BackgroundCardiac troponin I (cTnI) is useful for assessing hypertrophic cardiomyopathy (HCM) in cats.ObjectiveTo measure plasma cTnI concentrations in healthy cats and evaluate the clinical utility of cTnI in determining the severity of HCM.AnimalsClinically healthy cats (n = 88) and cats with HCM (n = 93).MethodsMulticenter prospective study. Cats with HCM, including hypertrophic obstructive cardiomyopathy at various stages, were diagnosed using echocardiography. Plasma cTnI concentrations were analyzed by a commercial laboratory. Receiver‐operating characteristic curve analysis was used to evaluate the accuracy of plasma cTnI concentrations to detect HCM.ResultsThe median cTnI concentration was 0.027 ng/mL (interquartile range, 0.012‐0.048 ng/mL) in healthy cats. Concentrations were significantly higher in diseased cats than in healthy controls, and concentrations were significantly higher in cats with heart failure than in asymptomatic cats. A plasma cTnI concentration of 0.163 ng/mL had a sensitivity of 62.0% and specificity of 100% when used to distinguish normal cats from asymptomatic HCM cats without left atrial dilatation. A cutoff of 0.234 ng/mL had high sensitivity (95.0%) and specificity (77.8%) for assessing heart failure. The areas under the receiver‐operating characteristic curves were 0.85 and 0.93, respectively.Conclusions and Clinical ImportanceIncreased cTnI concentrations reflect the severity of HCM. If other causes of cardiac injury are ruled out, plasma cTnI concentration may be useful for predicting the severity of HCM in cats.

Plasma N-terminal pro-atrial natriuretic peptide (NT-proANP) concentration increases with progression of myxomatous mitral valve disease (MMVD) in dogs. This multicentre, prospective study compared plasma NT-proANP, N-terminal pro-brain natriuretic peptide (NT-proBNP), ANP, and cardiac troponin I (cTnI) concentrations in dogs with MMVD for their characteristics and discriminatory ability to detect cardiac dilatation and congestive heart failure (CHF). Thirty-six healthy dogs and 69 dogs with MMVD were included. Clinical variables were obtained via physical examination, thoracic radiography, and echocardiography. The discriminatory ability of each cardiac biomarker (CB) to determine the presence or absence of cardiac dilatation (event 1) and CHF (event 2) was evaluated using the receiver operating characteristic curves. Plasma NT-proANP, NT-proBNP, and ANP concentrations showed a significant association with the left atrium/aorta ratio ( P <0.01). The area under the curve of plasma NT-proANP and NT-proBNP concentrations were 0.72 and 0.75, respectively in event1 and 0.72 and 0.76, respectively in event2. Plasma NT-proANP and NT-proBNP concentrations showed sensitivity 80.0 and 80.0%; specificity 67.6 and 64.7% in event1 (cutoff value; 8,497.81 pg/ml and 1,453.00 pmol/l, respectively) and sensitivity 85.7 and 81.0%; specificity 60.4 and 64.6% in event2 (cutoff value; 8,684.33 pg/ml and 1,772.00 pmol/l, respectively). In dogs with MMVD, plasma NT-proANP, NT-proBNP, and ANP concentrations increase with left atrial enlargement. Particularly, plasma NT-proANP and NT-proBNP concentrations appeared to be equally useful in the discriminatory ability to detect cardiac dilatation and CHF.

Several patients who had a progressive clinical course involving both the central and peripheral nervous systems have been reported, but the diagnostic marker has been remained uncertain. More recently, such patients were reported to have namely “encephalomyeloradiculoneuropathy (EMRN)” associated with anti-neutral glycosphingolipid (GSL) antibodies. These antibodies were reported to disappear from the serum in the recovery phase, but whether this finding applies to the cerebrospinal fluid (CSF) remains uncertain. We describe a 67-year-old man with EMRN in whom we measured anti-neutral GSL antibodies in serial serum and CSF samples. During the disease course, the optical densities of the positive band against the background intensity ratio (–<0.3; ±≥0.3 to <0.6; +≥0.6 to <1.0; 2+≥1.0 to <2.0; 3 +≥2.0) for serum and CSF anti-lactosylceramide (LacCer) antibodies were found to be as follows: 2+ and 1+ at the first admission, ± and − when the consciousness level improved after immunotherapy, − and 1+ at clinical relapse, and ± and − when the consciousness level improved after immunotherapy. This is the first time to document that clinical relapse occurred in EMRN, and at this time the negative anti-LacCer antibodies in CSF after the first course of immunotherapy turned positive, but this was not seen in serum samples.

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Sporadic Inclusion Body Myositis (sIBM) is a refractory myositis developing in the elderly. Recently, anti-cytosolic 5'-nucleotidase 1A (cN1A) antibodies were reported to be present specifically in sIBM. To assess the clinicopathological features and usefulness of anti-cN1A positivity in muscle specimens, we evaluated a group of Japanese patients with sIBM. Among Japanese patients with myositis who underwent a muscle biopsy from 1991 through 2014 in our hospital, we identified cases of sIBM that met the European Neuromuscular Center (ENMC) criteria. We then analyzed clinical course, pathological findings, and treatment response. Of 282 patients with myositis, 35 (12%) were given a diagnosis of sIBM (24 men and 11 women). The median age at onset was 67 ± 7 (55-81) years, and that at diagnosis was 70 ± 7 years. Remarkably, 5 (14%) patients concurrently had hepatitis C virus (HCV) infection and 4 (11%) had heart disease. Pathologically, we found rimmed vacuoles in 32 (91%) patients and anti-cN1A positivity in perinuclear regions and rimmed vacuoles in 31 (89%) patients. Remarkably, anti-cN1A antibody positivity was significantly higher in sIBM than in polymyositis (30%), dermatomyositis (10%), and morphologically normal cases (0%), suggesting its high specificity for sIBM. Twelve (34%) patients received immunosuppressants, 8 (23%) received prednisone, and 5 (14%) received intravenous immunoglobulins (IVIg). Clinical symptoms transiently improved in 5 patients given prednisone and in 4 patients given IVIg, but these treatments failed to be radical therapies. In our study of Japanese patients with sIBM, anti-cN1A antibody positivity in muscle specimens was highly sensitive and specific pathologically. Therefore, the expression of anticN1A antibody may be greatly useful for the diagnosis of sIBM. Although the concurrent presence of HCV infection and heart disease was notable, other epidemiological characteristics were consistent with the results of previous studies.