Epidemiology of heart disease in English Bull Terriers and echocardiographic characteristics of mitral valve abnormalities.

OBJECTIVES: To present the prevalence and distribution of heart disease as well as echocardiographic findings in English Bull Terriers. MATERIALS AND METHODS: One hundred and one English Bull Terriers were retrospectively included to evaluate the prevalence and distribution of heart disease. Secondly, a retrospective study on mitral valve abnormalities was performed on three groups: a control group (n=120, 19 breeds) used to establish reference intervals for mean transmitral gradient; a healthy English Bull Terriers group (n=25) and an English Bull Terriers group with mitral valve abnormalities (n= 18). Healthy English Bull Terriers for which mitral inflow parameters were not obtainable and English Bull Terriers with other types of heart disease were excluded. RESULTS: The prevalence of heart disease in English Bull Terriers was 65% (66/101), with mitral valve abnormalities (47%, 47/101) and aortic stenosis (29%, 29/101) being most common. The cut-off value for normal mean transmitral gradient was 3.5 mmHg in the control group. The mean transmitral gradient for healthy English Bull Terriers was higher than for other dog breeds. Healthy English Bull Terriers had a smaller mitral valve area and mitral annulus diameter compared with dogs with a similar body surface area. A high heart rate, smaller mitral valve area, mitral regurgitation, and volume overload are associated with increased mean transmitral gradient in English Bull Terriers with mitral valve abnormalities. CLINICAL SIGNIFICANCE: We suggest that mitral valve area, mitral annulus diameter and mean transmitral gradient measurements should be included in the echocardiographic protocol for English Bull Terriers.

Transthoracic two-dimensional and three-dimensional echocardiography for the measurement of mitral valve area planimetry in English Bull Terriers with and without heart disease.

INTRODUCTION: Mitral valve area (MVA) planimetry is used to diagnose and classify mitral stenosis (MS) in humans using two-dimensional and three-dimensional echocardiography (MVA2D and MVA3D). This study aimed to evaluate agreement, feasibility, and observer variability between MVA2D and MVA3D in English Bull Terriers (BT). Our hypotheses were (1) that the MVA of BT is generally smaller than that of breeds with similar body weight and (2) that these techniques could be used to diagnose MS in BTs. ANIMALS: Twenty healthy BTs, 15 healthy Boxers, and 49 BTs with heart disease. MATERIALS AND METHODS: A prospective diagnostic agreement study was conducted. All dogs underwent a thorough clinical examination, conventional transthoracic echocardiography, and three-dimensional echocardiography. RESULTS: Bland-Altman plots (limits of agreement: 0.12-1.5) showed consistent bias and poor agreement between MVA2D and MVA3D. For the 69 BTs, MVA3D (2.1 ± 0.50 cm2) measurements were significantly lower than MVA2D measurements (2.9 ± 0.60 cm2), and healthy BTs had significantly lower MVA parameters than healthy Boxers (p < 0.001). Intraobserver and interobserver variability were excellent for both MVA2D and MVA3D (intraclass correlation coefficient >0.9). Six BTs were diagnosed with MS, with MVA3D less than 1.8 cm2 and a mean transmitral gradient (MTG) of more than 5 mmHg. CONCLUSIONS: Both MVA2D and MVA3D are feasible, have low observer variability and can be used to diagnose MS in BTs. For assessing the narrowest orifice area, the preferred method is MVA3D. The smaller MVA in BTs compared to Boxers may indicate some degree of MS.

Symmetric Dimethylarginine in Cats with Hypertrophic Cardiomyopathy and Diabetes Mellitus.

BACKGROUND: Symmetric dimethylarginine (SDMA) has been increasingly used as a marker of early chronic kidney disease (CKD) in cats, but little is known about the influence of comorbidities on SDMA in this species. HYPOTHESIS: Hypertrophic cardiomyopathy (HCM) and diabetes mellitus (DM), independently of CKD, are associated with changes in serum SDMA. ANIMALS: Ninety-four cats (17 with CKD, 40 with HCM, 17 with DM, and 20 healthy controls). METHODS: Case-control study. Clinical examination, echocardiography, ECG, blood pressure, CBC, biochemistry, thyroxine, and SDMA measurement were performed. Urinalysis was performed in controls and cats with CKD and DM. Analysis of variance was used to compare overall differences in the log-transformed SDMA data among groups. A random forest algorithm was applied to explore which clinical and other factors influenced serum SDMA. RESULTS: Median (range) serum SDMA for the renal group (positive control) was 19 (10-93) µg/dL, whereas for the control group (negative control), it was 10 (5-15) µg/dL. For the cardiac and diabetic groups, serum SDMA was 9 (4-24) µg/dL and 7 (3-11) µg/dL, respectively. The renal group had significantly higher SDMA concentrations and the diabetic group significantly lower SDMA concentrations compared to all other groups. CONCLUSIONS AND CLINICAL IMPORTANCE: Serum SDMA concentrations in cats with HCM were not significantly different from those of healthy control cats. Cats with DM, however, had significantly lower SDMA concentrations than controls, a finding that needs further investigation and should be kept in mind when evaluating renal function of cats with this endocrinopathy.

Cardiac Troponins in Dogs and Cats.

Cardiac troponins are sensitive and specific markers of myocardial injury. The troponin concentration can be thought of as a quantitative measure of the degree of injury sustained by the heart, however, it provides no information on the cause of injury or the mechanism of troponin release. Conventionally, the cardiac troponins have been used for diagnosis of acute myocardial infarction in humans and have become the gold standard biomarkers for this indication. They have become increasingly recognized as an objective measure of cardiomyocyte status in both cardiac and noncardiac disease, supplying additional information to that provided by echocardiography and ECG. Injury to cardiomyocytes can occur through a variety of mechanisms with subsequent release of troponins. Independent of the underlying disease or the mechanism of troponin release, the presence of myocardial injury is associated with an increased risk of death. As increasingly sensitive assays are introduced, the frequent occurrence of myocardial injury is becoming apparent, and our understanding of its causes and importance is constantly evolving. Presently troponins are valuable for detecting a subgroup of patients with higher risk of death. Future research is needed to clarify whether troponins can serve as monitoring tools guiding treatment, whether administering more aggressive treatment to patients with evidence of myocardial injury is beneficial, and whether normalizing of troponin concentrations in patients presenting with evidence of myocardial injury is associated with reduced risk of death.

Cardiac troponin I and T as prognostic markers in cats with hypertrophic cardiomyopathy.

BACKGROUND: Myocardial injury detected by cardiac troponin I and T (cTnI and cTnT) in cardiac disease is associated with increased risk of death in humans and dogs. HYPOTHESIS: Presence of myocardial injury predicts long-term death in cats with hypertrophic cardiomyopathy (HCM), and ongoing myocardial injury reflects change in left ventricular wall thickness over time. ANIMALS: Thirty-six cats with primary HCM. METHODS: Prospective cohort study. Cats with HCM were included consecutively and examined every 6 months. Echocardiography, ECG, blood pressure, and serum cTnI and cTnT were evaluated at each visit. Cox proportional hazards regression analysis was performed to evaluate prognostic potential of serum troponin concentrations at admission and subsequent examinations. Correlations were used to examine associations between troponin concentrations and cardiac hypertrophy. RESULTS: Troponin concentrations at admission were median [range] 0.14 [0.004-1.02] ng/mL for cTnI, and 13 [13-79.5] ng/L for cTnT. Both were prognostic for death (P = .032 and .026) as were the last available concentrations of each (P = .016 and .003). The final cTnT concentration was a significant predictor of death even when adjusting for the admission concentration (P = .043). In a model containing both markers, only cTnT remained significant (P = .043). Left ventricular free wall thickness at end-diastole (LVFWd) at admission was correlated with cTnI at admission (r = 0.35, P = .035), however no significant correlations (r = 0.2-0.31, P = .074-.26) were found between changes in troponin concentrations and left ventricular thickness over time. CONCLUSIONS AND CLINICAL IMPORTANCE: Myocardial injury is part of the pathophysiology leading to disease progression and death. Low sensitivities and specificities prevent outcome prediction in individual cats.

Prediction of long-term outcome by measurement of serum concentration of cardiac troponins in critically ill dogs with systemic inflammation.

BACKGROUND: Myocardial injury, detected by cardiac troponin I and T (cTnI and cTnT), has been associated with long-term death in the noncardiac human intensive care unit (ICU). HYPOTHESIS: Presence of myocardial injury predicts 1-year case fatality in critically ill dogs with systemic inflammation. ANIMALS: Thirty-eight dogs with evidence of systemic inflammation and no primary cardiac disease. METHODS: Prospective cohort study. In dogs admitted to the ICU with evidence of systemic inflammation, blood samples were obtained at ICU admission for measurement of cTnI and cTnT, and cTnI was measured once daily during ICU hospitalization. Receiver operating characteristic (ROC) curves were used to examine prognostic capacity of admission cTnI, admission cTnT, and peak cTnI concentrations. RESULTS: One-year case fatality rate was 47% (18/38 dogs). Admission cTnI concentrations were (median [range]) 0.48 [0.004-141.50] ng/mL, and peak cTnI concentrations were 1.21 [0.021-141.50] ng/mL. Admission cTnT concentrations were 15 [<13-3744] ng/L. For each marker, non-survivors had significantly higher concentrations than survivors (P = .0082-.038). ROC analyses revealed areas under curves [95% CI] of 0.707 [0.537-0.843] for peak cTnI and 0.739 [0.571-0.867] for admission cTnT, respectively. At the optimal cut-off, concentrations were 1.17 ng/mL (peak cTnI) and 23 ng/L (admission cTnT), sensitivities were 72% and 72%, and specificities were 70% and 80%, respectively. CONCLUSIONS AND CLINICAL IMPORTANCE: While peak cTnI and admission cTnT are significantly related to 1-year case fatality in critically ill dogs with systemic inflammation, low sensitivities and specificities prevent their prediction of long-term outcome in individual patients. Troponins might play a role in identification of dogs at long-term risk of death.

Prognostic importance of myocardial injury in critically ill dogs with systemic inflammation.

BACKGROUND: In noncardiac critical disease in humans, myocardial injury as detected by cardiac troponin I and T (cTnI and cTnT) has been linked to high intensive care unit (ICU) death independent of prognostic composite scoring. HYPOTHESIS: Presence of myocardial injury predicts short-term death in critically ill dogs with systemic inflammation and provides additional prognostic information when combined with established canine prognostic composite scores. ANIMALS: Forty-two dogs admitted to the ICU with evidence of systemic inflammation and no primary cardiac disease. METHODS: Prospective cohort study. Blood samples were obtained at ICU admission for the measurement of cTnI and cTnT, C-reactive protein, and several cytokines. The acute patient physiologic and laboratory evaluation (APPLE) score and the survival prediction index were calculated within the first 24 hours of admission. Receiver operating characteristic (ROC) curves were used to examine the prognostic capacity of each biomarker and severity score. Multiple logistic regression analysis was performed to evaluate whether cardiac markers significantly contributed to severity scores. RESULTS: Twenty-eight day case fatality rate was 26% (11/42 dogs). cTnI concentrations were (median [range]) 0.416 [0.004-141.5] ng/mL and cTnT concentrations were 13.5 [<13-3,744] ng/L. cTnI, cTnT, and the APPLE score were all significant prognosticators with areas under the ROC curves [95% CI] of 0.801 [0.649; 0.907], 0.790 [0.637; 0.900], and 0.776 [0.621; 0.889], respectively. cTnI significantly contributed to the APPLE score in providing additional prognostic specificity (P = .025). CONCLUSIONS AND CLINICAL IMPORTANCE: Markers of myocardial injury predict short-term death in dogs with systemic inflammation and cTnI significantly contributes to the APPLE score.