Traumatic mitral valve avulsion from the annulus fibrosis producing acute left heart failure in a dog

Abstract

Traumatic detachment of the mitral valve from the annulus fibrosis occurred in a dog following blunt chest trauma. Euthanasia was elected approximately 7 months posttrauma due to refractory, chronic left heart failure. This is the first reported case of traumatic mitral valve rupture in a dog.

This report highlights a unique archived case from 1988 in which a 6.5-year-old, male Labrador retriever was referred to the Veterinary Medical Teaching Hospital at the University of Wisconsin, Madison, Wisconsin, USA, for evaluation of acute onset of dyspnea and a productive cough. Two days earlier, the owner reported falling on the dog during a disciplinary act, but no appreciable health problems or concerns with the dog were apparent immediately following the incident. Within 12 h posttrauma, the dog became noticeably lethargic, and within 24 h, he was both dyspneic and lethargic. Within 48 h posttrauma, the dyspnea progressed to a productive cough with pink, frothy nasal discharge.

Upon initial physical examination, the dog had a temperature of 38.2°C, a heart rate of 180 beats/min, and a respiratory rate of 100 breaths/min, characterized by severe expiratory dyspnea. Pink froth was present in the nose and mouth, suggesting possible hemorrhage from the lungs, nasal passages, or both. Harsh bronchovesicular lung sounds and a grade VI/VI holosystolic, left apical, plateau murmur were auscultated. The pulses were assessed to be fair and regular, with no appreciable deficits. A complete blood (cell) count (CBC) and an activating clotting time (ACT) were within normal limits, and heartworm tests were negative. Venous blood gas analysis was consistent with a respiratory alkalosis (pH 7.483; PCO₂ 36.3; PO₂ 48.9). Radiography of the thorax demonstrated a generalized interstitial and alveolar pattern, consistent with a diagnosis of pulmonary edema. The cardiac silhouette, including the left atrium, was normal in size. Sinus tachycardia was observed electrocardiographically. Two-dimensional and M-mode echocardiographic studies demonstrated a flapping mitral valve segment. The diameter of the left atrium (LA) and the ratio of LA to aortic root diameter were normal. The left ventricular systolic and diastolic chamber diameters and contractility were within normal limits. A preliminary diagnosis of ruptured chordae tendinae was made, based on the clinical and echocardiographic findings.

Therapy with furosemide (Lasix; Hoechsst Roussel Agri Vet, Somerville, New Jersey, USA), 4 mg/kg body weight (BW), IV, given once, followed by 2 mg/kg BW, IV, q12h; a transdermal nitroglycerin patch (Nitrostat; Lavipharm Corporation, East Windsor, New Jersey, USA) 5 mg, 2% ointment; and 40% oxygen administered via an O₂ cage was initiated. The dog improved dramatically and was removed from the O₂ cage after 14 h. In an attempt to further decrease the regurgitant fraction, hydralazine (Apresoline; Novartis Animal Health US, Greensboro, North Carolina, USA) therapy was initiated and titrated to a dose of 0.5 mg/kg BW, PO, q8h. The dog continued to improve and was discharged 4 d later. A sodium restrictive diet, furosemide (2 to 3 mg/kg BW, PO, q8h), and captopril (Capoten; Bristol-Myers Squibb, Syracuse, New York, USA) 0.8 mg/kg BW, PO, q12h, was the treatment recommended at discharge.

Six days after discharge, a follow-up physical examination revealed mild tachycardia, with a heart rate of 161 beats/min, and hematuria. Urinalysis revealed elevations outside of the normal range for both red blood cells and white blood cells, suggesting the presence of inflammation within the urinary tract. Electrocardiographic evaluation revealed sinus tachycardia and 5 to 10 atrial premature complexes/min. Left atrial dilation, as well as increases in left ventricular end-diastolic and systolic dimensions, consistent with volume overload and myocardial dysfunction, elevated afterload, or both, were present on echocardiographic evaluation. Clinical pathologic results revealed electrolyte abnormalities, including hyponatremia (142 mmol/L; reference range, 144 to 162 mmol/L), hypochloremia (96 mmol/L; reference range, 106 to 126 mmol/L), and hypokalemia (3.0 mmol/L; reference range, 3.6 to 6.0 mmol/L), which were likely clinically insignificant. Thoracic radiographs revealed slight left auricular enlargement with mild pulmonary edema. The therapy that was recommended included furosemide, 2.2 mg/kg BW, PO, q12h; captopril, 0.6 mg/kg BW, PO, q12h; and potassium chloride, 10 mEq, q24h. A transdermal nitroglycerin patch was to be applied 8 to 12 h/d.

Due to financial constraints, the owners did not return the dog for additional follow-up examinations. A letter from the owners, 7 wk after the incident, stated that the dog had to work harder to breathe and was developing a “barrel chest.” Syncopal episodes were reported, beginning 5 mo after the initial complaint. The dog had syncopal attacks for 10 wk, after which euthanasia was elected.

A necropsy was performed and the heart and hilar lung tissue were submitted in 10% phosphate-buffered formalin for gross and histopathological examination. The formalin-preserved heart weight was 426.2 g (estimated 1.02% of the initial BW at time of 1st presentation; normal values are 0.76% ± 0.09% BW [1]). The heart was sectioned using echocardiographic two-dimensional landmarks. The left atrium was markedly dilated, but there was no evidence of ruptured chordae tendinae. The caudal mitral valve apparatus was detached from the annulus fibrosis and a split in the left atrial wall separated the atrium into 2 chambers, the normal chamber and a second chamber caused by the rupture and subsequent dissection of the atrial wall. The second chamber communicated with the left atrium by a 0.5-cm longitudinal tear, 2 cm proximal to the atrial ventricular valve (Figure 1). The endocardial surface of the left atrium was roughened and white. The ratio between the right ventricular (RV) free-wall thickness and the left ventricular (LV) free-wall thickness was 0.77 (normal ratio of RV: LV wall thickness is 0.33 [2]), suggesting right and left ventricular hypertrophy due to chronic volume overload. All measurements were taken 1.0 cm distal to the annulus fibrosis.

Figure 1.

Upon cut section of the heart, a 0.5-cm longitudinal tear, 2 cm proximal to the atrial ventricular valve can be visualized, as indicated by the metal probe. A second chamber was created within the left atrium, resulting in blood accumulating within the dissected left atrial wall. The mitral valve appears roughened. The chordae tendinae are intact.

Multiple areas of the lung and heart were sampled by using routine histopathological processing techniques. Slides were stained with hematoxylin and eosin (H&E), Masson’s trichrome, Verhoeff elastic stain, and Movatt’s pentachrome. Two sections of lung revealed alveolar walls diffusely thickened with collagen. Occasional hemosiderin-laden macrophages were present within alveoli. Rare clusters of type II pneumocyte hyperplasia were observed. The adventitia of pulmonary arteries was distended with fluid. Irregular thickenings of the tunica intima of large pulmonary arteries were present. Mucous cells were numerous within bronchial epithelium. Evidence of chronic bronchitis was found in some large airways, indicated by fibrosis and the presence of lymphocytes and monocytes. Histopathologic findings suggested that chronic changes in the lung may have resulted from cardiogenic pulmonary edema and secondary pulmonary hypertension, as indicated by presence of pulmonary fibrosis.

Histopathologic examination of a large section of the left annulus fibrosis and mitral valve revealed a clear separation of the mitral valve from the annulus fibrosis. Accumulations of hemosiderin and hematoidin pigment were present, as was moderate thickening of the endothelium. The false chamber was irregularly lined with dense fibrous connective tissue, occasionally containing flattened cells (resembling endothelial lining cells) on the surface. Moderate endothelial fibroelastosis was present within the true, left atrial chamber. The myofibers of the left and right ventricles were hypertrophied.

The final pathological diagnosis was mitral valve rupture, which involved not the chordae tendinae, but the annulus fibrosis. In both human and veterinary medical literature, acute mitral regurgitation due to rupture of the chordae tendinae, which can occur spontaneously in normal hearts or, more often, secondarily to cardiac damage from endocardiosis or chest trauma, has been reported (3–6). A number of reports in human medical literature discuss valvular ruptures due to blunt chest trauma (7–9). Atrioventricular valvular ruptures following motor vehicle accidents or falls are most often reported (7). In one report, a previously healthy patient presented to hospital with rupture of both atrioventricular valves after sustaining a fall from an elevation of just 5 feet. During surgery, the patient was noted to have a transverse sternal fracture between the 5th and 6th intercostal spaces. Visualization of the mitral valve revealed a complete disruption of the anterior papillary muscle, as well as a tear in the posterior atrial wall (7). In humans, the tricuspid valve is particularly vulnerable because of the location of the right ventricle immediately behind the sternum. The purported mechanism of injury is compression of the heart during late diastole or isovolemic systole, when the cardiac chambers are full and the valves are closing or closed (10). Acute, significant thoracic compression transmits pressure, which likely leads to severe atrioventricular valve prolapse and rupture. Damage or disruption at the chordal or papillary muscle level is typical.

This is the first reported case in veterinary medicine of dissociation of the mitral valve from the annulus fibrosis. The presumed pathogenesis would include blunt trauma to the chest overlying the heart, rupture of the mitral valve from the annulus fibrosis and development of a false chamber within the left atrium. The development of this tear would result in the acute clinical signs and echocardiographic findings observed in this case. Awareness of the specific clinical features of mitral valve rupture and acute left heart failure will result in early diagnosis of this unique condition, especially in cases involving a recent history of blunt chest trauma. CVJ