Transvenous embolization of moderate to large patent ductus arteriosus in dogs using the Amplatzer vascular plug II.

BACKGROUND: Catheter-based occlusion of patent ductus arteriosus (PDA) can be performed using different devices. Transvenous embolization using the Amplatzer vascular plug II (AVP-II) has been studied in humans, but it has not been described in dogs. OBJECTIVE: Evaluate the feasibility and success of transvenous embolization of PDA using the AVP-II in dogs. ANIMALS: Nineteen client-owned dogs with left-to-right shunting PDA, with minimal ductal diameter >2.5 mm. METHODS: Prospective observational study using AVP-II with transvenous access for PDA closure in dogs. RESULTS: Angiography showed a conical ductus with a long (n = 17) or short (n = 2) ampulla. The minimal diameter of the duct was 4.34 ± 1.11 mm, and the maximal diameter of the ampulla was 13.18 ± 3.47 mm. Technical success was achieved in 18 of the 19 (94.7%) patients after the first intervention and in all 19 (100%) patients after the second intervention. Postrelease angiography documented complete occlusion of the PDA in 10 of 19 (52.6%) dogs. Mild flow acceleration or stenosis of the left pulmonary artery was found in 6 and 1 of the 17 analyzed cases, respectively, by Doppler examination. The closure rate 24 hours after intervention was 94.7% (18/19). The remaining dog had a moderate residual shunt, and delayed complete closure after 3 months led to a 100% closure rate. CONCLUSION AND CLINICAL IMPORTANCE: The AVP-II is a safe and effective device for transvenous embolization in dogs with moderate to large PDA.

Assessment of a bedside test for N-terminal pro B-type natriuretic peptide (NT-proBNP) to differentiate cardiac from non-cardiac causes of pleural effusion in cats.

BACKGROUND: Cats with pleural effusion represent common emergencies in small animal practice. The aim of this prospective study was to investigate the diagnostic ability of a point-of-care ELISA (POC-ELISA) for the measurement of N-terminal pro B-type natriuretic peptide (NT-proBNP) to differentiate cardiac from non-cardiac disease in cats with pleural effusion. The sample material for use of this rapid test was either plasma or diluted pleural effusion. Twenty cats with moderate to severe pleural effusion were prospectively recruited. The cats were grouped into two groups, with or without congestive heart failure (CHF; N-CHF), after complete work-up. Blood and effusion were collected in EDTA tubes. Plasma and pleural effusion supernatants were transferred into stabilizer tubes and frozen. POC-ELISA for NT-proBNP was performed with plasma and diluted effusion (1:1). Quantitative NT-proBNP measurement was performed in plasma and diluted and undiluted effusions. RESULTS: Six cats were assigned to the CHF group. Of the 14 cats in the N-CHF group, 6 had concurrent cardiac abnormalities that were not responsible for the effusion. For the detection of CHF, the test displayed respective sensitivities and specificities of 100% and 79% in plasma and 100% and 86% in diluted pleural fluid. Receiver operating characteristic (ROC) analysis for quantitative NT-proBNP measurement of plasma and diluted and undiluted pleural effusions displayed areas under the curve of 0.98, sensitivities of 100% and specificities of 86%. The optimum cut-off was calculated at 399 pmol/l in plasma and 229 pmol/l in the diluted effusion and 467 pmol/l in the undiluted effusion. CONCLUSIONS: POC-ELISA for NT-proBNP in both plasma and diluted pleural effusion was suitable to differentiate cardiac from non-cardiac causes of feline pleural effusion. According to our results, use of pleural effusion is feasible, but dilution of the effusion before measurement seems to improve specificity.

[Cyanosis in a calf with a double outlet right ventricle]. / Zyanose bei einem Kalb mit einem Double Outlet Right Ventricle.

A 4-day-old female Holstein Friesian calf was presented for evaluation of cyanosis and dyspnea. On auscultation, severe bronchovesicular sounds and a systolic heart murmur of grade IV/VI above the tricuspid valve were found. On echocardiography, a marked dextroposition of the aorta (> 50% originating from the right ventricle), leading to both great arteries arising from the right ventricle - a so-called double-outlet right ventricle - was detected. Two ventricular septal defects were present, one in the perimembranous, subpulmonary region, the other non-committed in the muscular region. The subpulmonary ventricular septal defect was responsible for the shunting of unoxygenated blood into the aorta. Additionally, an aneurysma-like atrial septal defect (type secundum) and a large patent ductus arteriosus were visualized. The main pulmonary artery was severely enlarged without the presence of a stenotic defect. The findings could be verified by angiography. Additionally, a diffuse hypoplastic ascending aorta was visualized. Necropsy confirmed the echocardiographic and angiographic findings.

Follow-up of troponin I concentration in dogs with atrioventricular block and dual-chamber pacing in a case-matched study.

BACKGROUND: Increased cardiac troponin I (cTnI) concentration has been reported in dogs with atrioventricular (AV) block before and shortly following pacemaker implantation. The role of AV dyssynchrony, age, or concurrent cardiac disease on cTnI concentration remains unknown. OBJECTIVES: To investigate change in cTnI concentration following dual-chamber pacemaker implantation on short- and long-term follow-up and to compare cTnI values to a case-matched control group. ANIMALS: Thirty-eight client-owned dogs with permanent AV block and 38 matched control dogs. METHODS: Retrospective review of medical records. Pacemaker group consisted of dogs with AV block and dual-chamber pacing. Control group matched the study population in age and cardiac disease. cTnI was compared between pacemaker and control group on short- and long-term follow-up. Different lead types and influence of arrhythmia on cTnI were tested. RESULTS: cTnI was high at presentation (median 0.66 ng/ml; range 0.03-18.6) and showed a significant reduction over time after pacemaker implantation (p < 0.0001). Median cTnI values were significantly different between pacemaker and control group on short-term (p = 0.0004; 0.11 ng/ml, range 0.03-1.36 versus 0.06 ng/ml, range 0.03-0.46), but not on long-term follow-up (p = 0.0547; 0.14 ng/ml, range 0.03-0.73 versus 0.07 ng/ml, range 0.03-0.46). Lead type and severity of arrhythmia did not show a significant correlation to cTnI concentration. CONCLUSIONS: On long-term follow-up, cTnI remained mildly elevated in some of the pacemaker dogs but was not significantly different to the matched control group.