Search

A 2.5-year-old castrated male domestic shorthair cat with a past pertinent history of FLUTD treatment 8 days earlier was presented during the night due to apathy and anorexia. Radiographs, ECG, blood pressure measurement and echocardiography revealed left-sided congestive heart failure, left ventricular concentric hypertrophy, left atrial dilation, severe diastolic dysfunction, hypotension, and vagotonus-associated sinus bradycardia with a first degree AV-block as well as a right bundle brunch block. NT-ProBNP and troponin I concentrations were elevated (NT-ProBNP > 1500 pmol/l, Troponin I 32.87 ng/ml). Presumptive diagnosis was acute myocarditis. Bartonella henselae PCR and Toxoplasma gondii IgM titer were negative. Initial IgG titer amounted to 1:32 (reference range: < 1:32) and on later testing this was negative. FeLV and FIV tests exhibited negative results. Coronavirus testing was not performed because the cat was vaccinated accordingly. A metastatic infection with Proteus mirabilis , which had been isolated from the urine, appeared possible. Alternatively, a hypersensivity reaction to drugs or a stress-induced myocarditis was taken into consideration. The hospitalized cat was treated with furosemide (initialy and in the course of further treatment), theophyllin (initially), continuous infusion with lactated Ringer's solution, pimobendan, and the addition of enrofloxacin to the ongoing amoxicillin/clavulanic acid administration. After 4 days, the cat's general condition improved satisfactorily and blood pressure returned to normal range. Left ventricular hypertrophy resolved, however, diastolic dysfunction as well as left atrial dilation persisted. Within the next 8 weeks, echocardiographic findings and cardiac biomarkers returned to near normal values. All medication was tapered and finally discontinued. During the last recheck examination 7 months following initial presentation, no cardiac changes were apparent., Competing Interests: Die Autorin bestätigt, dass kein Interessenkonflikt besteht., (Thieme. All rights reserved.)

Pulmonary hypertension (PH), together with its accompanying clinical signs and underlying causes, e.g. pulmonary thrombosis, are more and more recognized as an important clinical entity also in dogs. This article characterizes the clinical picture of 3 dogs with PH caused by natural infection with Angiostrongylus vasorum. All 3 dogs were of small breeds ( < 10 kg), the age at the time of diagnosis was 1, 2 and 11 years. Clinically, dyspnea and exercise intolerance were the predominating signs, 2 dogs developed hemoptysis, 1 dog developed right sided congestive heart failure. Severe arterial hypoxemia (PaO2 41 - 53 mmHg) reflected the severity of pulmonary parenchymal and vascular damage. Severe hyperglobulinemia (59 und 88 g/l) in two dogs implicated a long lasting infection. Anthelmintic treatment in 2 dogs resulted in quick clinical, radiographic and echocardiographic normalization. PH is the consequence of multiple causes and pathomechanisms, and the recognition of PH is primarily of differential diagnostic relevance. Prognosis and therapy in cases with PH mainly depend on the underlying cause, rather than on the PH and on its degree.

A case of endocarditis of the aortic valve in a 11 year old thoroughbred is presented. Diagnostic approach, the value of echocardiography, and the various symptoms, complications and prognosis are discussed. The horse with ruptured aortic valves due to endocarditis with severe aortic and mitral regurgitation causing congestive heart failure, was euthanised due to bad prognosis.

Plasma viscosity (PV) was examined in healthy (n = 122) and sick (n = 58) dogs. The mean value of PV in healthy adult dogs is 1.22 mPas. PV is remarkably increased in case of illness. In dogs with chronic heart failure the mean value was 1.46 mPas. Patients suffering from uraemia or pyometra revealed mean values of 1.90 mPas and 1.96 mPas respectively. An elevation of the PV is correlated with an increase of the "acute-phase-proteins". The examination of PV is useful for a better assessment of microcirculation. The PV is a parameter, which is important in diagnostics as well as in follow-up during special therapeutical procedures.

In this study 43 animals suffering from a decompensated heart failure were treated with one of two different ACE-inhibitors. 16 animals received Captopril, 27 were treated with Ramipril. A clinical examination was performed prior to the onset of therapy. Controls were performed two weeks, six weeks and seven months after the beginning of treatment. In the captopril-group 12 animals improved by at least one degree, four dogs died within the examination period. In the ramipril-group 16 of 27 dogs treated with a dosage of 0.125 mg/kg bw once a day showed an improvement of one or more degree and 6 animals died. In 8 animals the dose of 0.125 mg/kg bw once a day was increased to 0.125 mg/kg bw twice a day which consequently led to an improvement in 4 dogs. Ramipril and captopril were considered equal in tolerance. The study will be continued with a ramipril dosage of 0.25 mg/kg bw once a day in all further patients.

In this study 72 dogs the efficacy and safety of quinapril and captopril in the treatment of canine heart failure were found to be comparable. Differences exist between the dosage schedules of both ACE inhibitors. The recommended dosage schedule for the short acting captopril is three times daily 0.5 mg/kg bodyweight. Quinapril belongs to a newer generation of ACE inhibitors with a longer half life. Therefore a dosage of 0.5 mg/kg KGW once daily was in most cases sufficient for a successful therapy. This means that quinapril can ease the management of canine heart failure, because at least in dogs with mild to moderate heart failure the dosing interval is longer compared to captopril. Moreover, the treatment of small dogs is easier, because quinapril is available as 5 mg tablets whereas the smallest captopril tablets contain 12.5 mg agent.

The determination of the intracellular acid-base state is reported in this paper, using erythrocytic haemolysate in dogs as an example. Reference values are given for 217 clinically healthy dogs. The effects of various selected stages of illness and additional stresses on the erythrocytic acid-base equilibrium are reported and compared with acid-base changes in the blood. The metabolic acidosis observed may occur earlier and be stronger in the intracellular space than in the blood. There seems to be a closer correlation between a disturbed intraerythrocytic acid-base equilibrium and the degree of clinical symptoms than between the (commonly investigated) acid-base changes in the blood and the clinical presentations. The investigation of the blood alone does not provide a satisfactory indication of the patient's acid-base state and of the necessity for treatment.

Myocardial fibrosis and degeneration of unknown etiology is described in two adult, female goats of the Saanen and Pfauen breeds. Both animals presented with clinical signs of cardiac failure with subcutaneous edema, hydrothorax and ascites. The pathological lesions were characterized by cardiomegaly with ventricular and auricular dilatation and hypertrophy, massive subcutaneous edema and body cavity edema. The first goat additionally showed chronic liver congestion due to cardiac failure. Histologically, the most prominent changes were focally extensive cardiomyocyte degeneration and cardiac fibrosis. The clinical history and pathologic lesions are comparable to those of dilatative cardiomyopathy in SixRH cattle.

Between 1986 and 1989 there were 9 cases of idiopathic congestive heart failure at this clinic. Normally heifers in the last 1/3 of pregnancy and young cows aged between 2.5 and 3.5 years were affected, but the disease also occurred in one younger (1.5 years), one older (6 years) and in one male animal. In contrast to other reports, myocardial fibrosis in the State of Hesse was only seen in the Rotbunte breed. The animals suffered from a severe heart failure with venous congestion and congestive edema of the brisket, the submandibular area and the ventral abdomen. In most cases there is no precise difference in history, clinical findings and laboratory findings between myocardial fibrosis, traumatic pericarditis and endocarditis valvularis. Only pathological and histological examinations of the heart confirm a suspected myocardial fibrosis: The heart is enlarged and dilatated and seems to be non-elastic. Microscopically a scattered interstitial fibrosis and signs of myocardial degeneration are visible.

Atrial natriuretic peptide has been considered to be a major regulator in the body's water and salt homeostasis. Antagonizing those mechanisms leading to volume retention and overload (renin, angiotensin, aldosterone), ANP has been suggested to play a critical role in the pathology of certain diseases like renal failure, congestive heart failure or hypertension. In this regard, we measured ANP plasma concentration in normal healthy dogs and dogs with renal failure, congestive heart failure and Cushing syndrome. ANP levels were slightly decreased in dogs with Cushing disease (n = 9; 5.5 +/- 2 fmol/ml), increased in renal failure (n = 7; 16.2 +/- 5.8 fmol/ml, p less than 0.05) and markedly augmented in dogs with congestive heart failure (n = 14; 52.9 +/- 29.75 fmol/ml, p less than 0.01) as compared to healthy dogs (n = 6; 8.3 +/- 3.5 fmol/ml). Furthermore, characterization of the measured immunoreactivity (IR-ANP) revealed, that up to 50% of the IR-ANP in dogs with congestive heart failure corresponds to the ANP precursor molecule, not found in healthy subjects. This fact might present one possible explanation for the attenuated response to ANP in congestive heart failure. In addition, this finding may also serve a diagnostical purpose.

23 horses and one donkey with congestive heart failure are treated with a standardized methyldigoxin dose (0.0032 mg/kg of body weight). The therapy is controlled by the serum concentration of the cardiac glycoside. 4 horses have a higher and 13 horses a lower serum concentration as necessary for therapeutic approach. The influence of additional diseases and medications is demonstrated. Finally a rule for the evaluation of the individual therapeutic glycoside-dose is given.

32 dogs with congestive heart failure without sufficient reaction to a standardized therapy with glycosides are treated with an individual glycoside dose. The therapy is controlled by the serum concentration of the cardiac glycoside. The influence of additional diseases and medications is demonstrated. Finally a rule for the evaluation of the therapeutic glycoside dose is given.