Case Studies In Small Animal

Cardiovascular Medicine

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Case 18

Case Discussion

Grey was hospitalized and treated for his heart failure and diabetes mellitus. He responded poorly to therapy so the owner opted for euthanasia. Grey had been diagnosed as having restrictive cardiomyopathy over one year before his final visit. During that time he had problems with a chylous pleural effusion that was managed by performing intermittent pleurocenteses and administering Lasix and enalapril. One of the pleurocenteses had been performed at the UCD VMTH on the cat's first visit. On his second visit, Grey not only had pleural effusion but also had ascites and diabetes mellitus. His radiographs showed massive atrial enlargement and a very distended caudal vena cava. The echocardiographic examination revealed massive biatrial enlargement with ventricles that were normal to small (left) and mildly enlarged (right). This combination (nearly normal ventricles and large atria) are commonly the basis for diagnosing restrictive cardiomyopathy. Grey also had tricuspid regurgitation. It appeared that the regurgitant orifice was so large that he had laminar, rather than turbulent flow, across his tricuspid valve in systole. His tricuspid valve did not appear to be anatomically abnormal so the suspicion was that the regurgitation was secondary to other cardiac disease. He also had spontaneous contrast or echocardiographic "smoke." This occurs when red cell velocity decreases to a critical value and the red cells clump. One can readily see why the red cell velocity through the enlarged atria would be decreased. This is the same as what happens when a river widens in an area - flow velocity slows. Spontaneous contrast predisposes people, and probably cats, to developing a thrombus. In cats these usually form in the left atrium.

There was one additional abnormal diagnostic test in Grey - his ECG. First, he had no P waves. The lack of P waves in all leads is diagnostic of atrial standstill. Second, his heart rate was slow at 120 beats/minute. The normal feline AV node appears to depolarize at a rate between 90 and 120 beats/minute so the rate in this cat is compatible with a nodal escape rhythm. A nodal escape rhythm is common with atrial standstill. Third, the terminal (i.e., last) portion of his QRS complexes were oriented toward his head. It was difficult to tell if this was a terminal right or left axis deviation but was certainly abnormal. Consequently, the diagnosis in Grey was atrial standstill with a ventricular conduction abnormality. By far the most common cause of atrial standstill in a cat is severe hyperkalemia but Grey's serum potassium concentration was only mildly increased. In dogs, atrial standstill can also be caused by complete or almost complete loss of atrial myocardium where the myocardium is replaced by fibrous tissue. We had seen one case of this type of atrial standstill in a cat within the previous year so we were suspicious that Grey also had this abnormality, not restrictive cardiomyopathy. Pictures from the postmortem examination are below. In the top two pictures, the heart was filled with ultrasonic gel. It's blue color can be seen through the thin, translucent atrial walls.

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Right atrium and ventricle                                                     Left atrium and ventricle

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The bottom pictures were taken after the heart was opened and the gel washed out. The pathology pictures confirm the diagnosis of atrial standstill due to loss of atrial myocardium. One can readily appreciate that the only myocardium remaining in either atria is in the auricles. The body of both atria are made up purely of fibrous connective tissue. Since there was no atrial myocardium to depolarize, there were no P waves on the electrocardiogram. The sinoatrial (SA) node in Grey may have still been functional but since there was no myocardium or conduction pathways left between the SA and AV nodes, any SA node depolarization would have been unable to conduct to the AV node and beyond. Consequently, the AV node would have controlled Grey's heart rate and rhythm. Similarly, the SA node could have been destroyed by the same disease process that destroyed the atrial myocardium which again would have forced the AV node to take over the pacing function of the heart.

 

Mark D. Kittleson, D.V.M., Ph.D. All rights reserved.