(Circulation. 2005;111:e438-e439.)
© 2005 American Heart Association, Inc.
Images in Cardiovascular Medicine |
From the Department of Cardiology (Y.N., T. Aoyama, M.Y., T. Araki, S.F., K.Y.) and the Department of Respiratory Medicine (T.K., N.K., T.N., K.T.), Fukui Prefectural Hospital, Fukui, and the Molecular Genetics of Cardiovascular Disorders (Y.N., M.S., H.M.), Division of Cardiovascular Medicine, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan.
Reprint requests to Yoshihiro Noji, MD, Department of Cardiology, Fukui Prefectural Hospital, Yotsui 2-8-1, Fukui 910-8526, Japan. E-mail nojibon{at}nifty.com
A 71-year-old man with chronic obstructive pulmonary disease (severe pulmonary emphysema with home oxygen therapy) was referred to our hospital because of 1-day history of dyspnea at rest. His physical examination was remarkable for tachycardia (110 bpm) and tachypnea (32 breaths/min). The ECG demonstrated sinus tachycardia, S waves in leads I and aVL, transition zone to V5, and T-wave inversion in leads III and aVF. A transthoracic echocardiogram (TTE) performed on admission showed that the right atrium and right ventricle were apparently enlarged. The left ventricle had assumed a classic D-shaped configuration, which indicates impaired left ventricular relaxation, and severe tricuspid regurgitation was present. Systolic pulmonary artery pressure of up to 80 mm Hg was estimated on the basis of pulsed Doppler echocardiography. There were no signs of thrombus in the heart. Computed tomography of the chest revealed large thrombi in the right and left pulmonary arteries (Figure 1). The patient received immediate thrombolytic treatment with recombinant tissue plasminogen activator (Monteplase, Eisai Co, Ltd; 1 600 000 U) intravenously, followed by 15 000 U/d unfractionated heparin infusion over a 24-hour period, and both symptoms and pulse oximetry improved initially.
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However, on the fifth hospital day, he again became symptomatic, with acute deterioration of pronounced hypoxia. Simultaneous TTE revealed a large wormlike thrombus floating in the right atrium. The thrombus was highly mobile and eventually prolapsed into the right ventricle, then migrated into the pulmonary vasculature. The thrombus took on different shapes during examination (Figure 2). Unfractionated heparin (3000 U IV) was added. TTE repeated after 6 hours showed no signs of thrombus. Computed tomography showed thrombus in the right enlarged popliteal vein. An inferior vena cava filter was placed, and heparin was increased up to 25 000 U/d. His respiratory status had deteriorated, and he required 100% oxygen and then intubation. After that, his condition improved daily, and his trachea was extubated on the 12th hospital day. Heparin was transitioned to warfarin. The patient survived and is currently doing well without surgical embolectomy.
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Free-floating right heart thrombi are a rare phenomenon. Serial echocardiographic examinations are useful when the clinical status deteriorates, because they may demonstrate thrombus that was not detected on the initial examination.
Related Article:
Circulation 2005 111: 3185.
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