Circulation. 2008;118:2207-2208
doi: 10.1161/CIRCULATIONAHA.108.780601
(Circulation. 2008;118:2207-2208.)
© 2008 American Heart Association, Inc.
Images in Cardiovascular Medicine |
Regression of Thrombus and Electrocardiographic Changes With Thrombolytic Therapy in Acute Massive Pulmonary Embolism
Evin Bozcali, MD;
Yildiray Tutpinar, MD
From the Department of Cardiology, University of Istanbul, Cerrahpasa Faculty of Medicine (E.B.), and Department of Radiology, Medicana Hospitals Bahcelievler (Y.T.), Istanbul, Turkey.
Correspondence to Evin Bozcali, MD, Zeytinoglu Caddesi Sarikonaklar Sitesi B17/4, Akatlar Etiler Besiktas, Istanbul, Turkey 34335. E-mail ebozcali{at}gmail.com
A 57-year-old man who had undergone successful right coronary artery stenting 2 weeks previously was admitted to the emergency department with sudden onset of syncope, palpitation, hypotension (80/60 mm Hg), mild chest pain, and dyspnea. Coronary angiography, which was performed immediately with the suspicion of stent thrombosis, showed a patent stent in the right coronary artery without stenosis or thrombosis. Laboratory tests showed normal levels of creatine kinase and troponin I. Transthoracic echocardiography revealed right ventricular global hypokinesia with dilatation and impaired right ventricular systolic function. The systolic pulmonary artery pressure was estimated as 50 mm Hg from moderate-degree tricuspid regurgitation. A spiral thorax contrast-enhanced computed tomography scan showed that the right pulmonary artery was completely and the left pulmonary artery was partially obliterated by intramural thrombi (Figure 1A). An ECG illustrated abnormalities such as a prominent S wave in lead I and Q wave and inverted T wave in lead III (S1, Q3, T3 pattern), which were compatible with massive pulmonary embolism (Figure 1B). Because of his hemodynamic instability, the patient was immediately treated with intravenous tissue plasminogen activator (100 mg/2 h) and subcutaneous enoxaparin (1 mg/kg twice a day). Significant clinical improvement was achieved 3 hours after thrombolytic therapy. An ECG and echocardiogram taken on the next day of treatment showed resolution of the S wave in lead I and Q wave in lead III (Figure 2A) and normalization of right ventricular systolic function and dimension with a significant decrease in tricuspid regurgitation and an estimated systolic pulmonary artery pressure of 20 mm Hg. Bilateral lower-extremity venous Doppler ultrasonographic examination was negative for thrombus, including catheterization site. Consequently, the source of the pulmonary embolism was not determined.
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Figure 1. A, Contrast-enhanced thorax computed tomography reveals complete obliteration of the right and partial obliteration of the left pulmonary artery with intramural thrombi. B, An ECG shows a prominent S wave in lead I and Q wave and inverted T wave in lead III.
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Figure 2. A, An ECG shows resolution of the S wave in lead I and Q wave in lead III within 24 hours after application of thrombolytic therapy. B, On the third day, follow-up contrast-enhanced computed tomography illustrates significant regression of intramural thrombi in the right and left pulmonary arteries.
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Follow-up spiral computed tomography performed 72 hours after the administration of thrombolytic therapy revealed dramatic regression of the intramural thrombi in the right and left pulmonary arteries (Figure 2B).
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Acknowledgments
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Disclosures
None.
