Abstract
INTRODUCTION
In patients who are admitted to a hospital due to episode of syncope, acute pulmonary embolism (PE) is rarely considered as a possible cause. This report presents two cases illustrating PE as a cause of syncope with elevated cardiac troponin (cTn) and N-terminal pro-brain natriuretic peptide (NT-proBNP) levels despite normal echocardiographic examination and negative Doppler ultrasound imaging.
Case 1: An 83-year-old woman admitted to the ER due to episodes of recurrent syncopes. According to her anamnesis, she had four episodes of syncopes during last three weeks without chest pain, dyspnea, palpitation or hemoptysis. ECG revealed a normal sinus rhythm with a heart rate of 70 bpm without ischemic changes. Laboratory tests revealed raised levels of cTn and NT-proBNP. Transthoracic echocardiography (TTE) demonstrated preserved left and right ventricular systolic functions without
any cardiac chamber enlargement and mild tricuspid regurgitation with a PAP of 35 mmHg. Patient’s pre-test probability for pulmonary embolism was low (Wells’ score < 2) but D-dimer level was elevated. Doppler imaging for detection of deep vein thrombosis was negative. Computed tomography pulmonary angiography (CTPA) showed filling defects in the pulmonary arteries consistent with pulmonary embolism (Panel A). The patient was discharged with rivaroxaban therapy without any complication.
Case 2: A 69- year-old woman presented to ER with symptoms of chest pain and recurrent episodes of syncope for the last 2 days. Her medical history revealed hypertension and hyperlipidemia. On admission ECG showed a normal sinus rhythm with a heart rate of 105 bpm and T-wave inversions in inferior leads. Laboratory tests showed elevated levels of cTn and NT-proBNP. TTE demonstrated normal left ventricular systolic function with an ejection fraction of 55% and normal right ventricular function and chamber size with a tricuspid annular plane systolic excursion of 22 mm. Diagnostic coronary angiography was performed to exclude acute ischemia revealed non-significant coronary artery stenosis. Doppler ultrasound imaging for detection of deep vein thrombosis was negative. CTPA showed filling defects in the bilateral main pulmonary arteries consistent with acute bilateral pulmonary embolism (Panel B-C). The patient was discharged with rivaroxaban therapy after four days of hospitalization period without any complication.
CONCLUSION
Elevated cTn and NT-proBNP leves on admission strongly suggest transient hemodynamic impairment causing cardiac injury and syncope. Normal admission ECG and TTE can exclude most possible acute cardiac causes of syncope. Although acute right ventricular dsyfunction is the most frequent finding of acute massive PE causing hemodymanic impairment resulting with syncope, diagnosis of acute PE should only be excluded with CTPA in patients with similar clinical characteristics despite normal TTE and negative venous Doppler ultrasound imaging.
Abstract P1267 Figure
Doppler ultrasound imaging techniques for assessment of synovial inflammation
