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Background: Focused cardiac ultrasound (FCU) helps detect occult heart disease in human patients., Hypothesis: Focused cardiac ultrasound by a nonspecialist practitioner (NSP) will increase the detection of occult heart disease in asymptomatic cats compared with physical examination and ECG., Animals: Three hundred forty-three client-owned cats: 54 excluded and 289 analyzed., Methods: Multicenter prospective cohort study. Twenty-two NSPs were trained to perform FCU. Cats without clinical signs of heart disease were recruited, and NSPs performed the following in sequential order: physical examination, ECG, FCU, and point-of-care N-terminal pro-B-type natriuretic peptide assay (POC-BNP). After each step, NSPs indicated yes, no, or equivocal as to whether they believed heart disease was present. The level of agreement between the NSP diagnosis and a blinded cardiologist's diagnosis after echocardiogram was evaluated using Cohen's kappa test., Results: Cardiologist diagnoses included 148 normal cats, 102 with heart disease, and 39 equivocal ones. Agreement between NSP and cardiologist was slight after physical examination (kappa 0.253 [95% CI, 0.172-0.340]), did not increase after ECG (0.256 [0.161-0.345]; P = .96), increased after FCU (0.468 [0.376-0.558]; P = .002), and the level of agreement was similar after POC-BNP (0.498 [0.419-0.580]; P = .67). In cats with mild, moderate, and marked occult heart disease, the proportion of cats having a NSP diagnosis of heart disease after FCU was 45.6%, 93.1%, and 100%, respectively., Conclusions and Clinical Importance: Focused cardiac ultrasound performed by NSPs increased the detection of occult heart disease, especially in cats with moderate to marked disease. Focused cardiac ultrasound appears to be a feasible and useful tool to assist NSPs in the detection of heart disease in cats., (© 2019 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals, Inc. on behalf of the American College of Veterinary Internal Medicine.)

Objective: To compare cardiac troponin I (cTnI) concentrations determined by use of a point-of-care analyzer with values determined by use of a bench-top immunoassay in plasma samples obtained from clinically normal horses with and without experimentally induced cardiac disease, and to establish a reference range for plasma equine cTnI concentration determined by use of the point-of-care analyzer., Animals: 83 clinically normal horses, 6 of which were administered monensin to induce cardiac disease., Procedures: A blood sample was collected from each of the 83 clinically normal horses to provide plasma for analysis by use of the point-of-care analyzer; some of the same samples were also analyzed by use of the immunoassay. All 83 samples were used to establish an analyzer-specific reference range for plasma cTnI concentration in clinically normal horses. In 6 horses, blood samples were also collected at various time points after administration of a single dose of monensin (1.0 to 1.5 mg/kg) via nasogastric intubation; plasma cTnI concentration in those samples was assessed by use of both methods., Results: The analyzer-specific reference range for plasma cTnI concentration in clinically normal horses was 0.0 to 0.06 ng/mL. Following monensin treatment in 5 horses, increases in plasma cTnI concentration determined by use of the 2 methods were highly correlated (Pearson correlation, 0.83). Peak analyzer-determined plasma cTnI concentrations in monensin-treated horses ranged from 0.08 to 3.68 ng/mL., Conclusions and Clinical Relevance: In horses with and without experimentally induced cardiac disease, the point-of-care analyzer and bench-top immunoassay provided similar values of plasma cTnI concentration.

Background Hypothesis Animals Methods Results Conclusions and Clinical Importance Reliability of echocardiographic calculations for stroke volume and mitral regurgitant fraction (RFMR) are affected by observer variability and lack of a gold standard. Variability is used to calculate critical change values (CCVs) that are thresholds representing real change in a measure not associated with observer variability.Observed intra‐ and interobserver accuracy and variability in healthy dogs help model CCV for RFMR.Reliability cohort of 34 healthy dogs; allometric scaling cohort of 99 dogs with heart disease and 25 healthy dogs.Accuracy, variability, and CCV of 2 observers using geometric and flow‐based echocardiography were prospectively compared against a standard of RFMR = 0% and extrapolated across a range of expected RFMR values in the reliability cohort partly derived from cardiac dimensions predicted by the allometric cohort.Accuracy of methods to determine RFMR in descending order was 4‐chamber bullet (Bullet4CH), mitral inflow, cube formula, and Simpson's method of disks. Intraobserver variability was relatively high. The CCV for RFMR ranged from 28% to 88% and was inversely related to RFMR when extrapolated for use in affected dogs. For both observers, the Bullet4CH method had the lowest intraobserver CCV (Operator 1:28%, Operator 2:41%). Interobserver strength of agreement was low with intraclass correlation coefficients ranging from 0.210 to 0.413.Echocardiographic volumetric methods used to calculate stroke volume and RFMR have low accuracy and high variability in healthy dogs. Extrapolation of observed CCV to a range of expected RFMR suggests observers and methods are not interchangeable and variability might hinder routine clinical usage. Individual observers should be aware of their own variability and CCV. [ABSTRACT FROM AUTHOR]

Abstract: Background: Myocardial disease in camelids is poorly characterized. Nutritional (selenium deficiency) and toxic (ionophore toxicity) myocardial disease have been reported in camelids. Diagnosis and management of these and other myocardial diseases might be enhanced by evaluating cardiac troponin I (cTnI) concentrations. No information about cTnI reference intervals in camelids is currently available. Hypothesis/Objectives: (A) To determine cTnI concentrations obtained using a point of care i-STAT®1 analyzer (Heska Corporation) in healthy alpacas; (B) to compare alpaca cTnI concentrations between heparinized whole blood and plasma samples and between 2 different storage conditions (4 °C for 24 h or −80 °C for 30 days); (C) to examine assay reproducibility using the i-STAT®1. Animals, materials and methods: 23 healthy alpacas were evaluated. Blood and plasma samples were analyzed by the i-STAT®1 within 1 h of collection. Aliquots of plasma were stored at either 4 °C for 24 h or −80 °C for 30 days, and then analyzed. Assay reproducibility was determined by comparing 2 plasma or whole blood cTnI concentrations measured on the same sample over a 10 min period. Results: Analyzer-specific plasma cTnI concentrations in clinically normal alpacas had a median of <0.02 ng/mL (range: <0.02 ng/mL to 0.07 ng/mL). Plasma and whole blood concentrations showed good agreement. Storage did not affect cTnI concentrations (p > 0.75). Plasma cTnI concentrations had coefficient of repeatability of 0.02 ng/mL. Conclusions: The i-STAT®1 can measure cTnI in alpacas on both plasma and whole blood and provides similar values for both samples. Storage at 4 °C for 24 h or −80 °C for 30 days does not affect estimates of plasma cTnI. Evaluation of cTnI might be of value in assessing cardiac disease in this species. [Copyright &y& Elsevier]

The article focuses on a study which examined the effect of intragastric administration of sodium monensin on serum cardiac troponin I (cTnI) concentrations in four horses. The study evaluated the symptoms of cardiac disease within 24 hours of monensin administration, through elevated heart rate, echocardiography and cTnI increase. It observes that the highest concentrations of cTnI were found in two horses that died of severe cardiac disease within five days of monensin administration.

Focal adhesion kinase (FAK) is a cytoplasmic tyrosine kinase that plays a major role in integrin signaling pathways. Although cardiovascular defects were observed in FAK total KO mice, the embryonic lethality prevented investigation of FAK function in the hearts of adult animals. To circumvent these problems, we created mice in which FAK is selectively inactivated in cardiomyocytes (CFKO mice). We found that CFKO mice develop eccentric cardiac hypertrophy (normal LV wall thickness and increased left chamber dimension) upon stimulation with angiotensin II or pressure overload by transverse aortic constriction as measured by echocardiography. We also found increased heart/body weight ratios, elevated markers of cardiac hypertrophy, multifocal interstitial fibrosis, and increased collagen I and VI expression in CFKO mice compared with control littermates. Spontaneous cardiac chamber dilation and increased expression of hypertrophy markers were found in the older CFKO mice. Analysis of cardiomyocytes isolated from CFKO mice showed increased length but not width. The myocardium of CFKO mice exhibited disorganized myofibrils with increased nonmyofibrillar space filled with swelled mitochondria. Last, decreased tyrosine phosphorylation of FAK substrates p130Cas and paxillin were observed in CFKO mice compared with the control littermates. Together, these results provide strong evidence for a role of FAK in the regulation of heart hypertrophy in vivo. [ABSTRACT FROM AUTHOR]

Abstract: Atrioventricular (AV) canal defects comprise a rare category of congenital heart disease associated with abnormal development of the endocardial cushions. These anomalies include a broad spectrum of lesions involving the atrial septum primum, the inlet portion of the ventricular septum, and the atrioventricular valves. In severe cases heart failure may result. The present report describes cardiopulmonary findings in a six-week-old, female Thoroughbred foal with persistent tachypnea and tachycardia since birth. Clinical, echocardiographic, cardiac catheterization, and pathologic findings were compatible with complete AV canal defect with bi-directional shunting, congestive heart failure, and pulmonary hypertension. Gross cardiac pathologic findings included a large atrioventricular septal defect, a common atriovalvular orifice, five atrioventricular leaflets, with two free-floating bridging leaflets. Histopathologic lesions in the lung included hypertrophy of the pulmonary arteriolar walls due to thickening of the tunica media. This represents a well documented case of complete endocardial cushion defect with anomalous development of the atrioventricular valves and resultant pulmonary hypertension and heart failure. [Copyright &y& Elsevier]