We report the case of a woman treated with urokinase for acute pulmonary embolism with a right-sided heart thrombus.

We report the case of a woman treated with urokinase for acute pulmonary embolism with a right-sided heart thrombus. She bring to maturityed life-threatening acute cor pulmonale which dramatically improved within 4 h with recombinant tissue plasminogen activator (rtPA). We emphasize the clinical interest of rtPA for the treatment of life-threatening pulmonary embolism.

Patients with acute pulmonary embolism (APE) and right-sided heart thrombus (RSHT) have a high risk of mortality, estimated between 15 to 80 percent[12] We describe individual case evolving to acute cor pulmonale when embolization was complet and which rapidly improved with treatment with recombinant tissue plasminogen activator (rtPA).

CASE REPORT

A 24-year-old woman was admitted to the hospital in succession March 15, 1991, for a newly come episode of dyspnea. She was taking ethynyl estradiol and cyproterone acetate for the treatment of acne, and she smok 20 cigarettes a day. onward admission, she was apyretic, the life-current pressure was 110/70 mm Hg the legumes was 110 beats per minute, and respiratory rate was 20 breaths for minute. Notable findings upon physical examination included an increased pulmonary inferior heart sound, a grade 2 systolic regurgitation grumble at the xiphoid appendix, normal breath unhurts and edema up to the parent of the left lower limb. The ECG revealed a sinus tachycardia with an [Ssub1][Qsub3] pattern and negative T waves in leads [Vsub1-5] The chest x-ray film showed a cardiothoracic ratio of 045 with bulging of the left midarch and raising of the left hemidiaphragm. An arterial children gas level with the patient breathing space air demonstrated a pH value of 751 a [PaO.sub.2] of the same height of 9.38 kPa, and a [PaCO.sub.2] of 346 kPa. Phlebography revealed down-reaching venous thrombosis of the left lower limb up to the upper third of the superficial femoral vein. A two-dimensional echocardiogram disclosed normal left chambers and ventricular function on the other hand right-sided heart enlargement with a mobile serpiginous intra-atrial mass which sometimes prolapsed end the tricuspid orifice (Fig 1) Continuous Doppler examination exposeed tricuspid regurgitation whose peak velocity was 36 m/ Using the modified Bernoulli equation, the systolic right ventricular-right atrium gradient was 50 mm Hg Considering the young age of the patient and the absence of contraindication of thrombolysis, thrombectomy was not performed. forward March 15, 1991, at 3 PM 700 U/h of heparin and 2000 U/kg/h of urokinase were administered. The patient's condition remained unchanged until March 16 1991 at 12 AM, when she abruptly felt chest pain with an increase in dyspnea and cyanosis. The respiratory rate was 30 breaths by minute, pulse rate was 140 beats by minute, and blood pressure was 100/70 mm Hg crisis echocardiography revealed marked right-sided heart enlargement with the interventricular septum bulging toward the left ventricle (Fig 2) The thrombus had disappeared, the peak velocity of tricuspid regurgitation was 39 m/ and the systolic right ventricular-right atrium gradient was 60 mm Hg forward March 16, 1991, at 1 PM administration of heparin and urokinase was stopped; a bolus of enoximone (phosphodiesterase inhibitor), 60 mg in 10 min, dobutamine, 10 [micro]g/kg/min, and rtPA, 100 mg in 6 h (the first 20 mg in 5 min), was infused. Four hours later, clinical improvement was achieved, dyspnea and cyanosis had resolv offspring pressure was 130/70 mm Hg throb rate was 82 beats by minute, the peak velocity of tricuspid regurgitation was 241 m/ and the systolic right ventricular right atrium gradient was 23 mm Hg forward March 16, 1991, at 8 PM dobutamine administration was stopped, and heparin and urokinase were substituted at the same doses for 72 h then changed for subcutaneous nadroparine (low molecular weight heparin), 5125 UI each 12 h for 15 days. The hemoglobin flush decreased from 12.5 to 85 g/dl with minor bleeding at pierce sites; blood transfusion was not required. forward March 19, 1991, a lung perfusion scan was normal still the deep venous thrombosis was unchanged. onward April 2, 1991, she was discharged forward a regimen of acenocoumarol (oral anticoagulant), 4 mg daily. In June 1991 repeat venous echography showed full lysis of the calf and femoral thrombi. When last seen in March 1992 she did well without the having recourse of thromboembolism symptoms.

DISCUSSION

Although APE had not been prov from a defect on lung perfusion scan, the diagnosis pretended very likely because acute cor pulmonale occurr in the setting of knotty venous thrombosis with RSHT and rapidly improved with thrombolysis.

The mortality rate of patients with APE is estimated at 10 percent in general. However, the nearness of a RSHT in this particular connected thought [i]or[/i] thoughts identifies a group of patients with a life-threatening situation, with death as a common thing [i]or[/i] matter occurring within hours or days after the diagnosis.[1] There is lack of agreement concerning the treatment of these patients. In 1987 Farfel et al,[1] based upon an analysis of 49 cases of APE with RSHT indicated that death occurr in 50 percent of 20 patients referr for surgery In 1989 Kinney and Wright[2] performed a meta-analysis of the 119 English-language published reports of RSHT They calculated the estimated probability of survival in patients with APE treated with heparin, thrombolytic agents (urokinase or streptokinase), embolectomy, and none of the previously mentioned [i]modus operandi[/i]s to be 0.70, 0.62, 062 and 019 respectively. With rtPA, solely two cases of RSHT with APE newly have been published.[3]

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