39 research outputs found

    Czynniki ryzyka żylnej choroby zakrzepowo-zatorowej

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    Guidelines for primary treatment and secondary antithrombosis prevention of pulmonary embolism

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    Ostra zatorowość płucna prowadzi do gwałtownego wzrostu ciśnienia w naczyniach płucnych i przeciążenia prawej komory serca. O wyborze metody leczenia decyduje stopień zaburzeń hemodynamicznych i wynikające z tego ryzyko zgonu. Pacjenta w stanie stabilnym leczy się przede wszystkim przeciwzakrzepowo, natomiast chorzy z hipotonią, we wstrząsie wymagają natychmiastowego odblokowania tętnic płucnych, co uzyskuje się, podając leki trombolityczne lub wykonując embolektomię przeskórną albo chirurgiczną. Drugim istotnym problemem jest czas wtórnej profilaktyki przeciwzakrzepowej. Decydujące znaczenie ma w tym przypadku ryzyko nawrotu zakrzepicy, oceniane obecnie głównie na podstawie pierwotnej przyczyny żylnej choroby zakrzepowo-zatorowej oraz coraz częściej - stężenia D-dimeru miesiąc po odstawieniu leków przeciwzakrzepowych.Acute pulmonary embolism leads to sudden increase of pressure in pulmonary arteries and overload of the right ventricle. The management of pulmonary embolism depends on hemodynamic deterioration and consequent risk of death. All patients should be anticoagulated, however, subjects with hypotonia, in shock demand immediate resolving of thromboembolic obstruction of pulmonary arteries with thrombolysis or surgery/percutaneous embolectomy. The duration of secondary prophylaxis is a second important problem. The assessment of the risk of recurrent embolism is crucial and currently is based on primary reason of thromboembolic disease and on concentration of D-dimer one month after cease of anticoagulation

    Prophylaxis of pulmonary embolism in pregnancy and puerperium

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    Summary Pulmonary embolism is the main cause of death of pregnant women in developed countries. An increased prothrombotic activity is observed during pregnancy. Moreover, the risk of venous thromboembolic disease can be elevated in cases of inherited thrombophilia, antiphospholipid syndrome or previous venous thormboembolic events. According to presented guidelines of The Royal College of Obstetricians and Gynecologists and The American College of Chest Physicians, the risk stratification of venous thromboembolic disease during pregnancy and puerperium is a vital condition and proper antithrombotic prophylaxis should be implemented

    Diagnosis and treatment of pulmonary embolism in pregnancy

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    Abstract Pregnancy and puerperium increase the risk of venous thromboembolic disease. As it is potentially life-threatening, all patients with the suspicion of pulmonary embolism require proper diagnosis and, possibly, treatment. Venous ultrasonography is usually applied. However, in most cases the examinations with the use of ionized radiation – computer tomography or scintigraphy – are indispensable. In treatment of pulmonary embolism, low molecular weight heparins play the key role. However, in case of dramatic pulmonary embolism with shock and hypotension, thrombolytic therapy may be necessary. Low molecular weight heparins as well as oral anticoagulants can be used after the delivery

    Does kidney function matter in pulmonary thromboembolism management?

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    Cardiovascular circulation and kidney function are closely interrelated. The impairment of renal function is a well-known hazard of increased mortality and morbidity of patients with heart failure or coronary artery disease. Acute pulmonary embolism (APE) impacts pulmonary and systemic circulation, and can severely impair functions of other organs, including kidneys, as a result of hypoxemia and increased venous pressure. Previous studies indicate that renal dysfunction predicts short- and long-term outcomes and can improve the risk assessment in APE. However, renal function should also be cautiously considered during the diagnostic workup because the contrast-induced nephropathy after computed tomography pulmonary angiography (CTPA) is noticed more frequently in APE. Chronic thromboembolic pulmonary hypertension (CTEPH) is a rare but imminent complication of APE. This condition promotes renal impairment by increasing venous pressure and decreasing glomerular filtration. The renal function improvement and serum creatinine concentration reduction were noted in CTEPH subgroup with glomerular filtration rate ≤ 60 mL/min/1.73 m2 after successful treatment. In this review, we present the essential research results on the kidney function in thromboembolism disease

    Potential role of endothelin in patients with acute pulmonary embolism and chronic thromboembolic pulmonary hypertension

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    Endoteliny (ET) to rodzina trzech białek o bardzo silnych właściwościach wazokonstrykcyjnych. ET biorą udział w regulacji napięcia ściany naczyń i przepływu krwi. Synteza oraz degradacja ET odbywa się głównie w drogach oddechowych i naczyniach płucnych. Badania kliniczne nad zastosowaniem nieselektywnego antagonisty receptorów endotelinowych - bosentanu - wykazały poprawę w klasie czynnościowej u pacjentów z zatorowo-zakrzepowym nadciśnieniem płucnym (CTEPH). Donoszono, że endoteliny mogą mieć znaczenie w ostrej zatorowości płucnej, jednakże pełna ocena ich roli wymaga dalszych badań. W niniejszym opracowaniu omawiamy potencjalne znaczenie endotelin u chorych z przewlekłym zakrzepowo-zatorowym nadciśnieniem płucnym oraz w ostrej zatorowości płucnej.Endothelins (ET), a family of three peptides of strong vasoconstrictive properties, participate in the regulation of vascular tone and blood flow. The synthesis and degradation of the ET predominantly take place in the pulmonary vasculature. Elevated plasma ET levels were reported in various forms of arterial pulmonary hypertension including chronic thromboembolic pulmonary hypertension (CTEPH). Moreover, clinical studies with nonselective ET receptor antagonist - bosentan reported improvement in functional class in patients with CTEPH. It has been suggested that endothelins may play an important role in acute pulmonary thromboembolism (APE). However, further studies are necessary to verify these observations. In the current paper we discuss a potential role of endothelins in CTEPH and APE

    Increased systemic arterial stiffness in patients with chronic thromboembolic pulmonary hypertension

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    Background: Chronic thromboembolic pulmonary hypertension (CTEPH) is a complication of venous thromboembolism (VTE) resulting from non-dissolving thromboemboli in the pulmonary arteries. Previous observations indicate a higher prevalence of atherosclerosis and cardiovascular risk factors in patients with VTE and CTEPH. The purpose of the present study was to evaluate the arterial stiffening assessed by pulse wave velocity (PWV), a marker of arterial stiffness, in CTEPH patients in comparison with a matched control group (CG).Methods: The study group consisted of 26 CTEPH patients (9 male and 17 female, age 69 ± 10 years) and 22 CG (10 male, 12 female, age 67 ± 8 years). In all subjects a physical examination, carotid-femoral PWV and transthoracic echocardiography were performed. Right heart catheterization was done in all CTEPH.Results: Chronic tromboembolic pulmonary hypertension patients had significantly higher PWV than CG (10.3 ± 2.5 m/s vs. 9 ± 1.3 m/s, p < 0.05), even though systolic blood pressure was higher in CG (120 ± 11 vs. 132 ± 14 mmHg, p = 0.002). PWV correlated only with age and pulmonary vascular resistance (PVR) in CTEPH (r = 0.45, p = 0.03 and r = 0.43, p = 0.03, respectively). Arterial stiffening defined as PWV > 10 m/s was found in 11 (42%) CTEPH patients and in 5 (23%) cases from CG (p = 0.13). CTEPH patients with PWV > 10 m/s were older (74 ± 8 vs. 66 ± 10 years, p < 0.05), had decreased oxygen saturation (SaO2 89 [73–96]% vs. 96 [85–98]%, p < 0.01) and tended to have higher PVR (8.1 [3.1–14.0] vs. 5.2 [3.1–12.7] HRU, p = 0.10).Conclusions: Arterial stiffness, assessed with PWV, is increased in CTEPH. The elevated PWV is associated with older age, lower SaO2 and higher PVR in CTEPH

    Signs of myocardial ischemia on electrocardiogram correlate with elevated plasma cardiac troponin and right ventricular systolic dysfunction in acute pulmonary embolism

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    Background: Plasma cardiac troponins (cTn) are frequently elevated in acute pulmonary embolism (APE). ST-segment abnormalities on electrocardiography are also commonly observed in APE patients. However, it has not been defined which ventricle is a potential source of cTn release. We assessed the potential relationship between electrocardiographic signs of myocardial ischemia, systolic dysfunction of both ventricles at echocardiography and cTn levels in APE. Methods: We evaluated 94 consecutive patients (42 male, 52 female, aged 63 &#177; 19 years) with APE. On admission, blood samples were collected for cTnI or cTnT and standard 12-lead electrocardiogram was performed. The following signs of myocardial ischemia were analyzed: T-wave inversion [T (-)] and ST-depression or elevation (&#8805; 1 mV, at &#8805; 2 leads). The assessment of systolic function of both ventricles was performed by echocardiography. Results: In 33 (35%) patients, cTn exceeded the upper reference limit of our laboratory. The history of coronary artery disease (27% vs. 31%) and previous myocardial infarction (12% vs. 10%) did not differ in patients with elevated cTn [cTn (+)] and non-elevated cTn [cTn (-)]. In cTn (+) group T (-) or ST-depression were observed more frequently than in cTn (-) [32 (97%) vs. 46 (75%), p < 0.01]. However, both groups presented similar frequency of ST-elevation [7 (21%) vs. 11 (18%), p = NS). Interestingly, cTn levels correlated with the number of leads with T (-) or ST-depression (R = 0.30, p < 0.01). Moreover, in cTn (+) group right ventricular systolic dysfunction was more frequent [15 (54%) vs. 4 (7%), p = 0.0001], while left ventricle contractility abnormalities occurred similarly in both groups [3 (11%) vs. 8 (15%), p = NS]. Conclusions: Signs of myocardial ischemia (ST-segment changes) on electrocardiography in APE correlate with an elevated cTn and with the impairment of right, but not left, ventricle systolic function at echocardiography. (Cardiol J 2010; 17, 2: 157-162

    Peak systolic velocity of tricuspid annulus is inferior to tricuspid annular plane systolic excursion for 30 days prediction of adverse outcome in acute pulmonary embolism

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    Background: Tricuspid annular plane systolic excursion (TAPSE) is an established index of right ventricular (RV) systolic function and a significant predictor in normotensive patients with pulmonary embolism (PE). Recently, Doppler tissue imaging-derived tricuspid annular systolic velocity (TV S’), a modern parameter of RV function was reported to be useful in the diagnosis and prognosis of a broad spectrum of heart diseases. Therefore, herein, is an analysis of the prognostic value of both parameters in normotensive PE patients.Methods: One hundred and thirty nine consecutive PE patients (76 female, age 56.4 ± 19.5 years) were included in this study. All patients were initially anticoagulated. Transthoracic echocardiography was performed on admission. The study endpoint (SE) was defined as PE-related 30-day mortality and/or need for rescue thrombolysis.Results: Seven (5%) patients who met the criteria for SE presented more severe RV dysfunction at echocardiography. Univariable Cox regression analysis showed that RV/LV ratio predicted SE with hazard risk (HR) 10.6 (1.4–80.0; p = 0.02); TAPSE and TV S’ showed HR 0.77 (0.67–0.89), p &lt; 0.001, and 0.71 (0.52–0.97), p = 0.03, respectively. Area under the curve for TAPSE in the prediction of SE was 0.881; 95% CI 0.812–0.932, p = 0.0001, for TV S’ was 0.751; 95% CI 0.670–0.820, p = 0.001. Multivariable analysis showed that the optimal prediction model included TAPSE and systolic blood pressure (SBP showed HR 0.89 95% CI 0.83–0.95, p &lt; 0.001 and TAPSE HR 0.67, 95% CI 0.52–0.87, p&lt;0.03). Kaplan-Meier analysis showed that initially PE patients with TAPSE ≥ 18 mm had a much more favorable prognosis that patients with TAPSE &lt; 18 mm (p &lt; 0.01), while analysis of S’ was only of borderline statistical significance.Conclusions: It seems that TV S’ is inferior to TAPSE for 30 day prediction of adverse outcome in acute pulmonary embolism

    Is There a Relationship between Leptin Concentration, Sympathetic Nervous System and Left Ventricular Mass Index in Patients with Essential Hypertension According to Gender and Body Mass Index?

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    Wstęp Celem niniejszej pracy była ocena współzależności między stężeniem leptyny a układem współczulnym, ciśnieniem tętniczym i masą lewej komory serca u chorych z nadciśnieniem tętniczym pierwotnym w zależności od płci i wskaźnika masy ciała (BMI). Materiał i metody Badaniami objęto 46 chorych (21K, 25M; śr. wiek 44,0 &plusmn; 8,4 roku), z nadciśnieniem tętniczym pierwotnym. Grupę kontrolną stanowiło 37 ochotników (19K, 18M; śr. wiek 40,8 &plusmn; 9,8 roku). Badanych podzielono na grupy w zależności od płci i BMI (poniżej i powyżej 25). U wszystkich badanych oznaczano stężenie leptyny (RIA), noradrenaliny (NA) i adrenaliny (A) (HPLC) oraz NPY (RIA) we krwi; mierzono odsetek tkanki tłuszczowej i wykonywano badanie echokardiograficzne. Wyniki U chorych z nadciśnieniem tętniczym pierwotnym stężenie leptyny było podobne jak u osób bez nadciśnienia w porównywalnych grupach kontrolnych, było natomiast znamiennie wyższe u kobiet i u osób z nadwagą. Stężenie NA było istotnie wyższe u chorych z nadwagą. W badanych grupach nie wykazano różnic w stężeniu NPY, bez względu na płeć i BMI. Wskaźnik masy lewej komory serca (LVMI) był znamiennie wyższy u kobiet z nadciśnieniem tętniczym pierwotnym w porównaniu z grupą kontrolną, niezależnie od BMI. Wieloczynnikowa analiza regresji wykazała w całej grupie badanych (n = 83) związek między leptyną a płcią, BMI, wiekiem, ciśnieniem skurczowym i NA (r2 = 0,28, p < 0,0001), a u kobiet i mężczyzn z nadciśnieniem tętniczym pierwotnym - związek między leptyną a odsetkiem tłuszczu i NA (r2 = 0,34, p < 0,001). U chorych mężczyzn z nadwagą analiza regresji wykazała związek między leptyną a LVMI i ciśnieniem rozkurczowym (DBP), natomiast u chorych kobiet z nadwagą - z wiekiem, odsetkiem tłuszczu i LVMI. Wnioski Uzyskane wyniki mogą sugerować udział leptyny w regulacji ciśnienia tętniczego poprzez układ współczulny, jak również w patogenezie przerostu masy lewej komory serca.Background The aim of the study was to evaluate the relationship between plasma leptin, sympathetic nervous system, blood pressure and left ventricular mass index in patients with essential hypertension (EH) according to gender and BMI. Material and methods The study included 46 patients (21F, 25M; mean age: 44,0 &plusmn; 8,4 yrs) with EH. Control group consisted of 37 volunteers (19F, 18M; mean age 40,8 &plusmn; 9,8 yrs). All subjects were divided into subgroups according to gender and BMI (). Concentration of plasma leptin (RIA), catecholamines (HPLC), NPY (RIA) and body fat percentage were determined in all subjects. In addition ECHO test was performed. Results In patients with EH plasma leptin concentration was comparable to controls, but values were significantly higher in women and in overweight patients. Plasma NA concentration was significantly elevated in overweight EH patients. No difference in NPY concentration was found in none of compared groups. LVMI was significantly higher in women with EH in comparison with controls, independently on body mass index. Multiple regression analysis indicated the relation between leptin and gender, BMI, age, systolic blood pressure and NA (r2 = 0,28, p < 0,0001) in all investigated subjects, as well as between leptin and body fat % and NA in EH patients (r2 = 0,34, p < 0,001). Multiple regression analysis indicated also the relation between leptin and LVMI, A and diastolic blood pressure (r2 = 0,54, p < 0,05) in overweight EH men as well as between leptin and age, body fat % and LVMI in overweight EH women (r2 = 0,69, p < 0,05). Conclusion This study suggests that leptin may contribute to regulation of blood pressure through sympathetic nervous system and may have implication in pathogenesis of left ventricular hypertrophy
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