Calcified Amorphous Tumor-Induced Acute Cerebral Infarction

Abstract

SummaryWe report the case of a 38-year-old woman who was admitted for acute cerebral infarction linked to a cardiac calcified amorphous tumor (CAT) and related mitral annular calcification (MAC). The cardiac mass was removed, and mitral valve replacement surgery was performed. Pathological examination revealed an amorphous accumulation of degenerating material within both lesions, indicating that build-up of calcium along the mitral annulus and subsequent rupture of the fibrotic tissue may be involved in the initiation and progression of CAT.(Int Heart J 2018; 59: 240-242) Key words: Cardiogenic cerebral embolism, Echocardiography, Cardiac tumor C alcified amorphous tumor (CAT), first described by Reynolds, et al 1) in 1997, is a non-neoplastic cardiac tumor, and reports of some cases have suggested that CAT can cause cerebral infarction. The etiology of CAT remains unknown. CAT can arise from any of the four chambers of the heart or any of the four annuli. Most CATs originating from the mitral valve are related to extensive mitral annular calcification (MAC). 2-5)Regardless of the features of the CAT, including its site of origin, surgical excision is usually necessary. 6)Although CAT and MAC are related, there has been no reported histologic comparison of these two clinical entities. We encountered a MAC-related CAT that was responsible for a patient's cerebral infarction and also informative in terms of the tumor etiology. Case ReportA 38-year-old woman was referred to our hospital with acute right hemiplegia. She had been undergoing hemodialysis for 31 years because of chronic kidney failure resulting from systemic lupus erythematosus and secondary nephrotic syndrome and had been treated at various times with prednisolone, precipitated calcium carbonate, bixalomer, and/or cinacalcet hydrochloride. Her medical history also included rupture of a colonic diverticulum. Upon admission to our hospital, a systolic murmur was heard at the cardiac apex, and right hemiplegia with motor aphasia was observed. Brain magnetic resonance imaging showed acute cerebral infarction in the middle cerebral artery territory. Electrocardiography showed sinus tachycardia at 110 bpm.Both transthoracic echocardiography and transesophageal echocardiography revealed enlargement of the left atrium (50 × 42 mm), concentric left ventricular (LV) hypertrophy (LV mass index, 130 g/m 2 ; relative wall thickness, 0.50), mild mitral regurgitation, and a mobile cord-like structure and MAC at the middle part of the anterior leaflet ( Figure 1A, B). LV systolic function was normal with an LV ejection fraction of 67%, and LV wall motion was within normal range. No other potential source of cerebral embolism, such as a thrombus in the left atrial appendage, a patent foramen ovale, or an atrial septal aneurysm, was seen, there was no spontaneous echo contrast, and there were no physiologic or laboratory findings suggestive of infective endocarditis. No coronary artery stenosis was seen upon coronary angiography. The mobile cord-like structure was t...

Calcified amorphous tumor presenting with rapid growth in the ascending aorta

“…The best treatment strategy is controversial. However, there were several reports showing embolism from CAT 5,6 , so resecting the tumor as soon as possible is thought to be justified.…”