Anatomic, histologic, and two-dimensional–echocardiographic evaluation of mitral valve anatomy in dogs

Michele Borgarelli Department of Clinical Sciences, College of Veterinary Medicine, Kansas State University, Manhattan, KS 66505.

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Massimiliano Tursi Department of Animal Pathology, Faculty of Veterinary Medicine, University of Torino, 10095 Grugliasco, Italy.

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Giuseppe La Rosa Department of Animal Pathology, Faculty of Veterinary Medicine, University of Torino, 10095 Grugliasco, Italy.

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Paolo Savarino Department of Animal Pathology, Faculty of Veterinary Medicine, University of Torino, 10095 Grugliasco, Italy.

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Marco Galloni Department of Veterinary Morphophysiology, Faculty of Veterinary Medicine, University of Torino, 10095 Grugliasco, Italy.

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Abstract

Objective—To compare echocardiographic variables of dogs with postmortem anatomic measurements and histologic characteristics of the mitral valve (MV).

Animals—21 cardiologically normal dogs.

Procedures—The MV was measured echocardiographically by use of the right parasternal 5-chamber long-axis view. Dogs were euthanized, and anatomic measurements of the MV annulus (MVa) were performed at the level of the left circumflex coronary artery. Mitral valve leaflets (MVLs) and chordae tendineae were measured. Structure of the MVLs was histologically evaluated in 3 segments (proximal, middle, and distal).

Results—Echocardiographic measurements of MVL length did not differ significantly from anatomic measurements. A positive correlation was detected between body weight and MVa area. There was a negative correlation between MVa area and the percentage by which the MVL area exceeded the MVa area. Anterior MVLs had a significantly higher number of chordae tendineae than did posterior MVLs. Histologically, layering of MVLs was less preserved in the distal segment, whereas the muscular component and adipose tissue were significantly more diffuse in the proximal and middle segments.

Conclusions and Clinical Relevance—The MV in cardiologically normal dogs had wide anatomic variability. Anatomic measurements of MVL length were correlated with echocardiographic measurements.

Abstract

Objective—To compare echocardiographic variables of dogs with postmortem anatomic measurements and histologic characteristics of the mitral valve (MV).

Animals—21 cardiologically normal dogs.

Procedures—The MV was measured echocardiographically by use of the right parasternal 5-chamber long-axis view. Dogs were euthanized, and anatomic measurements of the MV annulus (MVa) were performed at the level of the left circumflex coronary artery. Mitral valve leaflets (MVLs) and chordae tendineae were measured. Structure of the MVLs was histologically evaluated in 3 segments (proximal, middle, and distal).

Results—Echocardiographic measurements of MVL length did not differ significantly from anatomic measurements. A positive correlation was detected between body weight and MVa area. There was a negative correlation between MVa area and the percentage by which the MVL area exceeded the MVa area. Anterior MVLs had a significantly higher number of chordae tendineae than did posterior MVLs. Histologically, layering of MVLs was less preserved in the distal segment, whereas the muscular component and adipose tissue were significantly more diffuse in the proximal and middle segments.

Conclusions and Clinical Relevance—The MV in cardiologically normal dogs had wide anatomic variability. Anatomic measurements of MVL length were correlated with echocardiographic measurements.

The MV apparatus is a complex anatomic structure consisting of MVLs, chordae tendineae, papillary muscles, and the MVa.1–3 This structure requires all of its components, together with adjacent atrial and ventricular musculature, to function properly.1,4,5 The MV has 2 mitral cusps (anterior [aortic] and posterior [mural]). This definition is equally applicable to humans and to other mammals.2 In humans, the distance from the base to the free edge of the AMVL is > 2 times that of the posterior cusp; however, because the PMVL is longer, the areas are nearly identical.1 The area of apposition of the 2 MVLs represents the MV commissure.6 However, there is not a consensus on this because authors in another study7 defined commissures as the end of the zone of apposition between MVLs, thus describing 2 commissures for the MV.

The MVa represents the fibrous support of the MVLs. In humans, the MVa is shaped more like the letter D than a true circle.4 There is marked variation in the structure of the MVa among clinically normal humans. In fact, it is uncommon to find a complete ring of connective tissue encircling the atrioventricular junction.8

The chordae tendineae and papillary muscles represent the tension apparatus of the MV. Chordae tendineae originate from the papillary muscles and insert into the free edge or onto the ventricular surface of the MVL. Several classifications have been proposed for the chordae tendineae in humans.4,9,10 Currently, the most accepted classification categorizes the chordae tendineae into commissural and MVL chordae tendineae.10 The commissural chordae tendineae have a fan-shape structure and support the commissural area. The MVL chordae tendineae are divided into zona rugosa and basal chordae tendineae. The zona rugosa chordae tendineae are those that provide the major support to the MVLs. They originate from both papillary muscles and distribute between the line of closure and the free margin of the MVL. The basal chordae tendineae originate from the ventricular free wall and are present in only the basal area of the PMVL. It has been suggested that the basal chordae tendineae reinforce the basal part of the PMVL during systole, although their function is not completely understood.9 Investigators in 1 study10 of 50 human hearts found basal chordae tendineae in only 31 specimens.

Histologically, the MVL has a layered aspect. The central structure, called fibrosa, is composed of collagenous fibers that run parallel to the surface of the MVL and extend into the chordae tendineae. On the atrial portion of the fibrosa, there is a variable amount of loose connective tissue (spongiosa). A thin fibroelastic layer covers approximately two-thirds of the length of the atrial and ventricular surfaces. Cardiac muscle and blood vessels can extend into the proximal and middle thirds of the atrial surface in dogs.2,3 Endothelium covers the fibroelastic layer on both sides. A dense nerve plexus with possible sensory or motor roles in valve function has been described in several species.11 In dogs, most of the nerve fibers are sympathetic and associated with the myocardium in the valve base.12

Few studies2,3 have been conducted to determine the anatomy of the MV in cardiologically normal dogs. This is surprising considering that chronic MMVD represents the most common acquired cardiovascular disease in dogs13 and that the disease shares many similarities with MV prolapse syndrome in humans.14 In dogs, diagnosis of the disease is usually made on the basis of detection of a systolic left apical murmur in a typically affected breed, and it must be confirmed echocardiographically.15,16 In humans, some studies17,18 have revealed a correlation between anatomic measurements of the MV apparatus and echocardiographic measurements. Moreover, there is evidence that some echocardiographic indices can be used to evaluate the amount of residual regurgitation through the MV after surgical repair.19 To our knowledge, no studies have been conducted to determine the correlation between echocardiographic measurements of MVs and anatomic measurements in dogs. Therefore, the purpose of the study reported here was to describe histologic characteristics of the MV in a group of cardiologically normal dogs of various sizes and breeds and to compare anatomic measurements with 2-D echocardiographic measurements.

Materials and Methods

Animals—Twenty-one client-owned cardiologically normal adult dogs examined at the Faculty of Veterinary Medicine of the University of Torino that were to be euthanized because of severe spinal cord disease were included in the study. The dogs (12 males and 9 females) represented various breeds. Body weight ranged from 12 to 64 kg (median, 22 kg), and age ranged from 1 to 11 years (median, 7 years). Dogs were considered cardiologically normal on the basis of results of physical and echocardiographic examination performed immediately prior to euthanasia. Dogs were excluded when any murmur or midsystolic click and regurgitation through the MV or MV prolapse were detected during echocardiographic examination. Dogs were included when nonrelevant regurgitation through the pulmonary or tricuspid valves was identified during echocardiographic examination. Informed written consent was obtained from each owner. The study was approved by the ethical committee of the Faculty of Veterinary Medicine at the University of Torino.

Echocardiographic measurements—All echocardiographic examinations were performed on conscious, unsedated dogs positioned in right lateral recumbency. All echocardiographic examinations were performed by 2 investigators (MB and PS), and the measurements were subsequently obtained from the digital recordings by a single investigator (MB). For each dog, MV diameter at the time of maximal opening of the MV was measured by use of the right parasternal 5-chamber long-axis view (Figure 1). This view corresponds to the anteroposterior diameter of the MVa.20 The same view was used to measure the length of MVLs at the time when both MVLs appeared as straight lines. To estimate intraobserver variability, analyses of the recorded images of 6 randomly selected dogs were repeated twice by the same observer, with a 1-week interval between the analyses. Recorded images were randomly ordered for the second analysis, with the observer not informed of the results for the first analysis. Intraobserver variability was quantified as the coefficient of variation by use of the following equation21: coefficient of variation = (mean difference between measurements/mean of measurements) × 100.

Figure 1—
Figure 1—

Right parasternal 5-chamber long axis Doppler ultrasonographic view obtained from a representative dog. Length of the MVLs (yellow lines) was measured when it was possible to see both leaflets as straight lines. The anteroposterior diameter of the MVa (white line) also was measured. Notice the ECG tracing in the lower left corner. The scale in the image is in centimeters.

Citation: American Journal of Veterinary Research 72, 9; 10.2460/ajvr.72.9.1186

Anatomic measurements—Dogs were anesthetized by administration of propofol (6 mg/kg, IV); anesthetized dogs were subsequently euthanized by IV administration of a solution of embutramide, mebozonium iodide, and tetracaine hydrochloride.a The heart of each dog was removed immediately after the dog was euthanized. Hearts were thoroughly washed with tap water and then placed in 4% formalin solution for at least 10 days before examination.

For the anatomic measurements, the atria were dissected. Long and short axes of the MVa, the MVa area, and the anteroposterior diameter of the MVa were measured at the level of the left circumflex coronary artery (Figures 2 and 3). The ratio between the long and short axes of the MVa was calculated from these measurements. The MV was then isolated from each heart, incised, and positioned in a straight line. Length and area of the AMVL and PMVL were measured. Intraobserver variability of anatomic measurements was assessed on 6 randomly selected valves, as described previously for the echocardiographic measurements.

Figure 2—
Figure 2—

Photograph of a heart obtained from the cadaver of a representative dog. The heart was fixed in 4% formalin solution for at least 10 days. The long and short axes (black lines) and MVa area (outlined shaded region) were measured at the level of the left coronary artery. The scale on the right is in centimeters.

Citation: American Journal of Veterinary Research 72, 9; 10.2460/ajvr.72.9.1186

Figure 3—
Figure 3—

Photograph of a heart obtained from the cadaver of a representative dog. The heart was fixed in 4% formalin solution for at least 10 days. The anteroposterior diameter of the MVa (red line) was measured at the level of the left coronary artery. The scale on the bottom is in centimeters.

Citation: American Journal of Veterinary Research 72, 9; 10.2460/ajvr.72.9.1186

To quantify the area of MVL for apposition, the difference between MVL area and MVa area was calculated as the percentage by which the MVL area exceeded the MVa area by use of the following equation: ([MVL area – MVa area]/MVL area) × 100. All anatomic measurements were performed by use of commercial image analysis software.b When limits of the MVLs were not clearly defined, the valve was photographed by use of a transillumination technique with polarizing light (Figure 4).

Figure 4—
Figure 4—

Photograph of the MV of a dog that was removed, incised, and positioned in a straight line. The photograph was obtained via transillumination with polarizing light. The AMVL is in the middle, and the PMVL has been divided and is on both sides. The measured length of the AVML (long blue line in middle) and PVML (short blue line on right) is indicated.

Citation: American Journal of Veterinary Research 72, 9; 10.2460/ajvr.72.9.1186

The numbers of total chordae tendineae, chordae tendineae originating from the anterior and posterior papillary muscles, branches originating from each chordae tendineae, chordae tendineae reaching each MVL, chordae tendineae attached to the zona rugosa of each MVL, and chordae tendineae attached to other areas of each MVL were evaluated in the MV isolated from 20 dogs. In 1 dog, evaluation of the chordae tendineae was not possible because of damage to the MV during removal from the heart.

Histologic examination—Histologic evaluation was performed using H&E staining by 1 investigator (MT). Histologic examination was performed on only 20 AMVLs and 16 PMVLs because of severe damage to 1 AMVL and 5 PMVLs during preparation for histologic examination. The presence of adipose tissue was confirmed via staining with Sudan black on cryosectioned histologic sections fixed in formalin to preserve the integrity of the lipid component.

Each valve was arbitrarily divided into 3 segments (proximal, middle, and distal). For each segment, the presence or absence of layered structure, muscular tissue, adipose tissue, myxomatous tissue, and mononuclear cells was evaluated. Myxomatous degeneration was defined as mild to moderate thickening of the spongiosa attributable to collagen disorganization and myxoid degeneration.

Statistical analysis—Statistical analysis was performed by use of a software system.c Normally distributed data were expressed as mean ± SD, and non-normally distributed data were expressed as median and range. The normality assumption was tested via the Shapiro-Wilk statistic. Differences between normally distributed variables were tested by use of an unpaired t test. Differences between nonnormally distributed data were tested by use of the Wilcoxon rank sum test. Analysis of correlation between variables was calculated by use of a Pearson product moment correlation test for normally distributed variables and a Kendall linear correlation coefficient for nonnormally distributed variables. Cross tabulations were performed by use of a Fisher exact test to evaluate differences in the distribution of layered structure, muscular tissue, and adipose tissue and the severity of myxomatous degeneration and mononuclear inflammation in the 3 segments of the MVs. Values of P < 0.05 were considered significant for all tests.

Results

Coefficients of variation—The intraobserver coefficients of variation for echocardiographic measurements of the AMVL, PMVL, and maximum anteroposterior diameter were 1.9%, 1.3%, and 0.4%, respectively. The intraobserver coefficients of variation for anatomic measurements of the AMVL, PMVL, anteroposterior diameter, MVa area, and MVL area were 0.04%, 0.1%, 0.04%, 0.04%, and 0.03%, respectively.

MV measurements—The mean ± SD echocardiographic length of the AMVL and PMVL was 21.36 ± 2.8 mm and 14.86 ± 3.23 mm, respectively. The mean maximum anteroposterior MVa diameter was 28.62 ± 5.9 mm. Anatomic measurements for MVa and MVLs were summarized (Table 1). The AMVL was significantly longer, compared with the length of the PMVL, for the echocardiographic (P = 0.007) and anatomic (P < 0.001) measurements. Echocardiographic measurements of AMVL and PMVL length did not differ significantly from the anatomic measurements. Median and interquartile range for echocardiographic and anatomic measurements were calculated (Figure 5). Echocardiographic measurements of the M V anteroposterior diameter were significantly (P < 0.001) larger than the corresponding anatomic measurements.

Figure 5—
Figure 5—

Box-and-whisker plots of echocardiographic (Echo) and anatomic (Anat) measurements of the length of the MVLs. The box represents the interquartile range (25th to 75th percentiles), the horizontal line in each box represents the median, the whiskers represent the extent of the data, and the diamonds represent outliers. Values did not differ significantly (P ≥ 0.05) between the anatomic and echocardiographic measurements.

Citation: American Journal of Veterinary Research 72, 9; 10.2460/ajvr.72.9.1186

Table 1—

Mean ± SD anatomic measurements of MVs in cadavers of 21 cardiologically normal dogs.

VariableMean ± SD
MVa area (mm2)477.20 ± 149.49
MVa long axis (mm)26.41 ± 5.37
MVa short axis (mm)21.18 ± 4.40
Ratio of the long axis of the MVa to the short axis of the MVa1.26 ± 0.20
MVa anteroposterior diameter (mm)19.23 ± 4.84
AMVL length (mm)22.86 ± 3.89
PMVL length (mm)15.24 ± 3.05
MVL area (mm2)749.85 ± 207.17
Percentage by which the MVL area exceeded the MVa area (%)35.08 ± 19.76

The ratio between the long and short axes of the MVa ranged from 1.02 to 1.68 (mean ± SD, 1.26 ± 0.19). Geometry of the MVa was not significantly correlated (r = 0.11; P = 0.64) with body weight. Both MVa area (r = 0.63; P = 0.003) and MVL area (r = 0.47; P < 0.001) had a significant moderate positive linear correlation with body weight. The percentage by which the MVL area exceeded the MVa area ranged from 14.67% to 63.15%. There was a significant moderate negative (r = 0.47; P = 0.002) correlation between this variable and MVa area (Figure 6).

Figure 6—
Figure 6—

Results of regression analysis between the MVa area and the percentage by which the MVL area exceeded the MVa area (y-axis). There is a significant negative correlation (r = 0.47; P = 0.002), whereby an increase in MVa area is associated with a decrease in the percentage of the MVL area that exceeded the MVa area.

Citation: American Journal of Veterinary Research 72, 9; 10.2460/ajvr.72.9.1186

Chordae tendineae—Data for chordae tendineae were summarized (Table 2). There were no differences in the number of chordae tendineae originating from the anterior and posterior papillary muscles and the number of branches from each papillary muscle. There was a significantly (P = 0.002) higher number of chordae tendineae reaching the AMVL than the PVML. This difference was attributable to the chordae tendineae attached to the zona rugosa. The number of branches for each chordae tendineae ranged from 2 to 5 (mean ± SD, 3.6 ± 0.58).

Table 2—

Mean ± SD and range values for the numbers of chordae tendineae in cadavers of 21 cardiologically normal dogs.

VariableMean ± SDRange
Total No. of chordae tendineae57.50 ± 9.2848–74
Anterior papillary muscle7.70 ± 1.496–11
Posterior papillary muscle8.15 ± 2.135–15
Branches  
   From anterior papillary muscle28.58 ± 5.6220–38
   From posterior papillary muscle28.65 ± 5.7320–39
AMVL23.80 ± 5.2917–33
PMVL18.30 ± 5.269–30
Reaching the zona rugosa of the AMVL18.25 ± 4.5813–26
Reaching the zona rugosa of the PMVL11.85 ± 3.486–19
Attached to other areas of the AMVL5.55 ± 2.312–9
Attached to other areas of the PMVL6.45 ± 3.381–16

Histologic examination—Histologic tissue distribution for the AMVL and PMVL was summarized (Table 3). For both MVLs, layering was significantly (P < 0.001) less preserved in the distal segment, compared with layering in the proximal and middle segments. The muscular tissue was significantly (P < 0.001) more diffuse in the proximal segment, compared with that in the middle and distal segments, and in the middle segment, compared with that in the distal segment, of the AMVL. In the PMVL, muscular fibers were significantly (P < 0.001) more diffuse in the proximal segment, compared with that in the middle and distal segments; however, muscular fibers were not significantly more diffuse in the middle segment than in the distal segment. Adipose tissue was significantly (P < 0.001) more diffuse in the proximal segment of both MVLs, compared with results for the middle and distal segments.

Table 3—

Tissue distribution in the proximal, middle, and distal segments of the AMVL and PMVL obtained from the cadavers of cardiologically normal dogs.

VariableAMVL (n = 20)PMVL (n = 16)
Layering  
   Proximal2013
   Middle1810
   Distal33
Muscular  
   Proximal199
   Middle113
   Distal00
Adipose  
   Proximal175
   Middle156
   Distal40
Myxomatous  
   Proximal00
   Middle15
   Distal1712
Inflammation  
   Proximal37
   Middle511
   Distal1814
   n = No. of dogs.  

Myxomatous degeneration was significantly more common in the distal segments for both MVLs. The PMVL had more myxomatous tissue in the middle segment than in the proximal segment. The severity of myxomatous degeneration was assessed as moderate in 9 of 20 distal segments of the AMVL, 2 of 16 middle segments of the PMVL, and 6 of 16 distal segments of the PMVL. Dogs with myxomatous degeneration in the MVLs had a higher mean ± SD age than did dogs without myxomatous degeneration, but the ages did not differ significantly (AMVLs, 7.89 ± 2.57 years vs 5.13 ± 3.75 years [P = 0.17]; PMVLs, 7.29 ± 2.93 years vs 5.85 ± 3.78 years [P = 0.52]).

Scant, mild mononuclear infiltrate was detected significantly (P < 0.001) more commonly in distal segments of both MVLs. The mononuclear infiltration was assessed as moderate in 5 of 20 distal and 1 of 20 middle segments for the AMVL and in 8 of 16 distal and 2 of 16 middle segments for the PMVL (Figure 7).

Figure 7—
Figure 7—

Photomicrograph of a tissue section from an MVL with mild myxoid degeneration and collagen disorganization in the distal segment. H&E stain; bar = 100 mm.

Citation: American Journal of Veterinary Research 72, 9; 10.2460/ajvr.72.9.1186

Discussion

Analysis of the results of the study reported here revealed that the MV apparatus in cardiologically normal dogs had a spectrum of anatomic variation, standard 2-D echocardiography was a reliable tool for measuring the height of MVLs in cardiologically normal dogs, and the MV in echocardiographically normal dogs had some histologic variations.

Several studies of human hearts have revealed that the MV apparatus has a wide spectrum of normality. In the present study, MVa geometry, which was measured by use of the ratio between the long and short axes, ranged from almost circular to elliptical. The geometry of the MVa represents an important variable for MV function.1,22 To exert an optimal force on an MVL, the papillary muscle–chordae tendineae tension system needs to be vertically aligned with the MVa. If the MVa is more rounded and left ventricular geometry is maintained, it may be possible that the systolic forces exerted by the tension apparatus are applied in a more lateral direction, which facilitates prolapse and incompetence of the valve.4,23 In an in vitro study,22 investigators found that MVa dilatation, but not left ventricular dilatation at the level of the papillary muscles, induces valvular failure. These results suggest that the morphology of the MVa is more important than is the morphology of the left ventricle for normal function of the MV. In the present study, morphology of the MVa did not correlate with body weight. However, in another study,d morphology of the MV in German Shepherd Dogs appears to be elliptical. Therefore, it can be hypothesized that MV geometry may be related to breed rather than to body weight.

One possible interesting result of the present study is that the percentage by which the MVL area exceeded the MVa area decreased with an increase in MVa area. Because MVa area and MVL area are positively correlated with body weight, it is likely that MVL area increases to a lesser extent with increasing dog size. This suggests that large-breed dogs may have more severe regurgitation through the MV despite less severe degeneration or prolapse because they may have a decrease in cooptation surface. Indeed, our research group has previously reported24 that large-breed dogs develop severe regurgitation with mild MV lesions that were detected during echocardiographic and postmortem examinations. In the study reported here, we measured MVa and MVL area on a 2-D image. Accordingly, these measurements cannot provide information about the height of an MV or take into consideration the 3-D morphology of the MV apparatus. Therefore, further studies that include the use of 3-D echocardiography will be needed to confirm our hypothesis.

In the present study, the standard 2-D echocardiographic measurements were not significantly different from the anatomic measurements, whereas echocardiographic measurements of the MVa exceeded the corresponding anatomic measurements. This is in agreement with results reported in 1 study18 in humans. In another study17 in humans, echocardiography was used to accurately estimate the length of MVLs surgically removed from patients with severe MV insufficiency, but the anatomic annular dimension was underestimated. The MVa is a dynamic structure in vivo, but this condition obviously is not maintained after death. We chose to measure MVa during diastole because this measurement has lower intraobserver variability than does measurement during systole. It is possible that anatomic measurements are more reflective of the systolic diameter. Shrinkage of the heart after fixation can also be an explanation for this observation.

The total number of chordae tendineae attached to the MV in dogs appears to be less than that reported in humans.10,17 It is also of interest that the number of chordae tendineae attached to the zona rugosa of the AMVL was significantly greater than the number attached to the zona rugosa of the PMVL. This is not a surprising finding because the AMVL is believed to sustain major stress, compared with the PMVL,1 and the AMVL chordae tendineae are vital for MV competence.25 Two studies8,17 in humans have indicated that variations in the distribution of AMVL chordae tendineae are associated with the MV prolapse syndrome. In the present study, we detected a wide variation in the total number of chordae tendineae reaching each MVL. Considering that the MV is subjected to considerable pressure and work over time, it can be speculated that a low number of chordae tendineae will result in increased and possibly unequal stress on MVLs, which, with time, may lead to MV changes and degeneration.8,17 Indeed, MMVD is more common in older dogs.13

Our histologic findings are similar to those reported in dogs3 and humans.4 It appears that the layered aspect of the MV is maintained in only the proximal and middle segments, whereas the distal segment has a less-organized structure. In contrast to results of other studies,2,3 we detected muscular fibers in approximately half of the PMVLs. Our observation that these muscular fibers were evident in the middle segment in 11 of 20 AMVLs and 3 of 16 PMVLs was also of interest. It has been suggested that muscular fibers are responsible for the earliest stages of narrowing of the mitral orifice during valve closure.1,2 Therefore, it is possible that dogs with a wider distribution of muscular fibers have a more efficient mechanism of closure of the MV.

To our knowledge, the study reported here provides the first description of adipose tissue as a constant feature of the MV structure. Because adipose tissue was more widely distributed in the proximal and middle segments of the MV, we speculate that it may have been functionally involved in partially absorbing the natural stresses to which the MV is subjected.

Finally, we believe that the mild to moderate myxomatous degeneration and scant mononuclear infiltration observed during histologic examination may be of particular relevance. These patterns were mainly evident in the distal segment of the MV. These regions of the valve are subjected to the most severe shear stress. Therefore, this finding would support the theory that continuous damage to and repair of the MV may play an important role in the pathogenesis of chronic degenerative MV disease in dogs and that myxomatous changes develop before they can be detected during clinical and echocardiographic examinations.13,14 In fact, all dogs included in the present study had no abnormalities detected during cardiovascular and echocardiographic examinations. Alternatively, it is possible that mild myxomatous changes represent an aging process; median age for dogs in the present study was 7 years.

The present study has some limitations. First, it was impossible to evaluate the variables for which shrinkage of the MV apparatus after fixation could have affected measurements. To our knowledge, no studies have been conducted on the effects of postmortem shrinkage on heart measurements. Because MVLs are primarily composed of connective tissue, it can be speculated that this effect was minimal. Second, although the study involved the description of the MV in a heterogeneous population of dogs, most dogs had a body weight > 20 kg. Consequently, it is possible that our findings cannot be applied to small-breed dogs, which are the breeds most frequently affected by MMVD.

For the study reported here, we concluded that the MV anatomy in cardiologically normal dogs has a wide range of anatomic variability. The MV in dogs has some specific peculiarities, such as a greater amount of muscular tissue and a lower number of chordae tendineae, compared with the number of chordae tendineae in humans. Furthermore, standard echocardiography in dogs can be used to provide an accurate measurement of MVL length, similar to the situation in human medicine. Our observation that the geometry of the MVa may vary considerably in cardiologically normal dogs should be taken into consideration when surgical management of MMVD is elected as a treatment option for affected dogs. This study also revealed that there is mild mononuclear infiltration and mild myxomatous degeneration in canine MVs, even in echocardiographically normal dogs. Therefore, it might be possible that such changes precede the development of more severe lesions or they may represent normal aging changes.

ABBREVIATIONS

AMVL

Anterior mitral valve leaflet

MMVD

Myxomatous mitral valve degeneration

MV

Mitral valve

MVa

Mitral valve annulus

MVL

Mitral valve leaflet

PMVL

Posterior mitral valve leaflet

a.

T-61, Intervet/Schering-Plough, Boxmeer, The Netherlands.

b.

Image Proplus software, Media Cybernetics, Betheseda, Md.

c.

R, version 2.9.0, R Foundation for Statistical Computing, Vienna, Austria. Available at: www.r-project.org/. Accessed Month, Day, Year.

d.

Borgarelli M. Mitral valve insufficiency in large breed dog. PhD thesis, Department of Animal Pathology, Faculty of Veterinary Medicine, University of Torino, Grugliasco, Italy, 2004.

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    Culshaw GJ, French AT, Han RI, et al. Evaluation of innervation of the mitral valves and the effects of myxomatous degeneration in dogs. Am J Vet Res 2010; 71: 194202.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 13.

    Haggstrom J, Kvart C, Pedersen HD. Acquired valvular heart disease. In: Ettinger SJ, Feldman EC, eds. Textbook of veterinary internal medicine. 6th ed. St Louis: Elsevier Saunders, 2005; 10221039.

    • Search Google Scholar
    • Export Citation
  • 14.

    Pedersen HD, Haggstrom J. Mitral valve prolapse in the dog: a model of mitral valve prolapse in man. Cardiovasc Res 2000; 47: 234243.

  • 15.

    Pedersen HD, Kristensen BO, Lorentzen KA, et al. Mitral valve prolapse in 3-year-old healthy Cavalier King Charles Spaniels. An echocardiographic study. Can J Vet Res 1995; 59: 294298.

    • Search Google Scholar
    • Export Citation
  • 16.

    Pedersen HD, Lorentzen KA, Kristensen BO. Echocardiographic mitral valve prolapse in cavalier King Charles spaniels: epidemiology and prognostic significance for regurgitation. Vet Rec 1999; 144: 315320.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 17.

    Virmani R, Atkinson JB, Byrd BF III, et al. Abnormal chordal insertion: a cause of mitral valve prolapse. Am Heart J 1987; 113: 851858.

  • 18.

    Gutgesell HP, Bricker JT, Colvin EV, et al. Atrioventricular valve anular diameter: two-dimensional echocardiographic-autopsy correlation. Am J Cardiol 1984; 53: 16521655.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 19.

    Yamauchi T, Taniguchi K, Kuki S, et al. Evaluation of the mitral valve leaflet morphology after mitral valve reconstruction with a concept “coaptation length index.” J Card Surg 2004; 19: 535538.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 20.

    Levine RA, Triulzi MO, Harrigan P, et al. The relationship of mitral annular shape to the diagnosis of mitral valve prolapse. Circulation 1987; 75: 756767.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 21.

    Schober KE, Bonagura JD, Scansen BA, et al. Estimation of left ventricular filling pressure by use of Doppler echocardiography in healthy anesthetized dogs subjected to acute volume loading. Am J Vet Res 2008; 69: 10341049.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 22.

    Espino DM, Shepherd DE, Buchan KG. Effect of mitral valve geometry on valve competence. Heart Vessels 2007; 22: 109115.

  • 23.

    Burch GE, Giles TD. Angle of traction of the papillary muscle in normal and dilated hearts: a theoretic analysis of its importnace in mitral valve dynamics. Am Heart J 1972; 84: 141144.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 24.

    Borgarelli M, Zini E, D'Agnolo G, et al. Comparison of primary mitral valve disease in German Shepherd Dogs and in small breeds. J Vet Cardiol 2004; 6: 2734.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 25.

    Espino DM, Shepherd DE, Hukins DW, et al. The role of chordae tendineae in mitral valve competence. J Heart Valve Dis 2005; 14: 603609.

  • Figure 1—

    Right parasternal 5-chamber long axis Doppler ultrasonographic view obtained from a representative dog. Length of the MVLs (yellow lines) was measured when it was possible to see both leaflets as straight lines. The anteroposterior diameter of the MVa (white line) also was measured. Notice the ECG tracing in the lower left corner. The scale in the image is in centimeters.

  • Figure 2—

    Photograph of a heart obtained from the cadaver of a representative dog. The heart was fixed in 4% formalin solution for at least 10 days. The long and short axes (black lines) and MVa area (outlined shaded region) were measured at the level of the left coronary artery. The scale on the right is in centimeters.

  • Figure 3—

    Photograph of a heart obtained from the cadaver of a representative dog. The heart was fixed in 4% formalin solution for at least 10 days. The anteroposterior diameter of the MVa (red line) was measured at the level of the left coronary artery. The scale on the bottom is in centimeters.

  • Figure 4—

    Photograph of the MV of a dog that was removed, incised, and positioned in a straight line. The photograph was obtained via transillumination with polarizing light. The AMVL is in the middle, and the PMVL has been divided and is on both sides. The measured length of the AVML (long blue line in middle) and PVML (short blue line on right) is indicated.

  • Figure 5—

    Box-and-whisker plots of echocardiographic (Echo) and anatomic (Anat) measurements of the length of the MVLs. The box represents the interquartile range (25th to 75th percentiles), the horizontal line in each box represents the median, the whiskers represent the extent of the data, and the diamonds represent outliers. Values did not differ significantly (P ≥ 0.05) between the anatomic and echocardiographic measurements.

  • Figure 6—

    Results of regression analysis between the MVa area and the percentage by which the MVL area exceeded the MVa area (y-axis). There is a significant negative correlation (r = 0.47; P = 0.002), whereby an increase in MVa area is associated with a decrease in the percentage of the MVL area that exceeded the MVa area.

  • Figure 7—

    Photomicrograph of a tissue section from an MVL with mild myxoid degeneration and collagen disorganization in the distal segment. H&E stain; bar = 100 mm.

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    Culshaw GJ, French AT, Han RI, et al. Evaluation of innervation of the mitral valves and the effects of myxomatous degeneration in dogs. Am J Vet Res 2010; 71: 194202.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 13.

    Haggstrom J, Kvart C, Pedersen HD. Acquired valvular heart disease. In: Ettinger SJ, Feldman EC, eds. Textbook of veterinary internal medicine. 6th ed. St Louis: Elsevier Saunders, 2005; 10221039.

    • Search Google Scholar
    • Export Citation
  • 14.

    Pedersen HD, Haggstrom J. Mitral valve prolapse in the dog: a model of mitral valve prolapse in man. Cardiovasc Res 2000; 47: 234243.

  • 15.

    Pedersen HD, Kristensen BO, Lorentzen KA, et al. Mitral valve prolapse in 3-year-old healthy Cavalier King Charles Spaniels. An echocardiographic study. Can J Vet Res 1995; 59: 294298.

    • Search Google Scholar
    • Export Citation
  • 16.

    Pedersen HD, Lorentzen KA, Kristensen BO. Echocardiographic mitral valve prolapse in cavalier King Charles spaniels: epidemiology and prognostic significance for regurgitation. Vet Rec 1999; 144: 315320.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 17.

    Virmani R, Atkinson JB, Byrd BF III, et al. Abnormal chordal insertion: a cause of mitral valve prolapse. Am Heart J 1987; 113: 851858.

  • 18.

    Gutgesell HP, Bricker JT, Colvin EV, et al. Atrioventricular valve anular diameter: two-dimensional echocardiographic-autopsy correlation. Am J Cardiol 1984; 53: 16521655.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 19.

    Yamauchi T, Taniguchi K, Kuki S, et al. Evaluation of the mitral valve leaflet morphology after mitral valve reconstruction with a concept “coaptation length index.” J Card Surg 2004; 19: 535538.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 20.

    Levine RA, Triulzi MO, Harrigan P, et al. The relationship of mitral annular shape to the diagnosis of mitral valve prolapse. Circulation 1987; 75: 756767.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 21.

    Schober KE, Bonagura JD, Scansen BA, et al. Estimation of left ventricular filling pressure by use of Doppler echocardiography in healthy anesthetized dogs subjected to acute volume loading. Am J Vet Res 2008; 69: 10341049.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 22.

    Espino DM, Shepherd DE, Buchan KG. Effect of mitral valve geometry on valve competence. Heart Vessels 2007; 22: 109115.

  • 23.

    Burch GE, Giles TD. Angle of traction of the papillary muscle in normal and dilated hearts: a theoretic analysis of its importnace in mitral valve dynamics. Am Heart J 1972; 84: 141144.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 24.

    Borgarelli M, Zini E, D'Agnolo G, et al. Comparison of primary mitral valve disease in German Shepherd Dogs and in small breeds. J Vet Cardiol 2004; 6: 2734.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 25.

    Espino DM, Shepherd DE, Hukins DW, et al. The role of chordae tendineae in mitral valve competence. J Heart Valve Dis 2005; 14: 603609.

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