Presentamos el caso de una mujer joven, que ingresa en nuestro hospital por dolor torácico de esfuerzo. Se realizó un ecocardiograma de estrés sin objetivar alteraciones de la contractilidad segmentaria en el ventrículo izquierdo, pero si dilatación y datos de sobrecarga de ventrículo derecho, sugestivos de un tromboembolismo pulmonar agudo. El diagnóstico se confirmó posteriormente con un angioTAC de arterias pulmonares. Son muy pocos los casos descritos en la literatura de tromboembolismos pulmonares detectados inicialmente por ecocardiografía de estrés. La paciente tuvo una buena evolución y fue dada de alta con antiocoagulación oral.
We report the case of a 71-year-old man, without any previous history of cardiovascular disease, who was derived to our echocardiography laboratory because of a six-month period of dyspnoea. In the echocardiographic examination, various pleural masses which depended from the left visceral pleura were found, surrounded by, what it seemed, an abnormally located severe anterior pleural effusion, which caused left lung atelectasis (jellyfish sign, complete atelectasis of a lung lobe which floats above a massive pleural effusion) with a less important pericardial effusion (Figure 1). After the echocardiographic findings, a total body Computed Axial Tomography (CAT) scan and a Positron Emission Tomography (PET) were performed, confirming various left pleural implants and a severe left pleural effusion causing a big left lung atelectasis with widespread cervical, thoracic and abdominopelvic adenophaties, suggestive of advanced lymphoma. The cytological exam of the pleural liquid obtained by the thoracentesis procedure, showed a monotonous population of predominantly medium size cells with signs of nuclear indentation compatible with a pleural affection by a germinal center follicular lymphoma. Pleural effusion is a common complication of lymphomas (20-30%) and is considered as one of the factors adversely influencing overall survival, as in most of the cases, serous cavity involvement is part of a disseminated disease process. The thoracic duct obstruction and impaired lymphatic drainage appear to be the primary mechanism for pathogenesis of pleural effusion in Hodgkin´s disease and direct pleural infiltration is the predominant cause in non-Hodgkin´s lymphoma. Because the descending thoracic aorta is interposed between the pericardium anteriorly and the pleura posteriorly, echocardiography may be a useful landmark in the differentiation of posterior effusions. However, sometimes due to the abnormal position of the effusion, it might be difficult to differentiate between pericardial and pleural effusions, with the need, as in our case, to perform a multi-modality imaging study with a CAT and PET scan, followed by a cytological exam, to confirm the diagnosis and to guide the posterior treatment. Finally, we would like to underline the importance of familiarizing ourselves on the basics of pulmonary echocardiography, as these findings are frequent during the performance of echocardiography in our daily practice. Abstract P1735 Figure. Jellyfish sign in pleural effusion
Acute inferior myocardial infarction can be complicated by conduction disorders and/or by extension to the right ventricle (RV). Both situations can resolve with an early percutaneous revascularization. We report a case of a 73-year-old woman, with arterial hypertension, dyslipidemia, and studied by cardiology for atypical chest pain, with several negative ischemia detection tests. She was brought to the Emergency Department due to oppressive chest pain irradiated to the left upper extremity. An electrocardiogram was performed, highlighting a complete atrioventricular block with suprahisian escape and ST segment elevation in inferior leads. Tendency to arterial hypotension and multiple episodes of asymptomatic non-sustained monomorphic ventricular tachycardias as well as self-limiting Torsade de Pointes were registered. The transthoracic echocardiogram (TTE) showed an akinesia circumscribed to the basal segment of the inferior left ventricle wall, a non-dilated RV with akinesia of its anterior wall and a new onset functional and asymmetric severe tricuspid regurgitation (TR) by tethering of the anterior leaflet. It was not possible to estimate the RV-RA gradient by obtaining a dense triangular doppler continuous wave jet contour with early peak. Vena contracta was 7 mm long. An urgent coronary angiography was performed in which the presence of an acute thrombotic occlusion of the proximal segment of the right coronary artery was confirmed. A drug-eluting stent was implanted, with good result. With all this, it was possible to stabilize the patient"s electrical and hemodynamic situation. A TTE was repeated one week after, in which mild to moderate tricuspid regurgitation was observed, coinciding with improvement of the RV systolic function and better mobility of the anterior tricuspid leaflet. Anatomically, the tricuspid valve consists of anterior, septal, and posterior leaflets. Each leaflet is connected via chordae tendineae to the anterior, posterior, and septal papillary muscles of the right ventricle, respectively. The cause of functional TR appears to be tricuspid annular dilatation and tethering of the tricuspid valve leaflets (because of LV failure, pulmonary hypertension, left-to-right shunt, or RV infarction). Primary disorders of the tricuspid valve causing TR are less common. RV myocardial infarction may involve the wall supporting the papillary muscle with resulting tension on the chordae causing TR. The 2D TTE demonstrates incomplete and often asymmetric closure of the tricuspid leaflets with apical displacement of the coaptation point. This phenomenon is similar to that seen with LV myocardial infarction with resulting loss of support of mitral papillary muscle and ischemic mitral regurgitation. We report a case of acute inferior myocardial infarction involving the RV that caused a transient dysfunction of the papillary muscle of the anterior tricuspid leaflet, generating a severe TR that resolved by early revascularization. Abstract P716 Figure. A: severe acute TR. B: few days after
A 67-year-old woman who had previous history of hypertension and hyperlipidemia was referred to the cardiologist because of nonspecific electrocardiographic abnormalities. During physical exam a systolic murmur was detected. Transthoracic echocardiography (TTE) showed aortic valve sclerosis with no evidence of valvular stenosis. An unexpected finding was the presence of a membrane at left atrium (LA) and a transesophageal echocardiography (TEE) was recommended with suspicion of cor triatriatum. No signs of obstruction to LA flow were demonstrable with pulsed-wave or colour Doppler analysis. On 3D TEE imaging, a structure compatible with a left atrial tendon was visualized. To complete the study computed tomography (CT) was performed, revealing the presence of a real membrane dividing the LA into two components, separating the pulmonary veins from the true LA chamber with the left atrial appendage (LAA), being the patient diagnosed of cor triatriatum. Cor triatriatum sinister (CTS) is a rare but well-recognised form of congenital heart disease. It is believed to reflect failure of incorporation of the common pulmonary vein into the LA. Defining the relationship between the CTS membrane and the LAA allows differentiation from a supramitral ring. In CTS, the membrane is located superior to the LAA (between the LAA and pulmonary veins), while a supramitral ring is located inferior to the LAA and is often adherent to, and constitutes part of, the mitral valve leaflets. The diagnosis of CTS may be made at any age. Most cases involve a nonobstructive membrane, diagnosis of which is facilitated by advances in imaging technology. TTE is adequate to define the clinical relevance of CTS but it may be more precisely tailored with cardiac CT or cardiac magnetic resonance (CMR) imaging. This case emphasizes the importance of a multimodality imaging approach. CTS can present as an isolated lesion, but it is more commonly seen in association with other congenital cardiac anomalies (patent foramen ovale, atrial septal defect, patent ductus arteriosus, coarctation of the aorta, persistent left superior vena cava, ventricular septal defect, anomalous pulmonary venous drainage, and a variety of left-sided cardiac abnormalities). Nonobstructive asymptomatic adults do not require intervention. However, onset of any cardiovascular symptom should prompt detailed evaluation. A turbulent jet arising from the opening in an obstructive CTS membrane may produce jet lesions on the structurally normal mitral valve causing damage and secondary mitral regurgitation. Surgical resection is the first line of management for an obstructive membrane in the LA. The development of atrial fibrillation in an individual with nonobstructive CTS may also constitute an indication for surgical resection as the presence of the membrane may increase the risk of thromboembolic events. Abstract P1335 Figure. Cor triatriatum sinister (TTE,3D-TEE,CT)
Interatrial communication is the most common congenital defect found in adulthood, being the most common ostium secundum variety (70-80%). Superior and inferior sinus venosus defects are less usual, found in the 5-10% of cases of interatrial communication and frequently associated with anomalous pulmonary venous return (APVR). These defects are located near the junction of the superior (5%) or inferior (<1%) vena cava with the right atrium, which makes them difficult to diagnose by transthoracic ecocardiography (TTE). Case description: A 44-year-old man who is being followed up in our electrophysiology consulting with suspicion of ARVC (suggestive CMR with no gene found) after an episode of ventricular tachycardia (VT) 11 years ago. Asymptomatic since then under treatment with atenolol, except for an episode of chest pain that required a coronary computed tomography which described an image compatible with a patent foramen ovale and normal coronary arteries. During the follow-up a cardio magnetic resonance (CMR) is performed which showed a severely dilated right ventricle with diskinetic areas, no volume changes since last CMR (5 years ago) and preserved ejection fraction. A small interatrial communication located infero-posteriorly in the septum drawed our attention. Estimated QP/QS was 1.4. After this finding, we reviewed the CT made 4 years ago, where a flow from the left atrium to the right atrium could be seen. We decided to ask for both a transthoracic echocardiography (TTE) and a transesophageal echocardiography (TEE). TTE showed normal left ventricle, a dilated right ventricle with preserved function, no valvulopathies and normal pulmonary pressure. Shunt test with agitated saline was slightly positive after Valsalva maneuver, and QP/QS was again 1.4. TTE showed a small interatrial communication measuring 1.9x0.8cm, next to inferior vena cava`s drainage. Since right ventricle dilation could be due both to the atrial septal defect (ASD) and to the dysplasia, the case was discussed in the heart team, and as the defect was small, QP/QS was 1.4 and pulmonary pressure was normal we adopted a conservative approach. Inferior sinus venosus defects are one of the least common atrial septal defects. They are located in the atrial septum immediately above the orifice of the inferior vena cava and are often associated with partial anomalous connection of the right pulmonary veins. This location makes it difficult to see by means of a common TTE or TEE, and usually as in our case multimodal approach can be very helpful. Usually patients with this kind of atrial septal defect (ASD), signs of significant shunt (right ventricular volume overload, QP/QS≥1.5) and systolic PA pressure less than 50% of systemic pressure (with pulmonary vascular resistance less than one third of the systemic vascular resistance) are suggested for surgery. In this case the possibility of two pathologies overlapping makes it challenging for diagnosis and treatment. Abstract P718 Figure. Multimodal imaging for diagnosis.
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