Indications for permanent pacing in dogs and cats.

Pacemaker implantation is considered as a standard procedure for treatment of symptomatic bradycardia in both dogs and cats. Advanced second-degree and third-degree atrioventricular blocks, sick sinus syndrome, persistent atrial standstill, and vasovagal syncope are the most common rhythm disturbances that require pacing to either alleviate clinical signs or prolong survival. Most pacemakers are implanted transvenously, using endocardial leads, but rarely epicardial leads may be necessary. To decide whether a patient is a candidate for pacing, as well as which pacing modality should be used, the clinician must have a clear understanding of the etiology, the pathophysiology, and the natural history of the most common bradyarrhythmias, as well as what result can be achieved by pacing patients with different rhythm disturbances. The goal of this review was, therefore, to describe the indications for pacing by evaluating the available evidence in both human and veterinary medicine. We described the etiology of bradyarrhythmias, clinical signs and electrocardiographic abnormalities, and the choice of pacing modality, taking into account how different choices may have different physiological consequences to selected patients. It is expected that this review will assist veterinarians in recognizing arrhythmias that may require permanent pacing and the risk-benefit of each pacing modality and its impact on outcome.

[Pulmonary arterial hypertension in adult patients with congenital heart disease]. / Ipertensione arteriosa polmonare nei pazienti adulti con cardiopatia congenita.

Pulmonary Hypertension (PH) is definited by a mean pulmonary artery pressure (PAPm) >25 mmHg at rest. The Dana Point 2008 Revised Classification System represents the most recent classification system update with respect of various etiologies of PH. About 10 % of adolescents or adults with uncorrected congenital heart disease (CHD) with left-to-right shunt and high pulmonary blood flow develop Pulmonary Arterial Hypertension (PAH) . Progressive vascular remodeling and increase in pulmonary vascular resistance (PVR) may ultimately lead to reversal of the shunt (pulmonary to systemic) causing cyanosis and determining the so-called Eisenmenger Syndrome (ES). Recent advances in the early diagnosis and medical targeted treatment of adult patients with CHD-PAH and ES can improve PAP, PVR and exercise tolerance, together with NYHA Class and survival, and may potentially reverse the vascular remodeling process in selected patients.

Interspecific competition between the nematode-trapping fungus, Duddingtonia flagrans, and selected microorganisms and the effect of spore concentration on the efficacy of nematode trapping.

The fungus, Duddingtonia flagrans, is able to trap and kill free-living nematode larvae of the cattle parasite Cooperia oncophora when chlamydospores are mixed in cattle faeces. Isolates of Bacillus subtilis (two isolates), Pseudomonas spp. (three isolates) and single isolates of the fungal genera Alternaria, Cladosporium, Fusarium, Trichoderma and Verticillium were isolated from cattle faeces and shown to reduce D. flagrans growth on agar plates. When these isolates were added to cattle faeces containing D. flagrans and nematode larvae of C. oncophora, developing from eggs, none of the isolates reduced nematode mortality attributed to D. flagrans. Similarly, the coprophilic fungus Pilobolus kleinii, which cannot be cultivated on agar, also failed to suppress the ability of D. flagrans to trap and kill developing larvae of C. oncophora. Increasing chlamydospore doses of D. flagrans in faecal cultures resulted in higher nematode mortality. Thus, no evidence of interspecific or intraspecific competition was observed. The consequences of these findings are discussed.

[Thrombosis and cardiovascular diseases]. / Trombosi e malattie cardiovascolari.

Thrombosis represents the propensity toward arterial and/or venous thrombotic events. Many causes of thrombosis are now known: clinical predisposing factors (recent major surgery, varices of lower limbs, prolonged bedrittening); immunological, hematological and liver diseases; inborn or acquired coagulation factors' or plasmatic proteins' deficiency; platelets disfunction. Thrombotic screening of affected individuals is fundamental to adjust dosage and length of therapy, for secondary prevention and for relatives evaluation.

Taste alterations in liver cirrhosis: are they related to zinc deficiency?

Patients with chronic liver disease may have taste impairment and altered zinc metabolism. We evaluated Taste Detection Thresholds (TDTs) in 60 patients with liver cirrhosis and correlated the findings with disease severity and alcoholic etiology. Plasma zinc levels and urinary output were also measured. A placebo-controlled treatment trial with zinc sulphate was made in 15 patients with compensated cirrhosis in order to ascertain whether zinc deficiency caused taste alterations. Taste detection of salty, sweet and acid tastants was significantly impaired in all cirrhotic patients in comparison with normal subjects. TDTs were not influenced either by the etiology or the severity of the disease. All groups of patients had low plasma zinc levels and decompensated cirrhosis had a significantly increased urinary output of zinc. No correlation was found between taste acuity and plasma zinc levels when only cirrhotic patients were considered. The effect of zinc supplementation on TDTs did not appear to be inferior to that of the placebo. Our results indicate that taste impairment in cirrhotics is due to the disease process per se and not to zinc deficiency.