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Serpentine Thrombus Traversing the Foramen Ovale: Paradoxical Embolism Shown by Transesophageal Echocardiography
- Sandra I. Barbour, MD;
- Keith F. Izban, MD;
- Cesar V. Reyes, MD;
- Thomas L. McKiernan, MD; and
- Eric K. Louie, MD
- From Loyola University Medical Center, Maywood, Illinois. Requests for Reprints: Eric K. Louie, MD, Division of Cardiology, Loyola University Medical Center, Building 110, Room 6228, 2160 South First Avenue, Maywood, IL 60153. Current Author Addresses: Dr. Barbour: The Permanente Medical Group, Inc., Department of Cardiology, 2025 Morse Avenue, Sacramento, CA 95825-2115.
Paradoxical embolism is a rare cause of myocardial infarction. We describe a patient in whom morbid obesity obscured clinical examination and rendered invasive diagnostic evaluation by angiography unfeasible. Transesophageal echocardiography showed the pathophysiologic basis for respiratory decompensation (pulmonary thromboembolism) and myocardial infarction (paradoxical embolism to a coronary artery) after transthoracic echocardiography and computed axial tomography had failed to distinguish among the initial differential diagnostic possibilities. These possibilities included left ventricular systolic dysfunction, pulmonary embolism, pulmonary sepsis, and acute decompensation of chronic pulmonary disease caused by morbid obesity.
Case Report
A 48-year-old man presented with progressive dyspnea and no history of other difficulties. Three weeks before admission, he had lost consciousness briefly and had had associated numbness in both hands and chest pain radiating to the left shoulder. The chest pain had resolved rapidly but had recurred intermittently over the following 3 days.
The patient weighed 177 kg; his body temperature was 38.5 °C, his respiratory rate was 30 breaths/min, his heart rate was 116 beats/min, and his blood pressure was 160/100 mm Hg. Breath sounds were diffusely diminished, and rales were heard bilaterally throughout the lower third of the thorax. Cardiac rhythm was rapid and regular and was associated with biventricular third heart sounds. Pitting edema was seen on the abdominal wall. The patient's extremities were cyanotic peripherally, but clubbing was absent. Moderate to severe pitting edema was present from the feet to the thighs.
Arterial blood gas samples taken while the patient was breathing room air showed a pH of 7.28 (normal range, 7.35 to 7.45), a PCO2 of 64 mm Hg (normal range, 30 to 50 mm Hg), and a PO2 of 51 mm Hg (normal range, 80 to 100 mm Hg). A chest radiograph showed cardiomegaly and bilateral pleural effusions. An electrocardiogram showed sinus tachycardia, right axis deviation, bi-atrial enlargement, and nonspecific ST-T wave changes.
The patient required intubation and mechanical ventilation after his respiratory condition deteriorated, but hypoxemia persisted despite the administration of an inspired fractional oxygen concentration of 100%. The patient's central venous pressure was 19 mm Hg (normal range, 2 to 8 mm Hg); his peak right atrial pressure was 25 mm Hg (normal range, less than 10 mm Hg); his right ventricular pressure was 68/12 mm Hg (normal range, 15/2 to 30/8 mm Hg); and his pulmonary artery pressure was 60/36 mm Hg (normal range, 15/4 to 30/12 mm Hg).
Transesophageal echocardiography showed a nondilated left ventricle compressed by a markedly enlarged right ventricle. A multilobed mobile mass adjacent to the catheter in the right atrium prolapsed across a tricuspid valve that otherwise appeared normal (Figure 1). The same mass formed a serpentine structure that traversed a patent foramen ovale, entered the left atrium, and crossed the mitral valve. Shaggy echo densities were imaged near the anterior mitral valve leaflet and the aortic valve. These echo densities were shown to be continuous, with the mass originating in the right atrium. Intravenous administration of systemic venous saline contrast fully opacified the right atrium and spontaneously crossed through the patent foramen ovale to the left atrium during positive-pressure ventilation. At this time, the patient's pulmonary arterial pressure was 70/46 mm Hg, and his systemic arterial pressure was 85/46 mm Hg.
The patient was not considered to be a candidate for surgery and died despite aggressive medical management. Autopsy showed a markedly enlarged heart with severe right ventricular dilation and hypertrophy causing substantial compression of the left ventricular cavity. A large thrombus, weighing 36 g, partially obstructed the tricuspid orifice and extended into the right atrium, the chordae tendineae, and the papillary musculature of the tricuspid valve (Figure 2). Patency of the foramen ovale was seen when a probe was used to displace the septum primum 1.2 cm from the limbus of the septum secundum. Examination of the lungs in situ showed multifocal hemorrhagic areas consistent with acute pulmonary infarctions. The lumen of a diagonal branch of the left anterior descending coronary artery contained a recent embolic thrombus, and there was evidence that an organizing myocardial infarction had occurred approximately 2 to 3 weeks earlier. The presumed mechanism of death was respiratory failure due to acute pulmonary thromboembolism complicated by acute myocardial infarction.
Discussion
The direct demonstration of paradoxical embolism by imaging a thrombus traversing the foramen ovale is unusual [1-3]. In our patient, transesophageal echocardiography showed three criteria for the diagnosis of paradoxical embolism [4, 5]. First, a large intracardiac thrombus (the embolic source) was seen in both the right and left sides of the heart. Second, the potential communication, a patent foramen ovale, was shown by the spontaneous transit of saline contrast between the atria, the physical presence of thrombus extending across the atrial septum at the fossa ovalis, and systemic hypoxemia despite a fractional inspired oxygen concentration of 100% [6-9]. Third, right ventricular enlargement and leftward ventricular septal displacement indicating severe pulmonary hypertension was the driving force for interatrial shunting and paradoxical embolism [10]. Evidence of several pulmonary infarctions found at autopsy provided one explanation for the pulmonary hypertension. Systemic embolism to the coronary vasculature and subsequent myocardial infarction shown by histologic studies resulted from embolization of the thrombus in the left side of the heart that was imaged by transesophageal echocardiography.
This patient was unusual because of the marked size and extent of the thrombus seen by transesophageal echocardiography in the right atrium and right ventricle and because of the demonstration of the propagation of the thrombus across a patent foramen ovale. Although the patient's dire clinical circumstances precluded surgical intervention, the transesophageal echocardiogram was critical in showing the potential for catastrophic systemic embolism as the thrombus propagated across the interatrial septum.
Dr. Izban: Loyola University Medical Center, Department of Pathology, 2160 South First Avenue, Maywood, IL 60153.
Dr. Reyes: 578-113 Room D121, Hines Veterans Administration Hospital, Hines, IL 60141.
Dr. McKiernan: Loyola University Medical Center, Division of Cardiology, Building 110, Room 6232, 2160 South First Avenue, Maywood, IL 60153.
Dr. Louie: Loyola University Medical Center, Division of Cardiology, Building 110, Room 6228, 2160 South First Avenue, Maywood, IL 60153.
- Copyright ©2004 by the American College of Physicians
