Stimpy is a seven year-old neutered male Persian cat presented to you for breathing difficulty.  Stimpy's owner says that he has been "...breathing really hard for the past few days and that he doesn't want to get out of the box he sleeps in."

Physical examination reveals a depressed, lethargic patient with abdominal distension. Palpation indicates ascites.  Stimpy's respiration is shallow and rapid and shortly after your examination he begins open-mouthed breathing.  You place Stimpy in an oxygen cage to ease his breathing out and calm him down so you can complete your examination. You tell the owner that Stimpy is in serious trouble and that you want to keep him for examination later on.

The owner was prepared to be told this, and has some things in his car. He returns with a blanket for the cat and a bag of food. "It's the only thing he'll eat," the man says.  You look at the bag and realize it's dry dog food.

After an hour in the oxygen cage, Stimpy's breathing has slowed somewhat and he is in much less distress.  You auscult Stimpy's lungs and notice a wet, crackling sound.  His heart sounds are really what you notice: they're severely muffled and you seem to hear a gallop beat.  The femoral pulse is weak and Stimpy's jugular veins appear to be distended. Thoracic radiographs show pleural effusion and a marked cardiomegaly of all four chambers.  The heart has lost its conical shape and looks like a softball.


Stimpy has dilated cardiomyopathy. This is fairly common myocardial disorder of cats whose cause is unknown, but it seems more likely that the disease has a genetic basis, which is certainly the situation in many human patients with this condition.

Dilated cardiomyopathy is a form of congestive cardiac insufficiency in which the heart cannot effectively pump blood to or from the systemic circulation.  In dilated cardiomyopathy the entire heart undergoes an increase in diameter with a concurrent decrease in muscle thickness and contractility. The result is a large, thin, round heart with little ability to pump blood into the lungs or into systemic circulation. Patients develop the symptoms Stimpy had: exercise intolerance, depression, lethargy, and ascites.  The condition is ultimately fatal.

Dilated cardiomyopathy involves both right and left heart failure.  Right failure causes venous stasis and passive congestion upstream from the heart; left failure involves congestion of the lungs and pleural effusion. Signs of right heart failure include distended jugular veins, a palpable jugular pulse, and ascites due to hepatic congestion.  Left heart failure is demonstrated principally through exercise intolerance and respiratory distress because of the diminished oxygenation of the blood.

Diagnosis of heart failure is made by analyzing the patient's history and clinical signs, and through auscultation, radiology, and response to therapy. In addition to the heart, other tissues can be examined for changes associated with heart failure.  Chief among these changes is the accumulation of hemosiderin in the parenchyma of various organs. Indeed, the presence of hemosiderin in the lungs is so closely associated with cardiac insufficiency that alveolar cells found containing the pigment are called "heart failure cells."


Right heart failure results in a pronounced hepatic venous stasis, leading to local hemorrhage and increased levels of erythrocyte destruction.  The destroyed red blood cells release their iron contents which have been taken up by the hepatocytes in the form of ferritin and hemosiderin. The accumulation of these pigments in hepatocytes and the resident macrophages of the liver is easily spotted as a brown granular material in H&E sections and as blue-black granules in the Prussian Blue stain. This condition is called hemochromatosis.

This image shows a sample of a portal drainage region of liver. The basic hepatic structure is retained but the interstitium has been distended by edema and hyperemia, consequences of portal hypertension. Some regions of the parenchyma appear darker than others. These are regions of relatively normal cells that appear darker due to the lighter color of the edematous regions around them. All of these these cells are being subjected to some degree of direct pressure, causing alterations in fuction and metabolism.


This is a closer view of the same region. The edema around the portal vein is easier to see, as is the subtle disturbance of the orderly arrangement of the hepatocytes.

In the image below left you can see small deposits of hemosiderin in the hepatocytes which with the H&E stain the hemosiderin appears a rusty brown color. If you look closely, you can see that the hemosiderin is deposited in discrete amounts and does not fill the cell as lipid or lipofuscin would. Venous drainage sites will always have a higher amount of debris an other accumulations than arterial sites.

At right is a slide of the same sample, stained with Prussian Blue to show iron. Hemosiderin is visible in many hepatocytes. The hemosiderin accumulates in closer to the site of venous drainage because as waste makes its way from the arterial supply through the tissue to the veins, it backs up in this region since the venous return has been compromised by the elevated pressures.

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