Henrik D. Pedersen

Indices for M-mode measurements in dogs usually have been based on the assumption that a linear relationship exists between these measurements and body weight (BW) or body surface area (BSA). The relationships between the geometry of 3-dimensional objects do not support this assumption. The purposes of this study were to retrospectively examine M-mode data from a large number of dogs of varying sizes and breeds that were examined by a large number of ultrasonographers, to use the allometric equation to determine the appropriate BW exponent required to predict these cardiac dimensions, and to determine normal mean values and prediction intervals for common M-mode variables. Linear regression analyses of data from 494 dogs (2.2-95 kg) revealed a good correlation between M-mode measurements and BW after logarithmic transformation of the data (r2 = .55-.88). Most variables were most closely related to an index of body length, BW(1/3), although the exponent that best predicted diastolic and systolic left ventricular wall thicknesses was closer to 0.25. No variable indexed well to BW or BSA. With these data, appropriate mean values and prediction intervals were calculated for normal dogs, allowing veterinarians to correctly and appropriately index M-mode values. The equations developed from this study appear to be applicable to adult dogs of most breeds.

Abstract Indices for M-mode measurements in dogs usually have been based on the assumption that a linear relationship exists between these measurements and body weight (BW) or body surface area (BSA). The relationships between the geometry of 3-dimensional objects do not support this assumption. The purposes of this study were to retrospectively examine M-mode data from a large number of dogs of varying sizes and breeds that were examined by a large number of ultrasonographers, to use the allometric equation to determine the appropriate BW exponent required to predict these cardiac dimensions, and to determine normal mean values and prediction intervals for common M-mode variables. Linear regression analyses of data from 494 dogs (2.2–95 kg) revealed a good correlation between M-mode measurements and BW after logarithmic transformation of the data (r2= .55-.88). Most variables were most closely related to an index of body length, BW1/3, although the exponent that best predicted diastolic and systolic left ventricular wall thicknesses was closer to 0.25. No variable indexed well to BW or BSA. With these data, appropriate mean values and prediction intervals were calculated for normal dogs, allowing veterinarians to correctly and appropriately index M-mode values. The equations developed from this study appear to be applicable to adult dogs of most breeds.

To examine the effects of regular participation in recreational soccer on health profile, 36 healthy untrained Danish men aged 20-43 years were randomised into a soccer group (SO; n = 13), a running group (RU; n = 12) and a control group (CO; n = 11). Training was performed for 1 h two or three times per week for 12 weeks; at an average heart rate of 82% (SEM 2%) and 82% (1%) of HR(max) for SO and RU, respectively. During the 12 week period, maximal oxygen uptake increased (p<0.05) by 13% (3%) and 8% (3%) in SO and RU, respectively. In SO, systolic and diastolic blood pressure were reduced (p<0.05) from 130 (2) to 122 (2) mm Hg and from 77 (2) to 72 (2) mm Hg, respectively, after 12 weeks, with similar decreases observed for RU. After the 12 weeks of training, fat mass was 3.0% (2.7 (0.6) kg) and 1.8% (1.8 (0.4) kg) lower (p<0.05) for SO and RU, respectively. Only SO had an increase in lean body mass (1.7 (0.4) kg, p<0.05), an increase in lower extremity bone mass (41 (8) g, p<0.05), a decrease in LDL-cholesterol (2.7 (0.2) to 2.3 (0.2) mmol/l; p<0.05) and an increase (p<0.05) in fat oxidation during running at 9.5 km/h. The number of capillaries per muscle fibre was 23% (4%) and 16% (7%) higher (p<0.05) in SO and RU, respectively, after 12 weeks. No changes in any of the measured variables were observed for CO. In conclusion, participation in regular recreational soccer training, organised as small-sided drills, has significant beneficial effects on health profile and physical capacity for untrained men, and in some aspects it is superior to frequent moderate-intensity running.

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.

Time for primary review 31 days. Mitral valve prolapse (MVP), i.e. abnormal systolic protrusion of mitral valve leaflets into the left atrium, is a common cause of severe mitral regurgitation (MR) requiring operation in people living in industrialized nations [1,2]. MVP has been reported to have many causes but in the majority of cases it is a primary condition (called primary MVP in this paper) characterized by a progressive myxomatous degeneration of the mitral valve leaflets and chordae tendineae [1–3]. The disease typically emerges in adolescence but complications such as severe MR usually do not occur until middleage or senescence [1–3]. An animal model with a shorter course of disease could be useful in several ways, for instance, by making it feasible to evaluate the effects of different drugs on disease progression. Despite this, no animal model of primary MVP has been described so far. From pathological studies, it has long been known that most dogs develop myxomatous mitral valve disease with age and that this disease is very similar macroscopically as well as microscopically to primary MVP in humans [4,5]. Traditionally, however, the canine disease has been given names other than MVP, including endocardiosis and chronic valvular disease. Recently, a number of studies, including many based on well-defined echocardiographic criteria for the diagnosis of MVP, have increased our understanding of this disease in the dog. The purpose of this article is to compare the knowledge which has been accumulated about myxomatous mitral valve disease/MVP in the dog with knowledge of primary MVP in humans. Pathologically, primary MVP in humans is very similar to canine myxomatous mitral valve disease [4,5]. In both species, the principal macroscopic findings are enlarged, thickened leaflets, interchordal hooding and elongated chordae tendineae (Fig. 1A, B) [4–9]. In addition, affected … * Corresponding author. Tel.: +45-35-282-526; fax: +45-35-282-525 hdp{at}kvl.dk