DESPITE medical progress in its diagnosis and treatment, acute pulmonary embolism (APE) remains an important cause of mortality, 30–35% in the absence of treatment, with delay of the diagnosis remaining the main cause of death from APE.1Spiral computed tomography as well as transthoracic echocardiography and/or transesophageal echocardiography (TEE) have become fast and successful examinations in the diagnostic strategy for this affliction.2We report two cases of bilateral APE without hemodynamic instability but complicated by the discovery of a thrombus trapped in a patent foramen ovale (FO) and floating on both sides in the right and left atrium. We also discuss the various therapeutic modalities.
A 73-yr-old woman was hospitalized after sudden onset of dyspnea. She had a medical history of recent discovery of an ovarian mass in the course of clarification, complicated with lower limb phlebitis treated by low-molecular-weight heparin for some days. At admission, her arterial blood pressure was 110/75 mmHg, with a pulse rate of 105 beats/min and a respiratory rate of 20 breaths/min. Laboratory findings showed hypoxemia at 65 mmHg, hypocapnia at 30 mmHg, and plasma D-dimers increased at 5 μg/ml. With the exception of a sinus tachycardia, the electrocardiogram was normal, and Doppler echography of the lower limbs confirmed left deep venous thrombosis. Pulmonary spiral computed tomography showed bilateral central APE. TEE showed normal right and left ventricular function but also revealed a snake-like thrombus trapped in the FO and floating in both atria. After insertion of a vena cava filter by the femoral route, the patient underwent an emergent surgical thrombectomy during cardiopulmonary bypass with closure of the FO. The patient's postoperative course was simple, and she left the intensive care unit after 5 days.
A 48-yr-old woman was admitted for acute dyspnea, hemoptysis, and chest pain for 3 days. Her arterial blood pressure was stable at 120/80 mmHg, and her respiratory rate was 30 breaths/min. The electrocardiogram showed a sinus tachycardia of 120 beats/min without S1Q3 pattern. Laboratory findings were hypoxemia at 60 mmHg, hypocapnia at 28 mmHg, and plasma D-dimers increased at 7.8 μg/ml. Spiral computed tomography confirmed clots in the main pulmonary artery and its right and left branches. The Doppler echography of the lower limbs revealed a right popliteal and posterior-tibial deep venous thrombosis without any floating thrombus in the femoral vein; therefore, intravenous heparin therapy was initiated. The next day, routine transthoracic echocardiography showed normal right and left cardiac function but also revealed a mobile structure in the right atrium. TEE confirmed the presence of a long serpentine thrombus trapped in the FO and floating in both the right and left atria (fig. 1). The patient was then transferred to our institution and, after deployment of an inferior vena cava filter by the femoral route, underwent surgical thrombectomy during cardiopulmonary bypass with closure of the FO. A 20-cm-long thrombus was removed from the FO (fig. 2), and others were removed from the pulmonary network. The patient's course was simple, and she left the intensive care unit after the third postoperative day.
The diagnosis of APE remains a challenge for physicians. Lorut et al. 2showed that the combination of ventilation/perfusion lung scan, spiral computed tomography, dosage of plasma D-dimer, and, in some cases, lower limb venous Doppler echography was an effective and noninvasive strategy to confirm APE. Echocardiography (transthoracic echocardiography and/or TEE) is a useful additional examination for the diagnosis of APE, particularly in hemodynamically unstable patients. Echocardiographic abnormalities are indirect signs of pulmonary arterial hypertension and right heart failure signs, which are right cavity dilation, hypokinetic right ventricle, and interventricular septum flattening, with even paradoxical motion.3,4Embolized thrombus visualization in the right cavities is rare, and its precise incidence is not known. Three types of thrombus can be identified according to their morphology, their origin, and their clinical meaning. The first one, type A, is an intracardiac floating thrombus, serpentine and highly mobile, which can even get through the tricuspid valve or even the pulmonary valve during cardiac beats. Type A thrombus is seen in patients with deep venous thrombosis and corresponds to the migration of a peripheral thrombus. The second type of intracardiac thrombus, type B, is similar to the thrombus of the left cavities and is rather well fixed to the cardiac walls. This thrombus is rarely associated with peripheral deep venous thrombosis but is generally seen in patients with cardiac, potentially thrombogenic, pathologies such as heart failure with cardiac blood flow stasis. Finally, type C is unlike type A, because it does not have the shape of a snake, and unlike type B, because it is very mobile and looks like a myxome.5The short-term prognosis of patients with type A thrombus is significantly worse than those with type B. In type A, early mortality (< 8 days) related to the thrombus is 40%, versus only 9% for type B. Therefore, discovery of an intracardiac type A thrombus must be considered as a real emergency, and treatment must be initiated immediately. The cause of death for type A is generally a massive and quickly fatal embolism, which is rarely the case for type B. Mortality is intermediate with intracardiac type C thrombus.5
We think that the systematic performance of TEE in all patients presenting with central APE, even those without hemodynamic compromise, is a minimally invasive and safe examination that would allow the early detection of an intracardiac floating thrombus and would allow one to choose the best therapeutic option. Echocardiographic studies including patients presenting with APE estimate the presence of an intracardiac floating thrombus from 3 to 23%, with, in these cases, short-term significant increased mortality of 26–50%, which is sharply superior to the 8–10% mortality associated with “isolated” APE.6–8Intracardiac tumor, vegetation, interatrial aneurysm, and embryonic remainder, such as the Chiari network, which is an embryologic membrane extending from the ostium of the inferior vena cava and the coronary sinus to the interatrial septum and the tricuspid valve or the thebesian and eustachian valves, are the main differential diagnoses to exclude.7–9
The prognosis of a typical type B thrombus is good, and intravenous heparin therapy is generally sufficient. However, there is currently no consensus for the ideal therapeutic management of APE associated with type A thrombus, and data in the literature vary greatly. On the basis of a comparable mortality for intravenous heparin therapy, systemic fibrinolysis, or surgical thrombectomy, Kinney and Wright10concluded in 1989 that intravenous heparin therapy was the first treatment of choice. Later, Rose et al. 5reviewed all of the cases of intracardiac thrombus published in the English-speaking literature between 1966 and 2000 that included sufficient clinical data. They thus analyzed 177 patients, among whom 98% presented with APE. The mortality rates associated with the absence of treatment, with anticoagulation therapy, with surgical thrombectomy, and with fibrinolysis were 100, 29, 24, and 11%, respectively, which suggests that thrombolytic treatment is the treatment of choice in the absence of any contraindication. However, it is important to note that the great majority of the reported cases corresponded to right cavity floating thrombi and that the rate of thrombus entrapped through the FO was extremely weak, even not clarified. It was not possible for us to find specific recommendations in the therapeutic management of these particular cases with high risks not only of pulmonary embolism but also of paradoxical embolism.11,12Given the high risks of massive pulmonary and systemic embolism, we chose the surgical option for the patients in these cases. This choice also allowed resection of the intracardiac thrombus, treatment of the clots located in the pulmonary arterial trunk and its main branches, and closure of the FO. Intravenous anticoagulation therapy with heparin was then introduced immediately in the postoperative period. We chose to use a vena cava filter in these two patients, but we recognize that there is considerable debate on this issue. The recognized indications are the extension of venous thrombosis or an ongoing pulmonary embolism in appropriately treated patients for more than 48 h and contraindications to anticoagulant therapy, whereas temporary filters may be discussed immediately after surgical embolectomy because of the increased risk of bleeding during the first 24–72 postoperative hours with full intravenous heparin therapy.13