Cardiac hydatidosis: a follow-up with cardiovascular magnetic resonance.

We present a case of a 38-year–old Turkish patient with a previously diagnosed cardiac hydatidosis, which is a parasitic infection most commonly induced by Echinococcus granulosus and with only rare cardiac involvement (0.5%– 2.0%). In 1998, the patient survived a cardiogenic shock caused by the rupture of 1 hydatic cyst and concomitant cardiac tamponade. Postsurgery, the patient was treated pharmacologically with albendazole. In 2006, a cardiac magnetic resonance and a computed tomography examination showed recurrent myocardial cystic formations (Figure 1). Disadvantageously, the largest cyst was located in the inferior wall of the left ventricle in close vicinity to the mitral valvular apparatus. An interdisciplinary conference came to the conclusion to neither treat the patient surgically, because of an extensive myocardial and perivalvular defect, nor pharmacologically with albendazole, because even anthelmintic medical intervention would have borne the risk of weakening the cystic wall and causing wall rupture. From 2006 to 2012, noninvasive clinical follow-up showed no major complications. In the last evaluation in 2012, the patient was asymptomatic, the ECG showed Q waves in the inferior wall (Figure 2), and the echocardiogram revealed the presence of the lesion, without clear demonstration of its morphology, however (Figure 3). In contrast, cardiac magnetic resonance illustrated morphological features of the cyst in greater detail and gave clear evidence of a cyst transformation from a World Health Organization (Table) type1 CE2, an active cyst with multivesicular, multiseptated, rosette-like or honeycomb-like aspect (Figure 4A through 4F), into a CE3B cyst, a transitional cyst with daughter cysts in a solid matrix (Figure 4G through 4J). Rapidly, only within 8 weeks, the lesion showed a marked cyst regression into an almost inactive CE4 form. Moreover, late gadolinium enhancement images showed a fibrous capsule surrounding the lesion, which might represent an inflammatory response contributing to the favorable evolution of the disease (Figure 5). With this report, we demonstrate a follow-up of a patient with cardiac hydatidosis in whom neither the published previously surgical treatment nor an anthelminthic therapy2 could be performed, but who nevertheless showed cystic