Background:The sonographic appearance of the cecum has been described previously in young cats.We believe that there may be different aspects of the cecum in healthy subjects of different ages. Purpose:The present study aims to describe the B-mode ultrasonographic appearance of cecum in healthy cats and its correlation with age. Methods:Twenty-nine clinically healthy cats underwent ultrasonographic evaluation (two-dimensional ultrasound with a 7.5-13 MHz linear transducer).The cecum was identified in transverse and longitudinal section.Two different patterns of ultrasonographic appearance were identified: hypoechoic homogenous and heterogeneous with a nonuniform hyperechoic band parallel to the lumen.Cecal content was recorded and wall measured (in longitudinal section) in the thin portion (S1, next to the colic junction) and in the thicker portion (S2, cul-the-sac).Medium values and standard deviations were recorded.Correlation between age and wall thickness (age/S1 and age/S2) was evaluated with Pearson correlation test.Friedman test was performed to examine the relationship between S1 and S2.Correlation between age and ultrasonographic appearance was evaluated with a logistic regression (using age as a continuous variable and binary output). Findings:Cats ranged from 1 to 14 years old (SD = 0.6).The cecal wall appeared hypoechoic homogenous in 19 cats while heterogeneous in 10.Logistic regression showed a correlation between age and ultrasonographic appearance (older cats tend to have an heterogeneous cecal wall, P = 0.016).Cecum content was gassy (15 cats) or mucous (14 cats).Medium thickness value was 0.20 cm (ranging 0.13-0.34cm, SD = 0.04) in S1 and 0.27 cm (ranging 0.16-0.38cm, SD = 0.05) in S2.Values of S1 and S2 were statistically different (P = 0).No significant statistical correlations were found between age/S1, age/S2, and age/luminal content (P > 0.05). Conclusion:Normal ultrasonographic appearances of feline cecum and their correlation with age are described.The cecal wall tends to be hypoechoic and homogenous in young cats, while heterogeneous in older individuals.We hypothesize that heterogeneous appearance of cecal wall could be explained by "cecal tonsil" theory: with aging, the immunostimulation of the lymphatic structures that are plenty in the cecal wall could lead to echostructural modifications.However, our hypothesis should be confirmed by histopathological examination even if all cats in our study were healthy and remained asymptomatic for 6 months after the initial evaluation.
We evaluated the long-term effect of early angiotensin-converting enzyme (ACE) inhibition (enalapril maleate) as monotherapy to postpone or prevent congestive heart failure (CHF) in asymptomatic dogs with mitral regurgitation (MR) attributable to myxomatous valvular disease (MVD) in a prospective, randomized, double-blinded, placebo-controlled multicenter trial involving 14 centers in Scandinavia. Two hundred twenty-nine Cavalier King Charles (CKC) Spaniels with MR attributable to MVD but no signs of CHF were randomly allocated to treatment with enalapril 0.25-0.5 mg daily (n = 116) or to placebo groups (n = 113). Each dog was evaluated by physical examination, electrocardiography, and thoracic radiography at entry and every 12 months (+/-30 days). The number of dogs developing heart failure was similar in the treatment and placebo groups (n = 50 [43%] and n = 48 [42%], respectively; P = .99). The estimated means, adjusted for censored observations, for the period from initiation of therapy to heart failure were 1,150 +/- 50 days for dogs in the treatment group and 1,130 +/- 50 days for dogs in the placebo group (P = .85). When absence or presence of cardiomegaly at the entrance of the trial was considered, there were still no differences between the treatment and placebo groups (P = .98 and .51, respectively). Multivariate analysis showed that enalapril had no significant effect on the time from initiation of therapy to heart failure (P = .86). Long-term treatment with enalapril in asymptomatic dogs with MVD and MR did not delay the onset of heart failure regardless of whether or not cardiomegaly was present at initiation of the study.
Summary Plasma concentration of immunoreactive atrial natriuretic peptide (ir- anp ) was investigated in 83 Cavalier King Charles Spaniels with variable severity of mitral regurgitation caused by chronic valvular disease ( cvd ). Severity of mitral incompetence was assessed by echocardiography. Significant differences in plasma concentrations of ir- anp were not found between clinically normal dogs (New York Heart Association functional class O), dogs with only cardiac murmur (class I), and dogs with echocardiographic evidence of slight to moderate left atrial and ventricular dilatation (class II). Dogs with severe left atrial and ventricular dilatation and clinical signs of congestion (classes III and IV) were found to have significantly ( P < 0.001) increased plasma concentration of ir- anp . Overall, moderate degree of association was found between plasma concentration of ir- anp and left atrial and left ventricular diameters (Pearson's r = 0.65, 0.60, respectively, P < 0.001), as well as heart rate ( r = 0.47, P < 0.01). However, left atrial enlargement was found to have the predominant effect on plasma ir- anp concentration. It is concluded that the plasma concentration of ir- anp did not become markedly increased before decompensation of chronic mitral regurgitation associated with severe enlargement of the left atrium and ventricle in Cavalier King Charles Spaniels.
We thank Dr Oyama for his comments and questions, which have prompted us to examine the changes in VHS more closely than was possible in the paper,1 which was strictly an evaluation of heart size and its rate of increase as diagnostic tests using the recommended monitoring intervals of dogs with mitral valve regurgitation.2 Concerning measurement variability, although the VHS velocity (∆VHS/month) around the cutoff value of 0.08 is much lower than the 95% limits of agreement3 for intra-observer variability in Table 3 of the paper,1 the actual ∆VHS values measured at Interval 1 (interval ending at CHF) (1.33; SD, 0.60), were above the range of intra-observer 95% limits of agreement (Fig 1) and at Interval 2, about the same (0.55; SD, 0.41). Only 9/93 ∆VHS values at CHF were lower than the 95% limits of agreement (Fig 1). The values of ∆VHS/month are much lower because ∆VHS is divided by the number of months in the interval. For measurements of intervals before interval 1, the ∆VHS values were small (mean 0.55) and the denominator large, about 12 (months), decreasing further the values and variability of ∆VHS/month. The measurement variability did not prevent the likelihood ratios for VHS velocity from having a large effect on pretest probability, because the overlap between CHF and not CHF was very small (Fig 1B of the paper).1 Although ∆VHS had a slight tendency to increase as the interval ending with CHF (interval 1) increased (y = 0.91 + 0.06 x, R2 = 0.13, P < .001), ∆VHS/month decreased logarithmically as the interval increased (Fig 2). This decreasing measured ∆VHS/month could not be dependent on ∆VHS but on the duration of the interval. The longer the interval, the greater the true or instantaneous velocity at CHF is underestimated, because ∆VHS is then averaged over more months. The true velocity can only be measured with a relatively short time interval. The shorter the interval, the higher the measured ∆VHS/month (Fig 2), and the closer it is to the true velocity. This explanation assumes that the heart size does not accelerate and then plateau for a while before CHF, an unlikely scenario.4 True velocities within a few months of CHF are probably close to, or even greater than, the higher values in Figure 2, but it would require frequent (monthly?) monitoring to measure them. To determine if absolute VHS at time 1 could "alert a clinician to recheck heart size more frequently in the subsequent months," we looked at the relationships among ∆VHS during interval 1, VHS at the observation before CHF (time 1), and interval 1. Shorter intervals (R2 = 0.13, P < .001) and higher VHS at time 1 (Fig 1) were associated with less increase in heart size (lower ∆VHS) during interval 1, just before CHF, and the relationship between VHS at time 1 and ∆VHS/month at CHF was not significant (P = .55, R2 = 0.04). Perhaps heart enlargement after time 1 is limited by interdependence with the lungs or pericardium restricting further dilation and the dog with a high VHS at time 1 may have progressed to a stage where little further change is required to cause the dog to develop signs of pulmonary congestion and edema. We then did a multivariate regression analysis with months to CHF as the dependent (outcome) variable and VHS at the last measurement and ∆VHS/month at CHF (interval 1) as the independent variables. As the data for ∆VHS/month were not linearly distributed (Fig 2) the values were converted to log10. R2 was considerably higher for ∆VHS/month (R2 = 0.51) than for VHS (R2 = 0.21) (both P < .001). Combining the two variables in the same model increased the R2 from 0.51 to 0.61 and both variables were still significantly associated with time to CHF. Finally, adding the interaction factor of VHS x ∆VHS/month only marginally increased the model R2 to 0.62 (ie, interaction factor was nonsignificant). These results imply that both VHS at the observation before CHF (time 1) and ∆VHS/month are independently predictive of time to CHF, and that ∆VHS/month is a more powerful predictor than VHS at time 1. A regression plot of months to CHF against VHS at all times gave a 95% confidence interval of 5–40 months to CHF for 11.6 VHS units, the cutoff point for dichotomized data at time 1, a range too great to be useful. The overlap between VHS at time 1 and at CHF (Fig 1A of the paper)1 was too much for VHS at time 1 to reliably detect dogs at risk of impending CHF as was also shown by the wide confidence intervals of the likelihood ratios of test 3 (Table 2 of the paper).1 Although absolute VHS is limited in its value to detect when "to initiate more frequent radiographic vigilance", an increase in VHS may be useful. Summary statistics for ∆VHS/month at the interval preceding CHF (interval 2) (Fig 2) were mean and median, both 0.03 ∆VHS units/month; 75th percentile, 0.04 (95% CI, 0.03–0.05); 90th percentile 0.06 (95% CI, 0.05–0.07), and 95th percentile 0.07 (95% CI, 0.06–0.13). At the annual measurement, those dogs which do not develop CHF before the rise is detected at the yearly examination and whose values exceed a selected percentile could be deemed to have entered the risk zone for impending CHF, and could be monitored more frequently, and a risk/benefit analysis done to determine if the veterinarian should "intervene and potentially change the outcome." We can only guess the most efficient interval (longest interval that gives the desired prediction) that gives the result of detecting impending CHF, as no prospective study has been done. Concerning "combining absolute VHS and rate of change of VHS" at suspected onset of CHF: when their dependence was taken into account,5 the interval likelihood ratios for both tests (Table 3 of the paper)1 being positive increased from 13 and 15 respectively to 130 (95% CI, 911-18), and for both tests being negative decreased from 0.04 and 0.05 to 0.01 (95% CI, 0.09-0.002). Simply multiplying them as if they were independent5 gave likelihood ratios of 195 and 0.002, the difference being due to the dependence between them. When the positive and negative interval likelihood ratios of the combined tests VHS and ∆VHS/month are applied to intermediate < 90 > 10%) pretest probabilities using the nomogram (Fig 3 of the paper),1 they practically rule in or out the diagnosis of CHF in Cavalier King Charles Spaniels. The limitations of VHS discussed in the paper1 also apply to the combined test results. In a previous study, 2D echocardiographic dimensions did not seem to have less interdog variability than VHS.4 Perhaps 3D echocardiographic measurements of chamber volumes and left ventricular eccentricity,6 independent of dog and breed variations and body size would have the desired accuracy to predict time to CHF, as they are calculated from a detailed reconstruction of the endocardial surface. To summarize: measurement variation had little effect on the accuracy of ∆VHS/month to diagnose onset of CHF; true ∆VHS/month was underestimated by averaging the change in VHS during the interval before CHF and the true velocity is likely to be much higher than the cutoff value (0.08 VHS units/month) used to derive the likelihood ratio to diagnose CHF; measured rate of change was affected by the time interval; VHS was of little use to predict time to onset of CHF; a rise of ∆VHS/month above a selected percentile of the values at the interval preceding the last one might be a useful sign of impending CHF; combining interval likelihood ratios for VHS and ∆VHS/month greatly improved the accuracy of diagnosis of CHF. The study shows the value of incorporating the element of time dependency from serial measurements as rate of change, a summary of the response over time of each subject.7
Two‐dimensional (2‐D) echocardiographic measurement of the left atrium (LA) has the potential to be more accurate than the standard M‐mode method, because the LA body can be measured. We evaluated a 2‐D method for measuring LA and aorta (AO) in a right parasternal short‐axis view and compared it to the M‐mode method. An index for LA size (LA/AO) was calculated in 166 cavalier King Charles spaniels, 56 normal and 110 dogs with mitral regurgitation (MR) of varying degrees secondary to chronic valvular disease. In normal dogs, the AO‐2‐D and LA/AO‐2‐D did not correlate to body weight (BW) or BW2; whereas, all M‐mode values and the LA‐2‐D were significantly ( p < .05) related to both BW parameters. In normal dogs, there was no difference between M‐mode and 2‐D indices. For all dogs (normal and dogs with MR) there was an 11% bias between the M‐mode and 2‐D index with the LA/AO‐2‐D being higher than the LA/AO‐M. The association between the mean and the difference of the indices demonstrated a quadratic relationship. Dogs with a mean LA/AO of 2.0–2.5 showed the largest difference between the two indices. Small values for the 2‐D coefficients of variation for respiration and stage of diastole were found; 3.4 and 3.1%, respectively. The 2‐D index is more sensitive to LA enlargement than the M‐mode index.
Cytogenetic findings and outcome of pregnancy are reported in 108 cases in which confined placental mosaicism (CPM, n = 101) or generalized mosaicism (n = 7) was found at or after first-trimester chorionic villus sampling. In all samples, a (semi)direct cytogenetic analysis of cytotrophoblast cells was performed. Two pregnancies with CPM ended in a spontaneous abortion before 28 weeks (1.9 per cent). In 15 cases the pregnancy was terminated: eight cases were shown to be examples of CPM; seven cases can be considered as examples of generalized mosaicism. A normal cytogenetic result was obtained after follow-up amniocentesis in 88 of the remaining 91 cases. In three cases, no amniocentesis was performed but confirmation of a normal karyotype was obtained in other cells. One of the 91 pregnancies was nevertheless terminated for psychosocial reasons. One child died perinatally and another on the seventh day after birth. The birth weight is known for 89 children; the curve shows a normal distribution. In 11 of these children (12.3 per cent), the birth weight was found to be below the tenth centile. The outcome in a subgroup of eight pregnancies with CPM and involvement of chromosome 13, 16, or 22, however, revealed two fetal losses and four children with a birth weight below the tenth centile (75 per cent).
