Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved. Hemodynamic and symptomatic improvement after delayed thrombolysis with Reteplase in a patient with massive bilateral pulmonary emboli Babak Sharif-Kashani a , Arda Kiani b , Mehrdad Bakhshayesh-Karam c , Faezeh Sheybani-Afshar a , Neda Behzadnia d and Farah Naghash-Zadeh a Most patients surviving the acute phase of pulmonary embolism will recover with no residue. But, 2–4% of patients will progress to chronic thromboembolic pulmonary hypertension. In this group, usually a ‘Honey moon’ period is seen but a few may show progression with ongoing symptoms despite medical treatment. In this case report, we review a patient in whom delayed thrombolytic therapy was administered due to progressive symptoms after 21 days. Her condition was stabilized. The early posttreatment computed tomographic pulmonary angiography (CTPA) showed incomplete resolution, but after 6 months she was functional class I with a normal CTPA and echocardiography. Blood Coagul Fibrinolysis 26:88–90 ß 2015 Wolters Kluwer Health, Inc. All rights reserved. Blood Coagulation and Fibrinolysis 2015, 26:88–90 Keywords: delayed diagnosis, pulmonary embolism, thrombolytic therapy a Lung Transplantation Research Center, b Tracheal Diseases Research Center, c Pediatric Respiratory Diseases Research Center and d Chronic Respiratory Diseases Research Center, National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran Correspondence to Babak Sharif-Kashani, MD, NRITLD, Shaheed Bahonar Avenue, Darabad 1956944413, Tehran, Iran Tel: +982127122626; fax: +982126109490; e-mail: babaksharifkashani@yahoo.com Received 7 October 2013 Accepted 26 December 2013 Introduction Pulmonary embolism is the most common cause of death from cardiovascular disease and ranks third after heart attack and stroke [1]. The morbidity and mortality associ- ated with venous thromboembolism (VTE) may be reduced with earlier diagnosis and treatment [2]. Yet, 2–4% of patients will progress to chronic thromboem- bolic pulmonary hypertension (CTEPH) [1]. However, data regarding the effect of delayed treatment of VTE on the acute syndrome as well as its progression to CTEPH are sparse [3]. Different mechanisms are involved in the setting of pulmonary hypertension due to pulmonary embolism including physical obstruction, in situ thrombosis and small arterial involvement. Case report A 27-year-old woman was referred to our center because of progressive shortness of breath starting 3 weeks ago. During this period, she had been evaluated at other centers and, in spite of there being no conclusive evidence, had been treated for allergic and obstructive airway disease with no apparent improvement. Prior to this illness, she enjoyed the benefits of full health and was an active athlete. She was married, had no children and was on no long-term medication. She was a nonsmoker and had no history of chemical or environ- mental exposure. Her family history revealed no signifi- cant finding also. Three weeks before she became symptomatic, she had started taking Cyproterone acetate for mild menstrual problems. She was a thin young woman who was symptomatic at rest. Her physical examination revealed tachypnea, tachycardia and central cyanosis while breathing room air. Her blood pressure and body temperature were normal. The jugular veins were engorged, and central venous pressure was elevated. The rest of the physical examination was normal except for a loud P2 and a II/VI systolic murmur best heard over the left sternal border. She had no peripheral edema or ascites. The patient was admitted with the possibility of pulmonary emboli. A radiograph X-ray was reported to be normal. The electrocardiogram showed right ventricle strain and sinus tachycardia, and the O 2 saturation on room air was 85%. D-dimer was elevated, and the pro-brain natriuretic peptide level was 2075 pg/ml. Screening tests for throm- bophilia as well as for rheumatologic tests were negative. A transthoracic echocardiographic study showed moder- ate pulmonary hypertension and failure of the right ventricle (RV) with mild RV/right atrium (RA) enlarge- ment (right ventricular systolic pressure ¼ 45 mmHg, tricuspid annular plane systolic excursion ¼ 1.7 cm, RV diameter ¼ 31 mm, RA diameter ¼ 33 mm). No clot was detected in the heart chambers, and Doppler sonographic examination of the lower extremities was negative for deep vein thrombosis. An initial computed tomographic pulmonary angiography (CTPA) was consistent with bilateral pulmonary emboli (Fig. 1). Although anticoagu- lation as well as supportive measures were started, 88 Case report 0957-5235 Copyright ß 2015 Wolters Kluwer Health, Inc. All rights reserved. DOI:10.1097/MBC.0000000000000087