A 19-year-old male Siberian tiger was presented with inappetence and paralysis of hind limbs. In a computed tomography (CT) scan, intervertebral disk disease at L3–L4 was detected. Cardiac arrest occurred during the surgery. At autopsy, myxomatous mitral valve degeneration (MMVD) and eccentric hypertrophy of the left heart were noted. The diagnosis was congestive heart failure caused by MMVD. Microscopically, myocardial and pulmonary fibrosis were observed in addition to the disintegration of the fibrosa layer and accumulation of glycosaminoglycans and proteoglycans in the spongiosa layer of the mitral valve. This is the first case of congestive heart failure with MMVD in a Siberian tiger.

Echocardiography is one of the most useful diagnostic techniques for differentiating heart disease as well as mitral valve lesion. Forty client-owned small breed dogs (weight, 2.3−13.2 kg) aged between 8−17 years with myxomatous mitral valve degeneration (MMVD) were included in the present study. The diagnosis of MMVD in dogs was made based on the clinical signs, chest radiography data, and echocardiographic findings. Echocardiographic examinations were conducted in accordance with recommended standards for dogs. M-mode, Doppler, and 2D echocardiography were performed in left and right lateral recumbency. 2D echocardiography was used to measure LA and Ao diameter from 2D short axis at the level of the aortic valve. In the comparison of conventional echocardiography indices in dogs with different stages of heart failure with MMVD, significant differences were observed in E/A ratio (p=0.005), EDV (p<0.001), EDVI (p<0.001), E-peak velocity (p= 0.001), ESV (p=0.028), ESVI (p=0.004), LA (p<0.001), LA/Ao Ratio (p<0.001), LVIDd (p<0.001), LVIDd/Ao Ratio (p<0.001), LVIDs (p=0.036), LVIDs/Ao Ratio (p=0.002), and MR Velocity (p=0.026). In addition, distinct correlations were found in EDV (r=0.712), LA/Ao ration (r=0.830), LVIDd (r=0.724), and LVIDd/Ao ratio (r=0.759). This study found that known conventional echocardiographic indices, including EDV, LA/Ao ratio, LVIDd dimension, and LVIDd/Ao ratio correlated with the severity of MMVD in point of significant differences and distinct correlations.

This study investigated the potential associations of dog characteristics with serum serotonin (5HT) concentration in dogs with degenerative mitral valve disease (DMVD). Client-owned dogs were prospectively recruited at the Veterinary Medical Teaching Hospital of Chungnam National University between 2010 and 2011. Forty-two dogs (22 females and 20 males) were enrolled in this study. DMVD dogs included Maltese (n=12), followed by Shih-tzu (n=10), mixed breed (n=5), Chihuahua (n=4), Miniature schnauzer (n=3), Miniature poodle (n=3), Miniature pinscher (n=1), Pomeranian (n=1), Yorkshire terrier (n=2), and Spitz (n=1). As inclusion criteria for the study, dogs had to show either direct or echocardiographic evidence of DMVD. Platelet count significantly differed among the three groups, as the moderate (P<0.05) and severe groups (P<0.05) showed significantly higher platelet counts than the mild DMVD group. Additionally, significantly higher LVIDd, LVIDs, fractional shortening (FS), and LA:Ao ratios were observed in dogs with moderate (P<0.05) and severe (P<0.05) DMVD compared to the mild group, respectively. Significant positive correlations between serum 5-hydroxytryptamine (5HT) concentration and platelet count (r=0.273, P=0.03), LA:Ao ratio (r=0.459, P=0.001), and LVIDd (r=0.319, P=0.013) were observed in DMVD dogs. Therefore, serum 5HT concentration may be a potential cause of DMVD progression.

Mitral valvular prolapse (MVP) in dogs is characterized by myxomatous valvular degeneration, which is caused by abnormal valvular thickening and incomplete coaptation of the mitral valve leading to mitral regurgitation. Mitral regurgitation causes left atrial and left ventricular enlargement. Pathogenesis of the disease is unknown, although some studies have suggested the involvement of endothelin and systemic connective tissue diseases. Mitral valvular prolapse in dogs commonly occurs in aged small dog breeds, including Malteses and Shih Zhus. This case study investigated the clinical features of an affected Maltese family and performed pedigree analysis. To the best of the authors’ knowledge, this is the first report of putative familial mitral valve prolapse and regurgitation in Maltese dogs. All family members in this study showed degenerative valvular changes and echocardiographic features of mitral valvular prolapse. Although disease progression differed, all dogs progressed to advanced heart failure stage within 2-3 years after diagnosis. Therefore, this is the first study to identify putative familial mitral valve prolapse in Maltese dogs. This finding suggests strong genetic etiology involved in the development of degenerative mitral valve disease in Maltese dogs. Furthermore, this finding could be a valuable resource for the identification of gene mutations in dogs with familial mitral valvular prolapse.

A 12-year-old spayed female Pomeranian (weighing 2.4 kg) was referred with primary complaints of acute dyspnea, cough, and lethargy. Diagnostic imaging studies found degenerative mitral valve cusps, chordae tendinae rupture, severe mitral regurgitation (5.45 m/s of peak velocity), and marked left atrial and ventricular dilation. The dog was diagnosed as having degenerative mitral valve disease (DMVD) with ISACHC stage IIIa heart failure. Her clinical condition was stabilized after administration of cardiac medication (e.g. diuretics and pimobendan). Ten months later, the dog was referred back to the clinic due to a sudden worsening of clinical signs. Echocardiographic study found pulmonary hypertension in addition to DMVD. After medication was adjusted, clinical signs were stabilized in 2 weeks. The patient was returned after 4 months for cardiac recheck and there was no obvious worsening of clinical signs. Incidental finding of a left-to-right atrial septal defect from rupture of the atrial septum secondary to marked left atrial dilation by DMVD was noted by echocardiography. To diminish left atrial volume overload, the frequencies of both furosemide and pimobendan were increased (i.e. from q 12 hr to q 8 hr) in addition to adding spironolactone (1 mg/kg q 12 hr). Based on diagnostic findings, this case was re-diagnosed as acquired atrial septal defect secondary to rupture of the atrial septum with advanced stage DMVD. The dog was then stabilized and is currently being regularly monitored.

Cerebral infarction is one of the leading causes of death worldwide and the most common cause of death from a singledisease in South Korea. Each year, 795,000 people in the U.S. experience a new or recurrent stroke. Approximately 15-30% of cerebral infarctions are of embolic origin related to cardiac abnormalities. Because determination of the etiology of cerebral infarction is crucial to acute management and future prevention, clinicians should pay attention to finding the cardiac source of embolism in patients with cerebral infarction. We report on a case of cerebral infarction by a small papillary fibroelastoma on the mitral valve. The patient was treated with open heart surgery and closure of the patent foramen ovale to prevent further embolic events.