the last two decades, in part as a result of the improved sophistication of non-invasive diagnostic techniques. The incidence of feline dilated cardiomyopathy has declined markedly since the discovery of taurine deficiency as an aetiological factor and subsequent modification of commercial diets. Hypertrophic cardiomyopathy now seems to be the commonest primary form and is characterised by unexplained left ventricular hypertrophy and diastolic dysfunction. Intermediate forms of cardiomyopathy are also recognised. Secondary cardiomyopathies are common; examples of causes include hyperthyroidism, systemic hypertension and acromegaly. Congenital cardiac disease is also well recognised and may lead to clinical signs even late in life.     

Feline hypertrophic cardio-myopathy: Variations on a theme

The history and the physical, radiographic, electrocardiographic, echocardiographic, haemo-dynamic and angiocardiographic findings from 18 cats with idiopathic hypertrophic cardiomyopathy are described. These data document a diverse spectrum of clinical manifestations of this disease in cats. The variety and complexity of feline hypertrophic cardiomyopathy complicate the diagnosis and challenge the idea that this disorder is a single disease entity.     

Feline bacterial urinary tract infections: An update on an evolving clinical problem

Although feline urine is increasingly submitted for bacterial culture and susceptibility testing as part of a more general diagnostic work-up for a range of presentations in veterinary practice, bacterial urinary tract infections (UTIs) are relatively uncommon due to a variety of physical and immunological barriers to infection. Culture positive urine is most often obtained from older female cats and the clinical history may include hematuria, dysuria and pollakiuria, or the infection may be occult. Urinalysis usually reveals hematuria and pyuria, and Escherichia coli and Gram-positive cocci are cultured most frequently. Most feline UTIs can be successfully treated using oral amoxicillin or amoxicillin/clavulanic acid administered for at least 14 days, but the prevalence of antimicrobial resistance amongst infecting bacterial species is a growing concern. There is currently no conclusive information on the safety and efficacy of alternative therapeutic agents for the treatment of feline UTIs.     

End-stage hypertrophic cardiomyopathy in a cat

A 14-year-old Persian cat was referred for evaluation of the progression of hypertrophic cardiomyopathy (HCM) after an acute episode of congestive heart failure. The diagnosis of HCM had been made almost 13 years ago. Echocardiography and electrocardiography revealed end-stage hypertrophic cardiomyopathy and multifocal atrial tachycardia. The patient was discharged on medical management with a grave prognosis.     

Cardiac troponin I in feline hypertrophic cardiomyopathy

Measurement of plasma cardiac troponin I concentration ([cTnI]) is a sensitive and specific means for detecting myocardial damage in many mammalian species. Studies have shown that [cTnI] increases rapidly after cardiomyocyte injury. The molecular structure of cTnl is highly conserved across species, and current assays developed for its detection in humans have been validated in many species. In this study, [cTnI] was quantified using a 2-site sandwich assay in plasma of healthy control cats (n = 33) and cats with moderate to severe hypertrophic cardiomyopathy (HCM) (n = 20). [cTnI] was significantly higher in cats with HCM (median, 0.66 ng/mL; range, 0.05-10.93 ng/mL) as compared with normal cats (median, <0.03 ng/mL; range, <0.03-0.16 ng/mL) (P < .0001). An increase in [cTnI] was also highly sensitive (sensitivity = 85%) and specific (specificity = 97%) for differentiating cats with moderate to severe HCM from normal cats. [cTnI] was weakly correlated with diastolic thickness of the left ventricular free wall (r2 = .354; P = .009) but not with the diastolic thickness of the interventricular septum (P = .8467) or the left atrium: aorta ratio (P = .0652). Furthermore, cats with congestive heart failure at the time of cTnI analysis had a significantly higher [cTnI] than did cats that had never had heart failure and those whose heart failure was controlled at the time of analysis (P = .0095 and P = .0201, respectively). These data indicate that cats with HCM have ongoing myocardial damage. Although the origin of this damage is unknown, it most likely explains the replacement fibrosis that is consistently identified in cats with moderate to severe HCM.     

Research on avian coccidia: an update.

Despite the availability of many anticoccidial drugs, infections caused by species of Eimeria continue to be a source of significant economic loss to the poultry industry. After two decades in which the use world wide of ionophorous antibiotics gave unparalleled control of coccidiosis, drug resistance is once again tipping the balance in favour of the parasites. The realization that even the most spectacularly successful drugs might, after all, have a finite life if not used conservatively, has focused attention on ways in which the life span of drugs can be prolonged. Many drugs with different (if unknown) modes of action are available, and a variety of shuttle and rotation programmes can be considered. In view of the limitations of chemotherapy, particularly for the rearing of replacement flocks, there is considerable interest in the development of vaccines. Prospects for the introduction of live vaccines based on attenuated parasites are now very good, but the availability in the future of genetically engineered vaccines is more uncertain as little is known about the parasite molecules that stimulate protective immunity and, even if isolated, how they can be administered to the host so that it responds in the immunologically correct manner. Current research on Eimeria spp. in the chicken is broadly representative of that being done on other coccidia. Many lines of investigation are not connected with the development of new drugs or vaccination per se (and therefore have no obvious practical applications), but they are providing new insights into the biological complexity of the organisms and the ways in which they interact with their hosts. It remains possible, however, that a more detailed understanding and analysis of the molecules that are essential in the maintenance of the parasitic life style can be exploited in the future to provide alternative targets for chemical or immunological attack. The research topics considered in this review are arbitrarily grouped as studies on: (1) the basic biology of parasites, including aspects of the life cycle, and structure and function of the apical organelles; (2) the molecular biology of the parasites, including analyses of the number and structure of chromosomes, characterization of DNA sequences, and an account of the viral RNA that has been found in some species of Eimeria; and (3) control of coccidiosis, encompassing first immunity and the development of vaccines, and secondly, chemotherapy.     

Prominent J wave in cats with hypertrophic cardiomyopathy

The J wave has never been documented in the electrocardiogram (ECG) of cats presenting with hypertrophic cardiomyopathy (HCM). The present study aimed to describe the presence, morphology, amplitude, and duration of J waves in cats with HCM. It included 20 apparently healthy cats and 45 cats diagnosed with HCM based on clinical, echocardiographic, ECG, and radiographic examination. The cats were of different breeds (Persian: 40, domestic short hair: 21, Siamese: 4), ages (6.01 ± 4.34 years), sexes (male: 33, female: 32), and weights (3.30 ± 1.51 kg). The J wave was absent in the ECGs of the healthy population, but was detected in 29 out of 45 cats with HCM (63%). The J waves were observed at the QRS-ST junction in more than one limb lead of the ECG. Only positive deflections with an amplitude ≥0.05 mV were included, as measured by an ECG ruler in three consecutive heart cycles. The J waves were mainly present in leads II (n=20) and III (n=16), with amplitudes of 0.06 ± 0.02 and 0.08 ± 0.03 mV; their mean (± SD) duration was 0.16 ± 0.05 msec in lead II and 0.18 ± 0.05 msec in lead III. They occurred in both notched and slurred morphologies, with the latter being more common. In conclusion, J waves were a common finding in the ECGs of cats with HCM.     

Cardiac troponin I in cats with hypertrophic cardiomyopathy

The molecular structure of cardiac troponin I (cTnI) is highly conserved across mammalian species and assays developed for its measurement in human patients have been validated in a number of veterinary species. A raised concentration of circulating cTnI is a sensitive and specific marker of cardiac myocyte injury. Raised levels have been documented in a variety of cardiac diseases in both human and veterinary patients. This study compared serum cTnI concentrations between 16 cats diagnosed with hypertrophic cardiomyopathy (HCM) using echocardiography and 18 control cats. The results show that cats with HCM have significantly higher concentration of serum cTnI (median 0.95 ng/ml, range 0.2-4.1 ng/ml) than control cats (median <0.2 ng/ml, range <0.2-0.25 ng/ml) [P<0.0001]. Furthermore in cats with cardiomyopathy a weak correlation was found between the thickness of the left ventricular freewall in diastole measured by ultrasound and serum cTnI concentration (r(2)=0.28;P=0.036). These results suggest that measurement of serum cTnI concentration may enable cats with cardiomyopathy to be distinguished from normal cats using the assay described here.