History
A 10-year-old spayed female domestic shorthair cat was evaluated because of acute-onset dyspnea. The cat had been treated for chronic kidney disease with daily SC administration of fluids for several years. On physical examination, the cat had pale mucus membranes and a thyroid nodule and was 5% dehydrated. The cat was dyspneic and tachycardic with a prominent cardiac gallop, dull lung sounds, and weak, synchronous pulses. The cat was thin and hypothermic with small, irregular kidneys on abdominal palpation.
Abnormalities detected on hematologic evaluation included azotemia (BUN concentration, 179 mg/dL [reference range, 15 to 34 mg/dL]; serum creatinine concentration, 4.3 mg/dL [reference range, 0.8 to 2.3 mg/dL]), hyperphosphatemia (phosphorus, 12.8 mg/dL; reference range, 3.0 to 7.0 mg/dL), hypokalemia (potassium, 2.9 mEq/L; reference range, 3.9 to 5.3 mEq/L), and anemia (Hct, 25%; reference range, 29% to 45%). The cat had a urine specific gravity of 1.014 (inactive sediment), a serum total thyroxine concentration of 4.4 μg/dL (reference range, 0.5 to 4.7 μg/dL), and a serum free thyroxine concentration > 10.0 ng/dL (reference range, 1.2 to 4.3 ng/dL). The cat's serum calcium-phosphorus concentration product was 123 mg2/dL2. Thoracic radiographs were obtained (Figure 1).
Right lateral (A) and ventrodorsal (B) radiographic views of the thorax of a 10-year-old spayed female domestic shorthair cat with acute-onset dyspnea obtained prior to thoracocentesis.
Citation: Journal of the American Veterinary Medical Association 245, 1; 10.2460/javma.245.1.45
Right lateral (A) and ventrodorsal (B) radiographic views of the thorax of a 10-year-old spayed female domestic shorthair cat with acute-onset dyspnea obtained prior to thoracocentesis.
Citation: Journal of the American Veterinary Medical Association 245, 1; 10.2460/javma.245.1.45
Right lateral (A) and ventrodorsal (B) radiographic views of the thorax of a 10-year-old spayed female domestic shorthair cat with acute-onset dyspnea obtained prior to thoracocentesis.
Citation: Journal of the American Veterinary Medical Association 245, 1; 10.2460/javma.245.1.45
Determine whether additional imaging studies are required, or make your diagnosis from Figures 1—then turn the page →
Diagnostic Imaging Findings and Interpretation
Pleural effusion is evident; cardiomegaly is suspected on the basis of tracheal elevation and an increase in the carinal-to-apical dimension of the heart. The pulmonary parenchyma appears to be retracted from the thoracic wall. Moderate pulmonary atelectasis and mineralization of the left ventricular myocardium are evident.
Thoracocentesis to remove plural fluid was performed; post-thoracocentesis thoracic radiography revealed a marked decrease in the pleural effusion and a mild, iatrogenic pneumothorax as well as mild, generalized cardiomegaly. Radiographic evidence of cardiac mineralization was unchanged (Figure 2).
Right lateral (A) and ventrodorsal (B) radiographic views of the thorax of the same cat as in Figure 1 that were obtained after thoracocentesis, which yielded 250 mL of fluid (modified transudate). Notice mineralization of the myocardium (arrows), pleural effusion, and mild, generalized cardiomegaly.
Citation: Journal of the American Veterinary Medical Association 245, 1; 10.2460/javma.245.1.45
Right lateral (A) and ventrodorsal (B) radiographic views of the thorax of the same cat as in Figure 1 that were obtained after thoracocentesis, which yielded 250 mL of fluid (modified transudate). Notice mineralization of the myocardium (arrows), pleural effusion, and mild, generalized cardiomegaly.
Citation: Journal of the American Veterinary Medical Association 245, 1; 10.2460/javma.245.1.45
Right lateral (A) and ventrodorsal (B) radiographic views of the thorax of the same cat as in Figure 1 that were obtained after thoracocentesis, which yielded 250 mL of fluid (modified transudate). Notice mineralization of the myocardium (arrows), pleural effusion, and mild, generalized cardiomegaly.
Citation: Journal of the American Veterinary Medical Association 245, 1; 10.2460/javma.245.1.45
Echocardiography revealed scant pleural effusion with left and right atrial enlargement. There was hyperechogenicity with hyperattenuating foci throughout the left ventricle and portions of the right ventricle (likely representing the mineralized areas seen on radiographs) as well as mild tricuspid insufficiency (Figure 3).
Right parasternal short-axis echocardiographic image of the heart of the same cat as in Figure 1. Notice the hyperechoic and hyperattenuating foci in the interventricular septum (arrows) and left ventricular free wall, consistent with myocardial mineralization. Image was obtained with a phased-array multifrequency-transducer, 5-MHz probe.
Citation: Journal of the American Veterinary Medical Association 245, 1; 10.2460/javma.245.1.45
Right parasternal short-axis echocardiographic image of the heart of the same cat as in Figure 1. Notice the hyperechoic and hyperattenuating foci in the interventricular septum (arrows) and left ventricular free wall, consistent with myocardial mineralization. Image was obtained with a phased-array multifrequency-transducer, 5-MHz probe.
Citation: Journal of the American Veterinary Medical Association 245, 1; 10.2460/javma.245.1.45
Right parasternal short-axis echocardiographic image of the heart of the same cat as in Figure 1. Notice the hyperechoic and hyperattenuating foci in the interventricular septum (arrows) and left ventricular free wall, consistent with myocardial mineralization. Image was obtained with a phased-array multifrequency-transducer, 5-MHz probe.
Citation: Journal of the American Veterinary Medical Association 245, 1; 10.2460/javma.245.1.45
Treatment and Outcome
At the time of initial evaluation, the cat was treated with furosemide (2.0 mg/kg [0.91 mg/lb], IV, q 8 h) and supplemental oxygen via an oxygen cage. Thoracocentesis yielded 250 mL of fluid (modified transudate).
Treatment with methimazole (0.50 mg/kg [0.23 mg/lb], PO, q 12 h) and aluminum hydroxide (8.0 mg/kg [3.64 mg/lb], PO, q 8 h) as well as oral administration of a potassium supplement was initiated. Treatment with pimobendan (0.25 mg/kg [0.11 mg/lb], PO, q 12 h) and enalapril (0.25 mg/kg, PO, q 24 h) was started after the echocardiogram was obtained. The amount of fluids administered daily SC was reduced. The cat did well with treatment for 8 months, at which time it was euthanized because of progressive renal failure.
Comments
Abnormal mineralization of the heart or aorta has been reported for several species, including cats, dogs, and cows.1–3 Soft tissue calcification can be idiopathic, dystrophic, or metastatic. Idiopathic calcification occurs without tissue injury or abnormal calcium-phosphorus metabolism.1,2 Dystrophic calcification can develop in injured tissue even when the calcium and phosphorus serum concentrations are within reference range.1,4
Metastatic calcification refers to calcium deposition in previously uninjured soft tissue due to a disorder in calcium-phosphate metabolism.4–6 Metastatic calcification is the most common form of soft tissue mineralization found in small animals and occurs with high serum concentrations of calcium, phosphorus, or both (serum calcium-phosphorus concentration product > 70 mg2/dL2).1 Metastatic calcification may be due to malignant or nonneoplastic conditions such as chronic renal failure, hyperparathyroidism, hypervitaminosis D, hypertension, bone disease, or blastomycosis.1,3,4 Unknown factors related to the individual's metabolism may also play a role, as not all animals with risk factors experience this phenomenon. Unfortunately, normalization of the serum calcium-phosphate concentration product does not always prevent or reverse the calcium deposits.7
In humans, calcium deposition within the myocardium is most commonly found on the anterior wall of the left ventricle toward the cardiac apex.7 In dogs, the most common area of mineralization is the ascending aorta followed by the caudal cardiac silhouette.2 Cardiac mineralization in cats is rare and therefore a common pattern of occurrence is not well characterized, although there are multiple reports1 of mineralized arteriosclerosis in cats secondary to systemic hypertension. The cat of the present report had diffuse mineralization throughout the left ventricle and portions of the right ventricle. Computed tomography is the gold standard for diagnosing this type of cardiac calcification.5,7 Calcium deposits can be associated with cardiac dysfunction or death, and coronary arterial calcium deposits are used as a marker of severity of coronary disease in humans.7
The cat of the present report appeared to have metastatic calcification of the myocardium owing to the longstanding hyperphosphatemia associated with chronic renal failure. It was thought the areas of ventricular mineralization were impairing systolic and likely diastolic function, leading to congestive heart failure
1. Lefbom BK, Adams WH, Weddle DL. Mineralized arteriosclerosis in a cat. Vet Radiol Ultrasound 1996; 37: 420–423.
2. Schwarz T, Sullivan M, Stork CK, et al. Aortic and cardiac mineralization in the dog. Vet Radiol Ultrasound 2002; 43: 419–427.
3. Lofstedt J, Hogan PM, Bildfell RJ, et al. Radiographic diagnosis of a calcific aortic arteriosclerosis in a Jersey cow. Can Vet J 1996; 37: 432–433.
4. Chan ED, Morales DV, Welsh CH, et al. Calcium deposition with or without bone formation in the lung. Am J Respir Crit Care Med 2002; 165: 1654–1669.
5. El-Bialy A, Shenoda M, Saleh J, et al. Myocardial calcification as a rare cause of congestive heart failure: a case report. J Cardiovasc Pharmacol Ther 2005; 10: 137–143.
6. Tam KF, Wang K, Fan WC. Metastatic calcification. J HK Coll Radiol 2002; 5: 186–189.
7. Catellier MJ, Chua GT, Youmans G, et al. Calcific deposits in the heart. Clin Cardiol 1990; 13: 287–294.
