358 A POSSIBLE RARE CASE OF VENTRICULAR LIPOMATOSIS: A STIMULUS FOR A PANORAMA OF FATTY CARDIAC LESIONS

Abstract

Abstract We exhibit the case of a 75 years-old man who undertook cardio-oncological assessment for Non-Hodgkin Lymphoma: baseline echo revealed typical features of lipomatous hypertrophy of the interatrial septum (LHIS) and an apical hypoechoic left ventricle (LV) lesion. Five years before, the patient performed MRI (Magnetic Resonance Imaging), which confirmed LHIS, but superabundant epicardial fat extended to the right ventricle and the apical junction between the two ventricles, both characterized by normal ejection fraction, and surrounded the origin of the pulmonary trunk. LV lateral and inferior walls presented lipomatous metaplasia foci and no history or ECG sign of previous myocardial injury could be pointed out. A slight band of late gadolinium enhancement at the basal infero-lateral wall of LV was highlighted. The patient referred episodes of fainting: the Holter-ECG showed pronounced bradycardia which couldn't be explained by other secondary causes. So a bicameral pace-maker was implanted. During our ambulatory evaluation, we decided to repeat MRI, which showed no difference in comparison with the previous one, so excluding malignant degeneration of the fatty mass surrounding the heart. Despite older age and the lack of sudden cardiac death family history we searched for pathognomonic arrhythmogenic cardiomyopathy (ACM) mutations. In consideration of the new evidence of the metabolic risk associated with abundant epicardial fat (EF) we asked for updated laboratory dosage of plasma glucose, LDL cholesterol and triglycerides and we recommended stricter control of blood pressure. From 4% to 52% of cardiac mass is made up of fat but only EF interacts with myocardium and coronary arteries. Anomalous growth of fat in the heart can present itself as LHIS, excessive lipomatous infiltration or cardiac lipomas (real capsulated tumors) but also ACM is histologically characterized by fibrofatty replacement of cardiomyocites. Overabundant and inflammed EF is now considered a surrogate of metabolic risk and is associated with multivessel coronary disease, the finding of chronic total occlusions (CTO) and microvascular angina. Identifying fatty heart lesions and defining their clinical and prognostic role remains an intriguing challenge. We suggest a general binary way to follow: the “mechanic one” for lipomas or lipomatous infiltration, that is paying attention to compression phenomena or the generation of arrhythmias, and the “metabolic one”, in other words optimizing cardiovascular prevention when EF is too much. A careful research of imaging features of ACM can't be omitted.