• Airway collapse;
  • Chronic bronchitis;
  • Left atrial enlargement


  1. Top of page
  2. Abstract
  3. Materials and Methods
  4. Results
  5. Discussion
  6. References


Cough in the geriatric small breed dog with myxomatous mitral valve degeneration (MMVD), a large left atrium, and absence of heart failure often is attributed to compression of the left mainstem bronchus by the left atrium. Studies investigating this syndrome are lacking in dogs.


Airway collapse is independent of left atrial enlargement.


A total of 16 dogs presenting with chronic cough in the absence of congestive heart failure. Group 1 dogs (n = 10) had moderate-to-severe left atrial enlargement based on an echocardiographically calculated left atrial:aortic surface area [LA:Ao(a)] > 6. Group 2 dogs (n = 6) had no to mild left atrial enlargement [LA:Ao(a) ≤ 6].


Dogs were prospectively evaluated. CBC, biochemistry, urinalysis, cervical and thoracic radiographs, fluoroscopy, echocardiography, and bronchoscopy were performed. Bronchoscopic abnormalities were compared between groups using Fisher's Exact Test. < .05 was considered significant.


Fluoroscopy identified airway collapse in both groups. Bronchoscopic evidence of airway collapse >50% was observed in multiple bronchi with no difference between groups. All dogs had inflammation on airway cytology with respiratory infection in 1 dog in group 2. Left atrial size was interpreted radiographically as enlarged in 9 of 10 group 1 dog and in 2 of 6 group 2 dogs. VHS was above normal in both groups of dogs regardless of echocardiographic evidence of cardiomegaly.


Results failed to identify an association between left atrial enlargement and airway collapse in dogs with MMVD, but did suggest that airway inflammation is common in dogs with airway collapse.


bronchoalveolar lavage


body condition score


left atrium:aorta


myxomatous mitral valve degeneration




vertebral heart score


Veterinary Medical Teaching Hospital

Chronic cough in the geriatric small breed dog presents a diagnostic and therapeutic dilemma. Such dogs often have heart murmurs associated with myxomatous mitral valve degeneration (MMVD) and many also are affected by airway disease. Therefore, cough may result from one of several different pathophysiologic mechanisms including airway collapse, chronic bronchitis, or pulmonary edema due to left heart failure.[1] In the presence of severe left atrial enlargement without heart failure, cough commonly has been anecdotally attributed to compression of the left mainstem bronchus by a large left atrium.[1-3] In people, the finding of an enlarged left atrium combined with increased pulmonary artery pressure is reported to lead to compression of the left mainstem bronchus and prompts aggressive treatment aimed at decreasing left atrial size.[4-6] However, studies investigating left atrial enlargement and compression of the left main stem bronchus are lacking in dogs.

Tracheobronchomalacia (TBM) refers to softening of the cartilaginous rings in the tracheal and bronchial walls, and breakdown of the elastic fibers in the dorsal tracheal membrane, elastic annular ligaments or both might also occur, resulting in a propensity for airways to collapse. The diagnosis is made by visual identification of >50% reduction in luminal diameter of the airway during bronchoscopy in humans or a >25% reduction in dogs.[5-7] In humans, TBM may be primary (congenital) or acquired (secondary).[5, 6] The etiology of TBM in dogs is unknown, but it may be a congenital cartilage disorder causing primary softening of the cartilage or an acquired syndrome secondary to chronic inflammation. Tracheobronchomalacia in dogs typically affects the cervical and intrathoracic trachea, as well as multiple lobar bronchi.[8, 9]

The purpose of this study was to investigate whether a relationship could be established between left atrial enlargement and airway collapse in dogs by comparing the incidence and distribution of airway collapse in small breed dogs with and without left atrial enlargement. We also aimed to describe patterns of airway infection or inflammation in these dogs. We hypothesized that airway collapse occurs in geriatric small breed dogs independent of left atrial size and that cough in dogs with large left atria but without pulmonary edema is a result of widespread structural deterioration, inflammatory airway disease, or both.

Materials and Methods

  1. Top of page
  2. Abstract
  3. Materials and Methods
  4. Results
  5. Discussion
  6. References

All small breed dogs evaluated at the William R. Pritchard Veterinary Medical Teaching Hospital (VMTH) at the University of California, Davis between January 2010 and February 2011 with a history of chronic cough (>3 months) were screened for inclusion in the study. Study dogs included those with (group 1) and without (group 2) moderate-to-severe mitral regurgitation (ie, moderately to severely enlarged left atrium) due to MMVD that were not in congestive heart failure. Dogs also were considered eligible to be included in group 1 if congestive heart failure had been diagnosed but was controlled by some combination of a diuretic, an angiotensin converting enzyme inhibitor, and pimobendan as deemed necessary by the primary clinician, and the cough persisted. All dogs had a CBC, serum biochemistry profile, urinalysis, cervical and 3-view thoracic radiographs, echocardiogram, and bronchoscopy performed. In most dogs, fluoroscopy also was performed during tidal respiration and induction of cough. Dogs were excluded if congenital cardiac disease, neoplasia, or systemic disease was detected. If no contraindication to anesthesia was identified, bronchoscopy and bronchoalveolar lavage under anesthesia were recommended for further evaluation of cough. This study was approved by the Institutional Clinical Trials Review Board and owner consent was obtained.

All dogs had age, breed, sex, neutering status, weight, body condition score (BCS), and the presence or absence of a murmur including its grade, timing, and point of maximal intensity recorded. Left lateral, right lateral, and dorsoventral thoracic and lateral cervical radiographs obtained during inspiration were evaluated. These were reviewed in random order by a board-certified radiologist (REP) who was masked to the group assignment of the case. Vertebral heart score (VHS) was calculated as previously described.[10] Enlargement of specific cardiac structures (left atrium, left ventricle and overall cardiac size) was graded as absent, mild, moderate, or severe for all cases. Collapse of the trachea and all visible bronchi was subjectively graded as not present, mild, moderate, or severe. A radiographic description of the pulmonary parenchymal pattern was recorded (normal, bronchial, interstitial, bronchointerstitial or alveolar) and was subjectively graded as mild, moderate, or severe and diffuse or focal.

Fluoroscopic examinations were obtained with the dog restrained in right lateral recumbency. Regular respiration was observed and recorded on video for future evaluation. Tracheal manipulation and compression were performed to allow fluoroscopic evaluation and recording of the trachea and bronchi during cough. Videos were examined in random order by a board-certified radiologist (REP) who was masked to the group assignment. Collapse of the trachea and left lobar bronchi during respiration and cough was subjectively evaluated and the results were recorded. More specifically, collapse of the cervical or thoracic trachea, carina, and bronchi to the cranial and caudal segments of the left cranial lung lobe and left caudal lung lobe was recorded as absent or present (>25% reduction in diameter).

Echocardiography1 was performed on all dogs by 1 investigator (MKS). Myxomatous mitral valve degeneration with mitral regurgitation was confirmed as the cause of the left apical systolic heart murmur in all group 1 dogs and in the group 2 dogs that had murmurs. The surface area and maximal diameter of the left atrium was measured and the size evaluated using left atrial:aortic surface area and diameter ratios (LA:Ao) from the right parasternal short-axis view.[11] Using the surface area method, a ratio of <3.7 was considered normal,[11] 3.7–<6 mild enlargement, 6–8 moderate enlargement and >8 severe enlargement (Singh MK and Kittleson MD, unpublished data). Dogs with moderate or severe left atrial enlargement (LA:Ao surface area ratio >6) were included in group 1 and those with no or mild left atrial enlargement (LA:Ao surface area measurement <6) were included in group 2.

Bronchoscopy with bronchoalveolar lavage (BAL) was performed in all dogs to document the distribution and severity of airway collapse and to determine the presence or absence of infection or inflammation. A balanced anesthetic induction plan was designed for each patient and anesthesia was maintained using a constant rate infusion of propofol at 0.1–0.4 mg/kg/min. Oxygenation was provided by jet ventilation at a rate of 180 breaths/min. An ECG, blood pressure, and pulse oximetry were constantly monitored throughout the procedure. Bronchoscopy was performed in sternal recumbency using a 3.8 mm × 55 cm flexible video endoscope.2 In each dog, the grade and extent of tracheal collapse were recorded according to a previously defined scheme based on the percent reduction in luminal size.[7] The canine bronchial map developed by Amis and McKiernan was used for examination of the lower airways.[12] For this study, bronchial collapse was identified as >50% loss in luminal diameter of individual bronchi due to static flattening of the lobar airways, circumferential narrowing or distortion of the normal round appearance of airway openings or as dynamic changes in luminal diameter with respiration or heart beat. This modified definition was used so that the presence of clinically relevant collapse could not be questioned. The site and extent of the airway collapse were recorded for each involved bronchial segment as well as for more distal airways.

BAL was performed at 1–2 bronchial segments at the discretion of the endoscopist by gently wedging the bronchoscope in a distal airway, instilling single 5-mL aliquots of warmed, sterile saline through the biopsy channel of the bronchoscope into each lobar segment, and retrieving the fluid with gentle hand aspiration. BAL fluid was submitted for cytologic assessment and for aerobic and Mycoplasma cultures. Reference values used for normal BAL cell and differential counts were 200–450 cells/μL comprised of up to 5–7 ± 5% neutrophils, lymphocytes, and eosinophils, and 65–85% macrophages.[13] Bacterial infection was confirmed when intracellular bacteria were identified on cytology in conjunction with isolation of pathogens on aerobic bacterial or mycoplasmal culture.[14] Inflammatory airway disease was characterized as neutrophilic, lymphocytic, or eosinophilic by the presence of >12% of the respective inflammatory cell.

Statistical Analysis

Data were examined for normality by the Kolmogorov–Smirnov test. Data with a normal distribution are reported as mean ± SD and were analyzed using a Student's t-test. Variables that were non-Gaussian in distribution are reported as median and range. Body weight, age, and BCS were compared between the 2 groups using a Student's t-test. Detection of fluoroscopically identified collapse during passive respiration and during cough was compared between group 1 and group 2 using Fisher's exact test. The distribution of airway collapse on bronchoscopy and presence of airway inflammation or infection were compared between groups 1 and 2 dogs also using a Fisher's exact test. For all statistics, < .05 was considered significant.


  1. Top of page
  2. Abstract
  3. Materials and Methods
  4. Results
  5. Discussion
  6. References

Ten dogs were enrolled in group 1 and 6 dogs in group 2. Dogs were presented for evaluation of a dry, harsh, or honking cough of long duration (group 1: 22.6 ± 17.5 months versus group 2: 10.2 ± 7.8, months, P = .12). Group 1 consisted of Shih Tzu (2), Terrier mix (2) and 1 each of Maltese, Miniature Poodle, Pomeranian, Chihuahua, Italian Greyhound, and Corgi mix. All dogs were castrated males. The ages ranged from 5 to 14 years with a median of 11.5 years. All 10 dogs had a left apical systolic murmur with grades ranging from III to V/VI. One dog had a history of congestive heart failure before entry in the study that was well controlled with furosemide, enalapril, and pimobendan. One dog had been treated with antibiotics (doxycycline) in the 4 weeks before bronchoscopy. Group 2 dogs consisted of 2 Chihuahuas and 1 each of Toy Poodle, Toy Poodle mix, Papillion, and Pomeranian. Four dogs were castrated males and 2 were spayed females. Ages ranged from 5 to 12 years with a median of 10 years. Two dogs had left apical systolic murmurs consistent with MMVD (grade II and III) and mild mitral regurgitation on echocardiogram. The other 4 dogs did not have heart murmurs or evidence of valvular regurgitation on echocardiogram. Two dogs had been treated with antibiotics (doxycycline in one and amoxicillin-clavulanic acid in the other) in the 4 weeks before bronchoscopy. There was no significant difference in age between groups. Body weight in group 1 dogs (6.5 ± 3.9 kg), did not differ from group 2 dogs (4.9 ± 4.2 kg), but body condition score was significantly lower in group 1 dogs (4.8 ± 0.8) compared with group 2 dogs (6.7 ± 1.0), (= .001).

LA:Ao ratio using the surface area method in group 1 dogs was between 7.0 and 10.1 (8.1 ± 0.9) and between 2.5 and 4.4 (3.4 ± 0.7) in group 2. LA:Ao measured using the short-axis diameter method was between 1.9 and 2.6 in group 1 dogs (2.2 ± 0.2) and 1.2 and 1.6 in group 2 dogs (1.4 ± 0.1).

Radiographic evidence of left atrial enlargement was subjectively reported as mild (1), moderate (7), and severe (2) in group 1 dogs and as mild (4) and moderate (2) in group 2 dogs. The dog with the grade III murmur in group 2 had its left atrium subjectively reported as moderately enlarged and had mild LA enlargement on echocardiography (LA:Ao surface area, 4.4). The other dog with moderate left atrial enlargement identified radiographically did not have a heart murmur or presence of left atrial enlargement on echocardiography (LA:Ao surface area, 2.5) (Fig 1). Left ventricular size was reported as normal (1), mildly enlarged (6), and moderately enlarged (3) in group 1 dogs and as normal in 3 dogs in group 2 and mildly enlarged in the other 3 (2 of the latter dogs had heart murmurs). VHS did not differ between group 1 dogs (11.6 ± 0.8) and group 2 dogs (11.5 ± 0.3), (= 0.90). VHS was outside the normal range (normal, 8.5–10.7)[10] in 9/10 group 1 dogs and 6/6 group 2 dogs.


Figure 1. A. Right lateral thoracic radiograph from a dog in group 2 showing extension of the left atrium dorsal to the carina (white arrows) with dorsal deviation of the trachea. Left atrial enlargement was graded as moderate and vertebral heart score was 11.8. Black arrowheads show collapse of the intrathoracic trachea. B. The dorsoventral radiograph of the dog in (A) showing a rounded, enlarged left atrium (white arrows). C. Left parasternal short axis echocardiogram of the LA:Ao from the dog in Figures 1A and 1B that shows that the dog does not have left atrial enlargement (LA:Ao [surface area] 2.5).

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Static radiography was considered supportive of tracheal collapse (cervical or thoracic) in 7/10 group 1 dogs and 4/6 group 2 dogs and of lower airway collapse in all dogs (Fig 2). In group 1, 8 of the 10 dogs had the classic appearance of a severely enlarged left atrium and left bronchial collapse. No dog in group 2 had this appearance. The number of bronchi observed to collapse radiographically did not differ between group 1 (4.2 ± 1.6) and group 2 (4.0 ± 0.6), (= .81). Radiography showed evidence of an abnormal pulmonary pattern (interstitial, bronchial, or alveolar) in 3/10 group 1 dogs and 3/6 group 2 dogs with no significant difference between groups (= 1.00).


Figure 2. A right lateral thoracic radiograph of a dog in group 1 with moderate collapse of the cervical and thoracic trachea (black arrowheads) and severe collapse of the carina (white arrowhead) and cranial segment of the left cranial lobar bronchus (black arrow). The left caudal lobar bronchus is also severely collapsed (white arrow).

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Fluoroscopy was performed in 8/10 dogs in group 1 and 5/6 in group 2. The remaining dogs were not able to undergo fluoroscopic examination due to lack of cooperation. During normal respiration, cervical tracheal collapse was identified in 5/8 group 1 dogs and 4/5 group 2 dogs. Collapse at the left cranial lobar bronchus was identified in 7/8 group 1 dogs and 5/5 group 2 dogs. Fluoroscopy performed during induction of cough showed evidence of lower airway collapse in all dogs examined in both groups.

Cervical and thoracic tracheal collapse was identified during bronchoscopy in both group 1 and group 2 dogs, but was subjectively less severe in group 1 dogs. Mild cervical tracheal collapse (grade 1–2) was present in 2/10 group 1 dogs and in 2/6 group 2 dogs, whereas grade 3–4 tracheal collapse was reported in no group 1 dog and in 4/6 group 2 dogs. Thoracic tracheal collapse was absent in 7/10 group 1 dogs and mild (grade 1–2) in 3/10 group 1 dogs. In contrast, 3/6 group 2 dogs had severe thoracic tracheal collapse (grade 3–4), whereas 1/6 had moderate collapse. In both groups of dogs, many bronchial segments were collapsed on initial entry to the airway indicating static bronchial collapse. Dorsal and ventral segments of the left cranial lobar bronchus were affected most commonly, followed by the left caudal and right middle lobar bronchi (Figs 35). There was no significant difference in site or severity of airway collapse between groups (Table 1). Localized regions of distal airway collapse were identified in 2/10 dogs in group 1 and 2/6 dogs in group 2.


Figure 3. Bronchoscopic evaluation of the left cranial (white arrow) and caudal segments (black arrow) of the left cranial lobar bronchus from a dog in group 1 (A) and a dog in group 2 (B) showing 80–100% static collapse of both segments.

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Figure 4. Bronchoscopic evaluation of the left caudal lobar bronchus (arrows) from a dog in group 1 (A) and a dog in group 2 (B) showing 100% static collapse.

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Figure 5. Bronchoscopic evaluation of right middle lobar bronchus (arrows) from a dog in group 1 (A) and a dog in group (B) showing 100% static collapse.

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Table 1. Distribution of airway collapse and airway inflammation detected by bronchoscopy and bronchoalveolar lavage.
 Group 1 (n = 10) Group 2 (n = 6) P value
  1. a

    Values from the dog with septic, suppurative inflammation were excluded here.

Lower airway collapse
Left cranial10  6  NA
Left cranial8  4  0.60
Right cranial4  3  1.00
Right middle8  6  0.50
Accessory4  4  0.60
Right caudal3  3  0.61
Mucosal hyperemia9  6  0.12
Mucosal irregularity6  3  1.00
Mucus accumulation4  4  0.60
  cell count  cell count  
BAL cytology 200–1500% 360–2840a% 
Neutrophilic5 13–67%4 12–56%a 
Lymphocytic4 16–52%1 23% 
Eosinophilic0  0   
Mixed1  1   
Intracellular bacteria0  1   
Positive aerobic culture7  3  0.22
Positive Mycoplasma culture1  0  1.00

Dogs in both groups had gross evidence of airway inflammation during bronchoscopy with hyperemia and mucus accumulation (Table 1). BAL was performed at 2 lung segments in 9/10 dogs in group 1 and 5/6 dogs in group 2. BAL cytology indicated suppurative, lymphocytic, or mixed inflammation in all dogs in both groups with no significant difference between groups. Parasitic larvae or ova were not found in any of the samples examined. In group 1, 7/10 dogs had small numbers of bacterial growth on airway BAL fluid in the absence of intracellular bacteria on cytology, suggesting airway colonization or contamination. In group 2, bacterial growth was noted in 3/6 dogs and was considered indicative of pneumonia in only 1 dog with septic, suppurative inflammation and growth of beta hemolytic Streptococcus spp. on culture. No Mycoplasma spp. were cultured, and there was no significant difference in detection of bacterial growth between the 2 groups (= .22) (Table 1).


  1. Top of page
  2. Abstract
  3. Materials and Methods
  4. Results
  5. Discussion
  6. References

Compression of the left mainstem bronchus by a severely enlarged left atrium is commonly hypothesized to be a cause for chronic cough in dogs with severe mitral valvular insufficiency that lack congestive heart failure.[3, 15] However, no specific studies have examined this hypothesis. Bronchoscopically, the left mainstem bronchus represents the segment of cartilaginous airway between the carina and the division into the left cranial and caudal lung lobes.[12] It arches over the dorsal aspect of the left atrium. The left pulmonary artery traverses the thorax dorsal to the left cranial lobe bronchus. Thus, the left mainstem bronchus is surrounded by the left pulmonary artery, the left pulmonary veins and the left atrium. Upward pressure by an enlarged left atrium lifts the left mainstem, cranial and caudal lobar bronchi; however, the left pulmonary artery would tend to prevent this elevation. It has been hypothesized that the 2 opposing forces result in bronchial compression in people.[4]

The current study was unable to document an association between moderate-to-severe left atrial enlargement and left bronchial collapse, and so failed to support the theory that a large left atrium either causes these structures to collapse or compresses already soft airways. In this study, all dogs with and without left atrial enlargement had collapse of the left cranial lobar bronchus, and the majority also had collapse of the left caudal and right middle lobar bronchi. There was no significant difference in the distribution of airway collapse between dogs with a severely enlarged left atrium and those with negligible left atrial enlargement.

The base of the heart occupies the space immediately adjacent to the lobar bronchi and it is plausible to hypothesize that cardiomegaly could result in compression of the bronchi. In a previous study of bronchomalacia,[8] affected dogs were significantly more likely to have heart murmurs associated with mitral regurgitation and to have radiographic evidence of cardiomegaly, although echocardiography was not routinely performed in that study and VHS was not calculated.[8] It was speculated that decreased lung volume due to airway collapse or decreased thoracic volume from obesity may have contributed to the radiographic impression of an enlarged cardiac silhouette in those dogs, or that the space occupying effect of an enlarged heart may have played a role in the bronchial collapse. In a separate study, dogs with a cough associated with cardiac or mixed cardiac and respiratory disease had a significantly higher VHS than those with a cough of purely respiratory origin.[1] The authors of that study concluded that a VHS < 11.4 might reasonably exclude cough of cardiac origin in dogs with MMVD, although some dogs with cough of noncardiac origin could have a VHS > 11.4.

In the present study, dogs with and without left atrial enlargement had a VHS greater than normal, with mean values exceeding 11.4, and there was no significant difference in VHS between group 1 and group 2 dogs. In contrast to an experimental study that found good correlation between VHS and echocardiographic parameters in dogs with experimentally induced cardiopulmonary disease,[16] in the dogs examined here, the VHS inappropriately identified cardiomegaly in dogs without clinically relevant cardiac disease on echocardiography. VHS has been found to vary significantly with breed and thoracic conformation.[17-19] It is possible that the reported normal range for VHS is inaccurate for the types of small dogs represented in this study.3 Although dogs in the control group had a significantly higher BCS than study dogs, any apparent fat on the periphery of the cardiac silhouette was not included in the VHS measurements in an attempt to minimize bias related to obesity. Nonetheless, the increased VHS and lack of difference in VHS between dogs with and without echocardiographic evidence of cardiomegaly in this study are important to note and indicate that the VHS measurement must be interpreted with caution. Radiography also reported mild (4 dogs) to moderate (2 dogs) subjective left atrial enlargement in group 2 dogs that were shown by echocardiography to have no left atrial enlargement or mild left atrial enlargement (1 dog), indicating a lack of agreement between these two imaging modalities.

Radiography was insensitive for detection of airway inflammation, showing evidence of a bronchial, interstitial or alveolar pattern in only 30% of group 1 dogs and 50% group 2 dogs. This is consistent with previous reports that found low sensitivity of radiography for the detection of chronic bronchitis in dogs.[20-22] Static radiography was supportive of tracheal or lower airway collapse at some location in all dogs examined. Previous studies have shown and the present study helps to confirm that the location of collapse identified radiographically correlates poorly with collapse identified on fluoroscopy or bronchoscopy.[8, 20] Fluoroscopy during normal respiration identified collapse of the left cranial lobar bronchus in the majority of dogs in both groups, and indicated collapse in all dogs during induction of cough. The latter had 100% correlation with bronchoscopy, reflecting the value of dynamic imaging studies for documentation of airway collapse.

All dogs, regardless of group, had bronchoscopic evidence of airway inflammation as indicated by gross findings (hyperemia, mucus) and results of airway cytology. Although the majority of dogs had neutrophilic inflammation, mixed and lymphocytic inflammation also was present and there was no difference between groups. Previous studies of bronchomalacia in dogs also reported a high percentage of inflammatory airway disease.[8, 20] The associations among cough, airway collapse, and airway inflammation are unclear. Mechanical trauma associated with coughing can induce neutrophilic or lymphocytic inflammation.[23, 24] Bronchomalacia is defined as a softening of bronchial walls resulting in collapse. It may be caused by an inherent abnormality in the cartilage, extrinsic compression or chronic inflammation.[5, 8, 20, 25] Acquired tracheobronchomalacia may develop in association with chronic cough caused by chronic bronchitis.[25] Additional studies are required to investigate the sequence of events leading to cough, lower airway collapse and inflammation in dogs.

Efficacious treatment of dogs with airway collapse has not been clearly established due to the lack of information regarding etiology of cough. Small breed dogs with MMVD, a large left atrium, and a chronic cough that are not in heart failure are commonly treated with narcotic cough suppressants.[3] However, cough suppression is not the treatment of choice in the presence of active airway inflammation[23, 26, 27] and dogs gradually develop tolerance to these drugs. An unexpected finding in this study was the presence of airway inflammation in all dogs with airway collapse, regardless of the presence or absence of left atrial enlargement. This finding suggests that use of an anti-inflammatory drug to control cough could be indicated in similarly affected dogs. Conversely, bacterial infection characterized by septic suppurative inflammation[14] was found in only 1 of 16 dogs. Although 1 dog in group 1 and 2 dogs in group 2 had been treated with antibiotics in the 4 weeks before bronchoscopy, these dogs showed minimal clinical improvement. This finding combined with the absence of septic inflammation on BAL led to the conclusion that isolation of bacteria in the remaining dogs was likely due to oropharyngeal or airway contamination. This finding is similar to that of other studies of both tracheal collapse and bronchomalacia and suggests that antibiotic therapy is rarely indicated in dogs with airway collapse.[8, 9, 20] Interventional therapy with stent placement has been reported in 2 dogs with left atrial enlargement due to MMVD and bronchoscopic evidence of airway collapse that lacked airway inflammation. This treatment resulted in 60% and 90% improvement in cough severity, although long-term outcome was not reported.4

There are several limitations to this study, most importantly that small numbers of dogs were included. The commonality of airway collapse in dogs,8,28 and particularly in small breed dogs that are also prone to MMVD, means that a very large study population would probably be required to identify significant differences between dogs with and without LAE. In addition, a control group consisting of dogs with large left atria but absence of cough was not included. During the design phase of this study, it was deemed improbable that owners would consent to a procedure such as bronchoscopy in a dog without clinical signs.

Despite these limitations, this study did not identify an apparent increase in the frequency or difference in distribution of airway collapse in dogs with MMVD and moderate-to-severe left atrial enlargement when compared with dogs without left atrial enlargement. Severe collapse, especially of the left cranial, left caudal, and right middle lobar bronchi was present in most dogs in both groups. Airway inflammation was common in this small group of dogs, although the association among cough, airway collapse, and inflammation remains unclear. Radiography was not considered accurate when compared with bronchoscopy for identification of airway collapse or inflammation or for documentation of cardiomegaly in this small group of dogs.

The question remains as to whether the entity of cough secondary to airway compression from a large left atrium actually exists. Additional studies are needed to identify factors contributing to airway collapse in dogs with a chronic cough with and without left atrial enlargement.

  1. 1

    Phillips iE33. Phillips Medical Systems, NA, Bothell, WA

  2. 2

    Olympus BF3C160, Olympus Corporation, Melville, NY

  3. 3

    Jepsen-Grant K, Johnson LR, Pollard RE. Vertebral heart scores in chondrodystrophic and brachycephalic breeds. 2011 ACVR Scientific Meeting, Albuquerque, NM (abstract)

  4. 4

    Kramer G, McKiernan B, Burk R. Bronchial stenting in dogs with chronic valvular heart disease and bronchial collapse. In: American College of Veterinary Internal Medicine Forum, Montreal, Canada 2009 (abstract)


  1. Top of page
  2. Abstract
  3. Materials and Methods
  4. Results
  5. Discussion
  6. References