Sample Echocardiography Case Submission

A Cavalier King Charles Spaniel, MI, 7y 5m old. He lives with an elderly couple in an assisted living facility, since the owners have Alzheimer’s disease. The couple’s daughter brings him in. His previous exam was 12/22/06, and at that time the daughter reported no problems, that he is being fed primarily people food. On exam his heart murmur has progressed from a Grade 4/6 on 6-16-06 to a Grade 6/6. Other clinical findings that day revealed severe dental disease with many previously extracted teeth, otitis, overweight by approximately 4lb, and coccidiosis on fecal flotation. Radiographs and an electrocardiogram were done, and there is cardiomegaly, with vertebral heart score of 11, and prominent vessels.

ECG: tachycardia, occasional premature ventricular contractions, and P mitrale.

CBC: Giant platelets, platelet count low, but considered by the consulting pathologist to be within the normal range for the breed. WBC and RBCs were normal in number, distribution, and morphology

Chemistry Profile: Alb-3.0, Glob-3.6, ALT- 150 (^, Normal-10-100), ALP-39, T. Bili-0.1, Amyl-762, BUN-22, Ca-10.2, Chol-200, Creat-1.3, Gluc-93, Phos 5.9.

Recommendations were to set up echocardiogram, treat the coccidiosis and otitis.

He had no clinical complaints up until he was dropped off for the echocardiogram; they reported that he coughed all the previous night.

Physical exam: Weight- 23.3lbs, Temp-101.4’F, Pulse-155, Respiratory rate-60.
Severe tartar and gingivitis and recession on remaining teeth. Mucous membranes- pink, CRT-1 second.

Grade 6/6 systolic murmur PMI mitral. Lung sounds have mild increase in harshness on inspiration, there is mild increase in respiratory effort, no cough elicited with moderate tracheal stimulation. Abdomen is mildly distended, and he is overweight. Prostate is symmetrically enlarged and non-painful on rectal exam.

Radiographs: progressive cardiomegaly, with tracheal elevation, and mild pulmonary edema.

Echocardiogram:

Right Parasternal Long Axis, 4 chamber

Long axis 4 chamber, shows pericardial effusion and mitral prolapse better.

Long axis 5 chamber.

Right Parasternal Short axis LA/Ao

Short axis Mitral view

Short axis Chordae level of LV

Short axis LV papillary muscle level

Left apical views, the second showing mitral valve prolapse.

LA/Ao M Mode

M mode Mitral

M mode LV

Right parasternal long axis 5 chamber with color flow Doppler

Left apical with color flow Doppler showing mitral regurgitation

Continuous wave Doppler showing mitral regurgitation

Heart rate measured systole to systole.

Left parasternal long axis right auricular view (tumor check)

Echocardiographic Findings:
Subjective Overview: There is mild pericardial effusion. There is no pleural effusion. Heart rate is increased, and rhythm appeared normal throughout the exam. The ventricular and atrial chambers appear dilated, but wall thickness appears normal. The mitral valve leaflets appear thickened, and there is mitral prolapse seen in the long axis views and in the left parasternal views. No masses are noted. A cursory abdominal ultrasound exam did not reveal any ascites.

Measurements: 
Ao-16.8mm        LA-44.1mm       LA/Ao-2.62
IVSd-7.1mm      IVSs-11.4mm    
LVDd-51.5mm   LVDs-27.9mm    FS-46%
PWd-6.1mm      PWs-10.1
HR-163-177       EPSS-1mm

Assessment: There is moderate to severe left atrial enlargement (2-2.5x normal).
Left ventricular wall thickness is normal in systole and diastole. LV chamber size is moderately to severely increased in diastole, and moderately increased in systole. Contractility (fractional shortening) is increased, consistent with mitral regurgitation. (1,2)
Heart rate is elevated. EPSS is decreased.
There is moderate to severe mitral regurgitation seen on color flow and continuous wave Doppler.
There is mild tricuspid regurgitation seen on color flow and continuous wave Doppler.
Aortic valve was normal. Despite the appearance in M mode that suggests the leaflets were not completely apposed in diastole, there was no aortic insufficiency noted.
Pulmonic valve showed very slight thickening on one of the leaflets. There was no insufficiency or congenital structural abnormalities noted.
Atrial septum and ventricular septum were bowed in appearance due to the volume overload on the left, but there were no septal defects.

 SUMMARY:

1. Severe mitral and mild tricuspid regurgitation secondary to chronic degenerative valvular disease, which is causing significant left atrial enlargement and left ventricular volume overload.
2. Left sided heart failure secondary to #1. (3,7,8)
3. Small volume pericardial effusion and no evidence of neoplasia. This appears secondary to congestive heart failure. (4) This was not enough to cause significant tamponade or other signs of right heart failure.

Treatment recommendations were to start Furosemide at 2.2 – 4.4mg/kg BID and Enalopril at 0.5mg/kg SID until the pulmonary edema has cleared, then the Furosemide can be reduced to the lowest effective dose. Additional medications were considered, but with the clients’ disabilities, it was decided to keep it to the most effective and simple treatment protocol. Close client follow up was also recommended. Ideally, a recheck exam in 3-7 days, sooner if coughing did not improve, is recommended to adjust dosages according to clinical response and client’s abilities.

The client received the medications with SID dosages on both labels. It is unclear if this was a mistake in labeling, or if the primary clinician decided that this would be more appropriate. They received a 30 day supply of the Furosemide at 12.5mg dose, and a 60 day supply of the 5mg enalopril. A request for refills of the medications was granted on 3/5/07. The report from the daughter at time is that Mohei is doing well and is back to his old self.  The recommendation at the time of the refills was to return for a recheck exam. The staff called on 4/20/07 with another reminder for this. No further entries have been made in the medical notes.

This is a good example of how some dogs with congestive heart failure can occasionally respond very well to minimal medical management. Since this is not the norm, my treatment recommendations will not be altered in future cases.

Degenerative (or myxomatous or chronic) mitral valve disease has been shown to be a hereditary disease in cavalier King Charles spaniels. (3, 5, 6, 9,) Male dogs have a lower threshold, so they tend to develop the disease earlier than females of this breed (5,6).  Chronic mitral valve disease is seen in 100% of dogs of this breed over 10 years of age, and in 56% of dogs over 4 years of age in one study. (9) Mitral valve prolapse is a common component of the disease in this breed, and has been noted as an early sign of the disease process that leads to mitral regurgitation. The degree of mitral regurgitation correlates positively with the murmur intensity, left ventricular end diastolic diameter, and left atrial diameter. (6)

Myxomatous degeneration may be detected on any of the four intracardiac valves. In Mohei’s case, there was evidence of it on the mitral valve most significantly, the tricuspid valve, and a very subtle suggestion of it seen even on the pulmonic valve. The incidence of valve involvement in dogs was found to be 62% of mitral valve alone, 32.5% incidence of mitral and tricuspid valves, and 1.3% incidence on the tricuspid valve alone. The pulmonic and aortic valves are less commonly affected. (5)

The other interesting finding in Mohei’s case was that of thrombocytopenia and macrothrombocytes. The association between this syndrome and mitral valve disease is reported in this breed, but the correlation does not appear direct. The macrothrombocytopenia shows an autosomal recessive inheritance pattern in this breed. (10) Platelet function correlated negatively to mitral valve regurgitation, in that there is decreased platelet aggregation with MR. (11)

1. Boon JA Manual of Veterinary Echocardiography Baltimore: Lippincott Williams and Wilkins, 1998.
2. Bonagura JD, O’Grady MR, Herring DS: Echocardiography: principles of interpretation Vet Clin North Am Small Anim Pract 15:1177, 1985
3. Kittleson MD: Myxomatous Atrioventricular Valvular Degeneration. In Kittleson MD, Kienle RD, eds:  Small Animal Cardiovascular Medicine St. Louis, 1998, Mosby.
4. Kienle RD: Pericardial Disease and Cardiac Neoplasia. In Kittleson MD, Kienle RD, eds:  Small Animal Cardiovascular Medicine St. Louis, 1998, Mosby.
5. Haggstrom J, Pedersen HD, Kvart C: New insights into degenerative mitral valve disease in dogs, Vet Clin North Am Small Anim Pract 34:1209-1226, 2004
6. Pedersen HD, Lorentzen KA, Kristensen BO: Echocardiographic mitral valve prolapse in cavalier King Charles spaniels: epidemiology and prognostic significance for regurgitation. Veterinary Record 144:315-320, 1999.
7. Kienle RD: Classification of Heart Disease by Echocardiographic Determination of Functional Status. In Kittleson MD, Kienle RD, eds:  Small Animal Cardiovascular Medicine St. Louis, 1998, Mosby.
8. Kittleson MD: Pathophysiology of Heart Failure. In Kittleson MD, Kienle RD, eds:  Small Animal Cardiovascular Medicine St. Louis, 1998, Mosby.
9. Beardow AW, Buchanan JW. Chronic mitral valve disease in Cavalier King Charles Spaniels: 95 cases (1987-1991). J Am Vet Med Assoc 203:1023-1029, 1993.
10. Singh MK, Lamb WA. Idiopathic thrombocytopenia in Cavalier King Charles Spaniels. Aust Vet J. 83(11):700-703, 2005.

News

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Certificate:
Drs. Bossung, Lindquist and Miller have successfully completed the IVUSS Ultrasound Certificate Program, which includes didactic training, case submission, practical exam and a written final examination.

Congratulations Amy, Eric and Chris!