Background: Pseudoaneurysm of the mitral-aortic intervalvular fibrosa (P-MAIVF) is an unusual complication related to various injuries or conditions which involve the mitro-aortic region; it communicates with the left ventricular outflow tract and is associated with a high-risk of redoubtable complications or sudden death. The cerebral and splenic localizations are frequently seen as manifestations of systemic embolism in infective endocarditis. Currently, there are no specific recommendations related to the diagnosis, management, treatment, or further evolution of patients with P-MAIVF and concomitant splenic infarction. This paper presents the case of a 43-year-old Caucasian woman with a late diagnosis of mixed bicuspid aortic valve disease, affected by an under-detected and undertreated episode of infective endocarditis leading to asymptomatic P-MAIVF. Prime clinical and imagistic diagnosis of splenic infarction indicated further extended investigations were required to clarify the source of embolism. Methods: Integrated multimodality imaging techniques confirmed the unexpected diagnosis of P-MAIVF. Results: The case had a fatal outcome following an uncomplicated yet laborious cardiac surgery. Patient death was attributed to a malignant ventricular arrhythmia. Conclusion: The present case raises awareness by highlighting an unexplained and unexpected splenic infarction association with P-MAIVF as a result of infective endocarditis related to mixed bicuspid aortic valve disease.

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The presence of the Fip1-Like1-platelet-derived growth factor receptor alpha (FIP1L1–PDGFRα) fusion gene represents a rare cause of hypereosinophilic syndrome (HES), which is associated with organ damage. The aim of this paper is to emphasize the pivotal role of multimodal diagnostic tools in the accurate diagnosis and management of heart failure (HF) associated with HES. We present the case of a young male patient who was admitted with clinical features of congestive HF and laboratory findings of hypereosinophilia (HE). After hematological evaluation, genetic tests, and ruling out reactive causes of HE, a diagnosis of positive FIP1L1–PDGFRα myeloid leukemia was established. Multimodal cardiac imaging identified biventricular thrombi and cardiac impairment, thereby raising suspicion of Loeffler endocarditis (LE) as the cause of HF; this was later confirmed by a pathological examination. Despite hematological improvement under corticosteroid and imatinib therapy, anticoagulant, and patient-oriented HF treatment, there was further clinical progression and subsequent multiple complications (including embolization), which led to patient death. HF is a severe complication that diminishes the demonstrated effectiveness of imatinib in the advanced phases of Loeffler endocarditis. Therefore, the need for an accurate identification of heart failure etiology in the absence of endomyocardial biopsy is particularly important for ensuring effective treatment.

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Blood platelets are pivotal cells in the process of hemostasis and thrombosis. In the majority of patients with severe liver disease, platelet function appeared defective. We determinate platelet adhesiveness, aggregability and MDA level, in rats with acute and chronic hepatopathy induced by CCl4 administration. Our data relieves that platelet functions are not only affected in chronic toxic affectation, but also in acute intoxication (p[0.05). Icosanoids production (expressed in MDA levels) are significantly decreased only in chronic CCl4 intoxication (p[0.001). Significant correlation appears between aggregability and MDA (r = -0.78) and adhesiveness and MDA (r = -0.57) in group C, with chronic CCl4 intoxication. The complexity of these platelet functions related to the hepatic disease is still a matter of debate and needs further investigation.