Short term clinical outcome of acute saddle pulmonary embolism.
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Biomedical subjects
Publications and source records attributed to A Torbicki.
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OBJECTIVE: To assess the value of transoesophageal echocardiography (TOE) for diagnosing suspected haemodynamically significant pulmonary embolism and signs of right ventricular overload at standard echocardiography. METHODS: 113 consecutive patients (58 male; 55 female), mean (SD) age 53.6 (13.3) years, in whom there was clinical suspicion of pulmonary embolism and right ventricular overload on transthoracic echocardiography, underwent TOE in addition to routine diagnostic procedures to identify pulmonary artery thrombi. RESULTS: TOE revealed thrombi in 32 of 51 patients who had suspected acute pulmonary embolism and in 31 of 62 with suspected chronic pulmonary embolism. In one patient a pulmonary angiosarcoma rather than chronic pulmonary embolism was found at surgery. The diagnosis of pulmonary embolism was confirmed in 77 patients by scintigraphy, spiral computed tomography, angiography, or necropsy (reference methods). While TOE failed to provide a diagnosis of pulmonary embolism in 15 of these 77 patients, no false positive findings were reported (sensitivity 80.5%, specificity 97.2%). In 11 and 26 cases, respectively, the thrombi were confined to the left or right pulmonary artery. Bilateral thrombi were found in 25 patients. Mobile thrombi were observed only in acute pulmonary embolism (in 19 of 32 patients). No complications of TOE were noted. CONCLUSIONS: TOE permits visualisation of pulmonary arterial thrombi, confirming the diagnosis in the majority of patients with pulmonary embolism and right ventricular overload. This may be useful for prompt decision making in patients with haemodynamic compromise considered for thrombolysis or embolectomy.
The history of pulmonary embolism cannot be reconstructed reliably beyond the last two centuries, starting with the Napoleon's times by the works of Laennec. We owe the first pathological and clinical descriptions to European scientists, especially French, German and Italian. Interestingly, some ideas regarding pathophysiology and even hemodynamics can be found in papers published as early as the end of the 19th century. Of note, the strong relationship between venous thrombosis and pulmonary embolism, suspected already in the middle of the 19th century, resulted later in a new clinical entity named venous thromboembolic disease. Only just before the second world war "modern" diagnostic tests entered into the clinical arena. Beginning with electrocardiography and X-ray techniques including pulmonary angiography, the progress in the field of imaging continued with lung scan, echocardiography, computed tomography, and finally still largely unexplored ultra-fast magnetic resonance imaging techniques: despite this technological development the correct diagnosis of pulmonary embolism in daily practice remains an important challenge. This is due to the lack of a single test which would combine high diagnostic power, round-the-clock availability and reasonably low cost. Though thrombotic origin of pulmonary embolism was well documented for almost two centuries, anticoagulation as a treatment for venous thromboembolism dates back much less than a century and thrombolysis was initiated only 30 years ago. What is even worse, those 30 years were not enough for us to identify clear-cut criteria in the selection between thrombolysis and anticoagulation in individual patients. Not to speak about the problem regarding optimal duration of secondary prophylaxis after a thromboembolic episode. Still how long shall we be debating about the same problems at the bed of our patients with venous thromboembolism? Or maybe the near future will bring completely new answers to our old questions? What type of case report related to pulmonary embolism will have the chance to be accepted for publication in the Italian Heart Journal in the year ... 2050? Future will show? But only if we help it....
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While highly specific for detecting thromboembolism in proximal pulmonary arteries, spiral computed tomography (spiral CT) cannot reliably exclude pulmonary embolism. Therefore "negative" spiral CT in patients with high clinical probability of acute pulmonary embolism should be considered as non-conclusive. The goal of our study was to check whether echo/Doppler could stratify patients with suspected pulmonary embolism according to the chance of obtaining a conclusive spiral CT result. Echo/Doppler recordings of 51 patients (27 F, mean aged 50 +/- 19) admitted to ICU with high probability of acute pulmonary embolism were compared with the results of spiral CT of pulmonary artery. Pulmonary embolism was revealed by spiral CT in 36 pts. who at echocardiography were found to have shorter acceleration time (AcT 86 +/- 27 vs 117 +/- 7 ms, p < 0.00001) and right ventricle enlargement (PK 30 +/- 5 vs 25 +/- 2 mm p < 0.0001). The velocity of tricuspid regurgitation (TVPG) could not be measured in 19 patients. Among patients with long AcT (> or = 120 ms) or without right ventricle enlargement 8 of 14 and 14 of 28 patients, respectively had no intrapulmonary clots at spiral CT. Echo/Doppler helps in preselection of patients in whom confirmation of PE with spiral CT is highly probable. In patients without indirect echocardiographic sings of pulmonary embolism, despite high clinical probability the chance of a conclusive spiral CT is 40-50%. This should be kept in mind when selecting the most effective diagnostic strategy in individual cases.
D-dimer measurement with highly sensitive tests seems useful to rule out pulmonary embolism (PE) and deep vein thrombosis (DVT). However, nonspecific increase in d-dimer is common among inpatients. The aim of our study was to check: 1) whether the frequency of normal DD level in inpatients justifies its assessment as a part of diagnostic strategy for VTE, 2) whether tests that we are using are sensitive enough to exclude PE and DVT. In 27 (47%) out of 58 hospitalised patients evaluated by ultrafast ELISA (VIDAS bioMerieux), but in none of 20/58 patients with confirmed VTE, DD-level was found normal. In 35 of those patients DD was measured also with microlatex tests--Tinaquant and BC d-dimer. In 14/35 patients imaging test confirmed VTE. Sensitivity, specificity and negative predictive value (NPV) respectively were following: VIDAS: 100%, 80%, 100%, Tinaquant: 100%, 48%, 100%, BC d-dimer: 29%, 90%, 70%. Our results suggest that: 1) the relatively high frequency of normal DD-level among inpatients justifies its use in diagnostic strategies involving hospitalised patients, 2) negative VIDAS test confirms its as reliability for excluding VTE while 3) high sensitivity found for Tinaquant test encourages further prospective studies, 4) sensitivity of BC d-dimer is too low to be useful for excluding VTE.
It is not clear whether right ventricle to pulmonary artery coupling is modified by the site of vascular obstruction in patients with chronic severe pulmonary hypertension. We compared invasively (Swan Ganz) and non-invasively (echo/ /Doppler) assessed hemodynamics between two groups of patients with severe chronic thromboembolic pulmonary hypertension (CTEPH)--(n = 6; 52 +/- 24 yrs) and pulmonary arterial hypertension (PAH) (n = 5; 42 +/- 9 yrs) who had similar invasively measured right ventricular systolic pressure (CTEPH: 78 +/- 14 mm Hg; PAH: 83 +/- 17 mm Hg; p = NS), mean pulmonary arterial pressure (CTEPH: 51 +/- 10; PAH 56 +/- 11 mm Hg, p = NS) and pulmonary vascular resistance (CTEPH: 15.6 +/- 4.4 l/min; PAH: 19.2 +/- 6.1; p = ns). Patients with CTEPH have significantly shorter acceleration time corrected to ejection time (RVET): (AcT/RVET % = 24 +/- 5% vs 32 +/- 6% in PAH; p = 0.04) as well as AcT corrected by RR distance was highly significantly shorter (8 +/- 2% vs 12 +/- 2%; p = 0.006). AcT in the CTEPH group was shorter than in the PAH (60 +/- 5 vs 75 +/- 15; p = 0.047). The mid-systolic deceleration was significantly more frequent in the CTEPH group than in the PAH group (88% vs 30%; p = 0.005). If the mid-systolic deceleration was present in patients with PAH, the time to mid-systolic deceleration (t-N) had tendency to be longer in CTEPH group (118 +/- 22 ms vs 150 +/- 28 ms in PAH; p = 0.09). Significant differences appeared after correction t-N to RVET (t-N/RVET % = 46 +/- 9% vs 61 +/- 4%; p = 0.027) and to RR interval (t-N/RVET % = 16 +/- 2% vs 24 +/- 1%; p = 0.002). Doppler derived RV index proposed by Tei was slightly higher in CTEPH (0.81 +/- 0.18 vs 0.65 +/- 0.32 in PAH) but not significantly. Taken together our observations indicate that dynamical coupling between RV and pulmonary arteries is more disturbed in CTEPH than in PPH despite similar levels of chronically increased PAP.
20 consecutive patients with thromboembolic pulmonary hypertension underwent pulmonary thromboendarterectomy. Mean pulmonary artery pressure decreased from mean 49.9 +/- 9.8 to 25.1 +/- 8.8 mm Hg (p < 0.0001), pulmonary vascular resistance decreased from mean 5.58 +/- 2.58 to 1.62 +/- 0.79 mm Hg/l*min-1 (p < 0.0001) and cardiac output increased from 3.71 +/- 1.18 to 6.92 +/- 1.64 l/min. Sixteen patients had marked clinical improvement. Two patients died in early and 2 patients in late postoperative period due to unrelieved pulmonary hypertension and postoperative complications.
The aim of the study was to assess effectiveness and safety of the LGM inferior vena cava (IVC) filters in patients with venous thromboembolic disease. In the Department of Internal Medicine of Institute of Tuberculosis and Lung Diseases in Warsaw 79 LGM IVC filters have been inserted since 1993. Indications for filters placement were as follows: recurrent pulmonary embolism (pe) despite anticoagulation--17 patients (pts), severe bleeding complications of thrombolytic or anticoagulant therapy--11 pts, contraindications for thrombolytic and/or anticoagulant treatment--5 pts, massive pe--14 pts, chronic thromboembolic-major vessel pulmonary hypertension (CTEPH)--30 pts, extensive deep vein thrombosis of lower limbs or vena cava inferior in patients with urgent indications for surgery--24 pts. Each filter placement was preceded by cavography. The diagnostic procedures (mainly ultrasonography) were performed after 3-6 and 12 months in the first year then once yearly during follow-up period. Oral anticoagulants (OA) or low-molecular-weight heparins (LMWH) were instituted in the majority of patients. 58 patients are still alive, 21 patients died. Only two non-fatal episodes of recurrent pe were documented. Other complications were rare and insignificant. We have not observed excess rate of recurrent deep venous thrombosis nor thrombosis at the filter site. The LGM IVC filters are effective and safe in such selectively chosen group of patients.
UNLABELLED: Patients with acute pulmonary embolism (PE) may require prompt confirmation of PE before aggressive therapy such as embolectomy or thrombolysis. However, emergency availability of routine diagnostic tests often remains a problem. Therefore, we assessed prospectively the diagnostic value of transesophageal echocardiography (TEE), recently reported to be useful in the diagnosis of PE. TEE was performed in 76 consecutive patients (42 F, 34 M) aged 66.7 +/- 15.8 yrs with suspected acute PE with echocardiographic signs of right ventricular pressure overload, but without known coexisting cardiorespiratory diseases. Pulmonary artery thrombi (TH) were visualized at TEE in 69.7% (53) pts. PE was confirmed by high probability lung scintigraphy and/or spiral CT in all these cases. Additionally, PE was diagnosed in 11 others without TEE-reported TH. In the 12 remaining patients PE was eventually excluded (specificity 100%, sensitivity 82.8%). Therefore, TEE in the diagnosis of hemodynamically significant PE reached 100%. No clinically important adverse events were observed during TEE. CONCLUSION: Transesophageal echocardiography is reliable and safe method of prompt confirmation of hemodynamically significant acute pulmonary embolism with relatively high sensitivity in adequately preselected patients. However, due to topographic limitations negative result of TEE does not exclude PE.
A broad spectrum of indications for low molecular weight heparin (LMWH) requires an assessment of side effects especially during prolonged administration. There are common risk factors for venous thromboembolism (VTE) and osteoporosis; heparin is "the drug of choice" for VTE treatment. The aim of our study was to assess the effect of treatment and prophylaxis with LMWH (enoxaparine sodium) and oral anticoagulant (acenocoumarol) for bone structure. Material consists of in- and outpatients. 49 densitometries were performed in 31 patients (in 15 cases double examination). We observed a decrease of bone mineral density in comparison to the initial examination in most cases: mean change of bone mass for examined areas was 3.05%.
Switching from heparin to acenocoumarol was complicated by severe retroperitoneal bleeding in a 50-years old patient with massive pulmonary embolism and deep venous thrombosis. The haematomas were evacuated by surgical procedure. Planned insertion of a vena cava filter was abandoned because of a mobile clot in inferior vena cava (IVC) reaching above renal veins as evidenced by spiral computed tomography (SCT). Patient was transferred to the Surgical Department of Medical Academy in Warsaw where thrombectomy was performed. In spite of mechanical and pharmacological methods of venous thrombosis prophylactic, thrombectomy was complicated by massive proximal deep venous thrombosis of right leg and distal part of IVC. Patient was successfully treated with UFH i.v. followed by low molecular weight heparins. No bleeding complications were observed. Screening for thrombophilia and cancer were negative. This case report is an example of difficulties in clinical management in a patient who has both life-threatening thromboembolic disease and bleeding.
A case of 68 years old women suffering from chronic anemia, myelodysplastic syndrome and treated with progestogen due to endometrial hypertrophy is presented. Initially she was admitted to a regional hospital because of progressive weakness and exertional dyspnea. Three months earlier she reported an episode of acute dyspnea and chest pain. On the basis of clinical symptoms and perfusion lung scintigraphy pulmonary embolism (PE) was diagnosed. Patient received i.v. heparin which was changed to s.c. nadroparine subcutaneously. Platelet count dropped to 55,000'/ml on fifth day of treatment from initial level of about 200,000'/ml. Heparin induced thrombocytopenia was diagnosed, heparin was stopped and ticlopidine was recommended. After 3 weeks symptoms suggesting recurrent PE were observed. The patient was transferred to National Tuberculosis and Lung Diseases Research Institute. Recombinant hirudine (Refludan) was administrated (bolus 0.4 mg/kg and initial dose of infusion 0.1 mg/kg/h) overlapping with acenocoumarol from second day. Dose of r-hirudine was adjusted to achieve APTT prolongation 1.5 to 2.5 times of mid-normal range. During treatment with r-hirudine no bleeding and new thromboembolic complications occurred. Platelets count remained within normal range. After 14 days clinical improvement was observed, though symptoms of right ventricular overload and hypoxemia were still present after 6 months of treatment with oral anticoagulants suggesting chronic thromboembolic pulmonary hypertension.
Intraluminal caval filter placement can be applied in order to prevent pulmonary embolism. When surgery has to be performed in the patient with proximal deep venous thrombosis anticoagulant therapy should be reduced and filter placement is indicated. Temporary filter appears an interesting option, as it can be removed shortly after surgical intervention, when contraindications to anticoagulation no longer exist. However, obligatory removal of a temporary device in case of suspected filter or vena cava thrombosis emerges as a new clinical problem. We present a ease of 20 year old woman with proximal deep venous thrombosis and high risk of pulmonary embolism in whom temporary vena caval filter with heparin infusion were chosen as a method of perioperative pulmonary embolism prevention.
Analysis of the systolic flow velocity curve (SFVC) in the right ventricular outflow tract is considered as an alternative to the tricuspid valve pressure gradient (TVPG) method for echo-Doppler assessment of pulmonary arterial pressure (P(pa)). The present study checked whether or not SFVC is affected by the cause of pulmonary hypertension. Doppler recordings of 86 patients (39 female, aged 55.5+/-15.2 yrs) with acute (AP-PE) or chronic (CP-PE) proximal pulmonary embolism, chronic obstructive pulmonary disase (COPD) or primary pulmonary hypertension (PPH) were retrospectively analysed by two observers unaware of the purpose of the study. Despite having the lowest TVPG (48+/-13 mmHg), patients with AP-PE had the shortest acceleration time (t(acc); 56+/-15 ms) and time to midsystolic deceleration (t(msd); 105+/-16 ms). t(acc) <60 ms in patients with TVPG <60 mmHg had 98% specificity and 48% sensitivity for AP-PE. In PPH, SFVC was less abnormal (t(acc) 64+/-14 ms, t(msd) 125+/-25 ms, both p<0.03) despite having a TVPG twice as high (92+/-12 mmHg, p< 0.001). In contrast to t(acc), TVPG showed strong correlation with direct P(pa) measurements whenever performed (r=-0.43, p=0.02, versus r=0.80, p<0.001; n=30). There was no correlation between t(acc) and TVPG in a pooled study group and SFVC seemed strongly affected by the presence of both AP-PE and CP-PE. While potentially useful for evaluation of the true right ventricular afterload during pulsatile flow conditions, the systolic flow velocity curve does not provide a reliable estimate of pulmonary arterial pressure.