Whether syncope as a presenting symptom independently classifies acute pulmonary embolism (APE) into a high mortality risk group remains a matter of controversy. We retrospectively included all consecutive patients admitted to our clinic with APE from January 2014 to December 2016. Our sample consisted of 76 patients with a mean age of 69 ±13.6 years, 64.5% female. 14.3% presented with syncope at admission. In-hospital mortality was 20.8%. Patients with syncope were more likely to require inotropic support (OR = 5.2, 95 % 1.17-23.70, p=0.03) due to the association of cardiogenic shock (OR= 15.95% CI 3.02-74.32, p < 0.001) and systolic blood pressure below 90 mmHg (OR=5.52, 95% CI 1.24-24.47, p=0.03). Patients with syncope had a higher PESI score (150.9 ± 51.1 vs 99.9 ± 30.1, p < 0.001) and a greater in-hospital mortality (OR= 4.5, 95% CI 1.14-17.62, p=0.03). However, multivariate logistic regression equations did not identify syncope as an independent predictor of mortality. In our sample, syncope did not independently reclassify the patient in a higher mortality group, but due to the association with hemodynamic instability, which remains the primary tool in therapeutic decision-making.

e 461Objective: The thrombolytic therapy in patients with intermediary risk pulmonary embolism is a debated subject. According to the ESC Guidelines for the Management of Acute Pulmonary Embolism (2014) the thrombolytic therapy in patients with intermediary -high risk pulmonary embolism (defined as PESI score >85, echocardiography signs of RV dysfunction, biochemical signs of RV dysfunction (NtproBNP and cTnT elevated)) -IIa class indication. Secondary to thrombolytic therapy a hypertensive rebound can occure as a result of the improvement of the RV systolic function (echocardiography assessed) Design and method:We selected 25 patients with intermediary-high risk pulmonary embolism with no contraindications for thrombolytic therapy, aged below 75yo, no severe renal failure, normal left ventricle systolic function. The patients received thrombolytic therapy 10 mg t-PA followed by 90 mg t-PA in 2 h. From this patients 66% were diagnosed with ambulatory primary hypertension. The echocardiographic makers of RV dysfunction were assessed on admission and on 72 h after thrombolytic treatment (TAPSE, S wave velocity assessed by TDI, RV diastolic diameter, dyskinetic IVS, the severity of tricuspid regurgitation). We assessed the hypertensive profile by 24 h hypertension monitoring on 72 h after thrombolytic therapy.Results: Only 25% of the included patients presented high blood pressure on admision, the medium SBP on admision was 135.8mmHg. The echocardiographic markers of RV dysfunction were concordant with the acute PE, as the mean S wave velocity by TDI was 10.8 cm/s, the medium TAPSE was 13.5 mm, the medium RV diastolic diameter 44.8 mm and 25% of the patients had dyskinetic IVS. Postthrombolytic therapy the assessment of RV function revealed an increasing TAPSE by 54%, an increasing S wave velocity by 44.8%, the medium RV diameter 38.6 mm and only 2 patients with dyskinetic IVS. Regarding the hypertensive profile on 24 h the medium SBP was 158.5mmHg with a hypertensive load of 44.5%. It is obvious a correlation between the posthrombolytic hypertensive rebound and the improving markers of RV pressure overload. Conclusions:The results reveal a possible correlation between the improving RV dysfunction assessed by echocardiography and the posthrombolytic rebound in patients with acute intermediary-high risk PE.