Detection of right heart thrombi (RHT) in the context of pulmonary thromboembolism (PE) is uncommon (4–18%) and increases the risk of mortality beyond the presence of PE alone. Type A thrombi are serpiginous and highly mobile and are thought to be originated from large veins and captured in-transit within the right heart. Optimal management of RHT is still uncertain. A 79-year-old woman, with a history of recent total hysterectomy with adnexectomy and a Wells procedure, presented to the emergency department following an episode of syncope. Computed tomography revealed bilateral PE and the presence of a right atrial thrombus. Transthoracic echocardiography demonstrated a free-floating type A thrombus in the right atrium, protruding into the right ventricle, and signs of pulmonary hypertension and right ventricle dysfunction. Considering the recent surgery and clinical stability, treatment with heparin alone was decided. Subsequent clinical improvement was observed and echocardiographic follow-up revealed complete thrombus dissolution and complete recovery of right ventricle function. Most authors recommend treatment of PE with RHT with thrombolysis or embolectomy followed by anticoagulation, although evidence is scarce. Individual risk of hemorrhage and operatory-related mortality should be taken into account when defining the treatment strategy especially when benefit is not firmly established.

Cardiomyopathy is a manifestation of mitochondrial cytopathies, but rarely constitutes the dominant feature, especially in adults. We report the case of a 59-year-old male with a personal and maternal history of diabetes and deafness, who presented with cardiomyopathy and kidney disease. We diagnosed the patient as having a mitochondrial cytopathy resulting from the 3243A>G mutation on the tRNA^Leu(UUR) gene in the mitochondrial DNA. The family history, broad spectrum of clinical manifestations and fluctuant clinical course provided clues to the diagnosis. We discuss the possible mechanisms underlying the phenotypic variability and fluctuant clinical course of mitochondrial disorders and the potential usefulness of coenzyme Q10 and L-carnitine in 3243A>G mutation patients.

Mitral and aortic valve aneurysms are uncommon, but the coexistence of both mitral and aortic valve aneurysms in the same patient is a rather unusual finding in the literature. We report a rare clinical case of a patient with both mitral and aortic valve aneurysms and a rupture of the mitral valve aneurysm, as the main echocardiographic manifestations of infective endocarditis. This clinical case emphasizes infective endocarditis as the most frequent cause of valve aneurysms, reminding that this diagnosis should be suspected even in the absence of vegetations. This case demonstrates that transoesophageal echocardiography plays a major role on diagnosis of valve aneurysms, revealing the rupture of the mitral valve aneurysm and defining this rupture as the main mechanism of mitral valve regurgitation. This case also underlines the role of transoesophageal echocardiography on management decisions, allowing a morphological evaluation of the mitral valve and selection of the appropriate surgical strategy.

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