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.

Accuracy and sensitivity of three-dimensional echocardiography to detect changes in right ventricular volumes: comparison study with cardiac magnetic resonance.

We aimed to investigate the ability of three-dimensional transthoracic echocardiography (3DE) to detect changes in RV volumes compared to cardiac magnetic resonance (CMR). Eighty-five subjects including 45 with no known cardiac disease and 40 patients with a variety of cardiac diseases were included. Two- and three-dimensional echocardiography as well as CMR of the RV was performed before and after infusion of on average two litres of saline. Examinations were analysed with estimation of RV dimensions, volumes and ejection fraction (RVEF). Intra- and inter-examiner variability was evaluated in 25 patients randomly selected from the cohort. Three-dimensional echocardiography underestimated volumes and RVEF compared to CMR with mean differences and 95% limits of agreement of 110.3 ± 59 mL for RV end-diastolic volume (RVEDV), 43.3 ± 32 mL for RV end-systolic volume (RVESV) and 3.5 ± 10.7% for RVEF. CMR was more reproducible than 3DE, with intra-observer coefficient of variation (CV) of 4% vs. 14.2% for RVEDV, 9.7% vs. 16.7% for RVESV and 6.3% vs. 8.6% for RVEF. The RVEDV, RVESV and RV stroke volume (RVSV) by CMR significantly increased after saline infusion by 15.3 ± 16.2 mL, 3.5 ± 14.2 mL and 11.8 ± 12.6 mL, respectively, as well as RVEF by 1.5 ± 4.6% (p < 0.05). However, 3DE was not able to detect any of these changes in RV volumes (p ≥ 0.05). Compared to CMR imaging of the RV, three-dimensional echocardiography appears unable and unreliable in detecting RV volume changes of less than 15%, highlighting the need for cautious utility of 3DE in these circumstances.

Low adiponectin levels at baseline and decreasing adiponectin levels over 10 years of follow-up predict risk of the metabolic syndrome.

AIM: Adiponectin is the most abundant adipokine and may play a key role in the interplay between obesity, inflammation, insulin resistance and the metabolic syndrome (MetS). Thus, this large population-based cohort investigated whether adiponectin at baseline and/or a decrease in adiponectin during follow-up is associated prospectively with the risk of incident MetS. METHODS: Using a prospective study design, the development of MetS was examined in 1134 healthy participants from the community. Plasma adiponectin was measured at study entry and again after a median follow-up of 9.4 years (IQR: 9.2-9.7). During follow-up, 187 participants developed MetS, and 439 presented with at least two components of MetS. RESULTS: During follow-up, adiponectin decreased in participants who developed MetS, whereas adiponectin was increased in those who did not develop MetS (P<0.001). Those with low adiponectin levels (quartile 1) at baseline had an increased risk of developing MetS (OR: 2.92, 2.08-6.97; P<0.001) compared with those with high levels (quartile 4). After adjusting for confounding variables, low adiponectin levels at baseline remained independently associated with MetS (OR: 2.24, 1.11-4.52; P=0.017). Similarly, participants with a decrease in adiponectin during follow-up also had an increased risk of MetS (OR: 2.96, 2.09-4.18; P<0.001). This association persisted after multivariable adjustments, including for baseline adiponectin (OR: 4.37, 2.77-6.97; P<0.001). Finally, adiponectin levels at follow-up were inversely associated with an increase in the number of components of MetS (P<0.001); geometric mean adiponectin levels were 9.5mg/L (95% CI: 9.0-10.0) for participants with no components vs 7.0mg/L (95% CI: 6.3-7.9) for those with four to five components. CONCLUSIONS/INTERPRETATION: Low plasma adiponectin levels at baseline and decreasing adiponectin levels during follow-up are both associated with an increased risk of MetS.

Optimisation of coronary vascular territorial 3D echocardiographic strain imaging using computed tomography: a feasibility study using image fusion.

Current echocardiographic assessments of coronary vascular territories use the 17-segment model and are based on general assumptions of coronary vascular distribution. Fusion of 3D echocardiography (3DE) with multidetector computed tomography (MDCT) derived coronary anatomy may provide a more accurate assessment of left ventricular (LV) territorial function. We aimed to test the feasibility of MDCT and 3DE fusion and to compare territorial longitudinal strain (LS) using the 17-segment model and a MDCT-guided vascular model. 28 patients underwent 320-slice MDCT and transthoracic 3DE on the same day followed by invasive coronary angiography. MDCT (Aquilion ONE, ViSION Edition, Toshiba Medical Systems) and 3DE apical full-volume images (Artida, Toshiba Medical Systems) were fused offline using a dedicated workstation (prototype fusion software, Toshiba Medical Systems). 3DE/MDCT image alignment was assessed by 3 readers using a 4-point scale. Territorial LS was assessed using the 17-segment model and the MDCT-guided vascular model in territories supplied by significantly stenotic and non-significantly stenotic vessels. Successful 3DE/MDCT image alignment was obtained in 86 and 93 % of cases for reader one, and reader two and three, respectively. Fair agreement on the quality of automatic image alignment (intra-class correlation = 0.40) and the success of manual image alignment (Fleiss' Kappa = 0.40) among the readers was found. In territories supplied by non-significantly stenotic left circumflex arteries, LS was significantly higher in the MDCT-guided vascular model compared to the 17-segment model: -15.00 ± 7.17 (mean ± standard deviation) versus -11.87 ± 4.09 (p < 0.05). Fusion of MDCT and 3DE is feasible and provides physiologically meaningful displays of myocardial function.

Genotype-phenotype correlation between the cardiac myosin binding protein C mutation A31P and hypertrophic cardiomyopathy in a cohort of Maine Coon cats: a longitudinal study.

OBJECTIVES: A missense mutation (A31P) in the cardiac myosin binding protein C gene has been associated with hypertrophic cardiomyopathy (HCM) in Maine Coon cats. The aim of this study was to investigate the effect of A31P on development of HCM, myocardial diastolic dysfunction detected by color tissue Doppler imaging and occurrence of cardiac death during longitudinal follow-up in a cohort of Maine Coon cats. ANIMALS: The original cohort comprised 282 cats (158 of wild-type genotype, 99 heterozygous for A31P and 25 homozygous for A31P). METHODS: Prospective longitudinal study including echocardiography and registration of survival. RESULTS: The median age at the initial examination was 1.7 years (range, 0.8-9.2 years) and 6.4% (18/282) of the cats were diagnosed with HCM. One hundred sixty-five cats were eligible for echocardiographic re-examination, and during an average follow-up period of 2.7 years an additional 6.7% (11/165) of the cats developed HCM. Survival data could be obtained for 262 of the cats originally included, and among these 9.2% (24/262) died of causes that met the study criteria for cardiac death. In the homozygous group 80% (20/25) of cats included were diagnosed with HCM and 48% (12/25) suffered cardiac death during follow-up. These results corresponded to a significantly higher risk for cats homozygous for A31P to develop HCM (p<0.001) and die from cardiac-related causes compared with both other genotypes (p<0.001). CONCLUSIONS: Homozygosity for A31P was associated with a high penetrance of HCM and a substantial risk for cardiac death in the study population.

A simple linear model for the effect of changes in metabolic risk factors on coronary heart disease.

OBJECTIVES: The risk of having one or more metabolic risk factors in the development of coronary heart disease (CHD) is well estimated, but it still remains to be shown which influence any given change in the number of risk factors has on the overall risk of CHD. DESIGN: In this prospective cardiovascular population study, 10 194 participants were examined twice with a 5-year interval for metabolic risk factors such as obesity, hypertension, hypercholesterolaemia and diabetes mellitus. RESULTS: During 14 years of follow-up, 1724 incident cases of CHD were identified, 973 in men and 751 in women. The effect of an increase in the number of metabolic risk factors during a 5-year interval on the relative risk of CHD could be determined to be statistically significant for both genders. But only for men, the effect of a decrease in the number of metabolic risk factors was statistically significant during the same time interval. Hence, by statistical analysis, a simple linear model could be constructed for men with two linear trend parameters, one corresponding to the number of metabolic risk factors at the first examination and one corresponding to the change in the number of metabolic risk factors from the first to the second examination. The parameters were 1.50 (1.39-1.63); P < 0.001 and 1.29 (1.18-1.41); P < 0.001, respectively. CONCLUSIONS: This study suggests that it is possible to fit a simple linear model for the effect of changed number of metabolic risk factors on the risk of CHD.