Témata prací (Výběr práce)Témata prací (Výběr práce)(verze: 336)
Detail práce
  
Vztah reperfuze plicních tepen po akutní plicní embolii k rozvoji chronické tromboembolické plicní hypertenze.
Název práce v češtině: Vztah reperfuze plicních tepen po akutní plicní embolii k rozvoji chronické tromboembolické plicní hypertenze.
Název v anglickém jazyce: Relation between the reperfusion of pulmonary arteries after an acute pulmonary embolism to the development of chronic thromboembolic pulmonary hypertension.
Klíčová slova: plicní embolie, reperfuze, chronická tromboembolická plicní hypertenze, hemoglobin
Klíčová slova anglicky: Pulmonary embolism, reperfusion, chronic thromboembolic pulmonary hypertension, hemoglobin
Akademický rok vypsání: 2013/2014
Typ práce: disertační práce
Jazyk práce: čeština
Ústav: II. interní klinika – klinika kardiologie a angiologie 1. LF UK a VFN (11-00520)
Vedoucí / školitel: prof. MUDr. Pavel Jansa, Ph.D.
Řešitel: skrytý - zadáno a potvrzeno stud. odd.
Datum přihlášení: 13.08.2014
Datum zadání: 13.08.2014
Datum potvrzení stud. oddělením: 13.08.2014
Datum a čas obhajoby: 12.09.2019 10:00
Místo konání obhajoby: Fyziologický ústav 1. LF UK, Albertov 5, 128 00 Praha 2
Datum odevzdání elektronické podoby:13.05.2019
Datum proběhlé obhajoby: 12.09.2019
Předmět: Obhajoba dizertační práce (B90002)
Oponenti: doc. MUDr. Hana Maxová, Ph.D.
  prof. MUDr. Martin Hutyra, Ph.D.
 
 
Seznam odborné literatury
1. Kittnar O. Lékařská fyziologie, Grada, Praha, 2011.
2. Ganong WJ. Přehled lékařské fyziologie, dvacáté vydání, Galén, Praha, 2005.
3. McIntyre KM, Sasahara AA. The hemodynamic response to pulmonaryembolism in patients without prior cardiopulmonary disease. Am J Cardiol 1971; 28(3): 288–294.
4. Smulders YM. Pathophysiology and treatment of haemodynamic instability in acute pulmonary embolism: the pivotal role of pulmonary vasoconstriction. Cardiovasc Res 2000; 48(1): 23–33.
5. Nečas E. Pafologická fyziologie orgánových systémů část 1, Karolinum, Praha 2006.
6. Lankhaar JW, Westerhof N, Faes TJ, et al. Quantification of right ventricular afterload in patients with and without pulmonary hypertension. Am J Physiol Heart Circ Physiol 2006; 291(4): H1731– H1737.
7. Marcus JT, Gan CT, Zwanenburg J, et al. Interventricular mechanical asynchrony in pulmonary arterial hypertension: left-to-right delay in peak shortening is related to right ventricular overload and left ventricular underfilling. J Am Coll Cardiol 2008; 51(7): 750–757.
8. Begieneman MP, van de Goot FR, van der Bilt IA, et al. Pulmonary embolism causes endomyocarditis in the human heart. Heart 2008; 94(4): 450-456.
9. Ribeiro A, Lindmarker P, Johnsson H, et al. Pulmonary embolism: a follow-up study of the relation between the degree of right ventricle overload and the extent of perfusion defects. J Intern Med 1999; 245(6): 601-10.
10. Stein PD, Yaekoub AY, Matta F, et al. Resolution of pulmonary embolism on CT pulmonary angiography. Am J Roentgenol 2010; 194: 1263-8.
11. Fox EA, Kahn SR. The relationship between inflammation and venous thrombosis: a systematic review of clinical studies. Thromb Haemost 2005; 94: 362–365.
12. Jezovnik MK, Poredos P. Idiopathic venous thrombosis is related to systemic inflammatory response and to increased levels of circulating markers of endothelial dysfunction. Int Angiol 2010; 29(3): 226-31.
13. van Aken BE, den Heijer M, Bos GM, et al. Recurrent venous thrombosis and markers of inflammation. Thromb Haemost 2000; 83(4): 536-9.
14. Oger E. Incidence of venous thromboembolism: a community-based study in Western France. EPI-GETBP Study Group. Groupe d'Etude de la Thrombose de Bretagne Occidentale. Thromb Haemost 2 2000; 83(5): 657-60.
15. Heit JA. The epidemiology of venous thromboembolism in the community. Arterioscler Thromb Vasc Biol 2008; 28(3): 370–372.
16. Cohen AT, Agnelli G, Anderson FA, et al. Venous thromboembolism (VTE) in Europe. The number of VTE events and associated morbidity and mortality. Thromb Haemost 2007; 98(4): 756–764.
17. Meignan M, Rosso J, Gauthier H, et al. Systematic lung scans reveal a high frequency of silent pulmonary embolism in patients with proximal deep venous thrombosis. Arch Intern Med 2000; 160(2): 159- 64.
18. Laporte S, Mismetti P, De´cousus H, et al. Clinical predictors for fatal pulmonary embolism in 15,520 patients with venous thromboembolism: findings from the Registro Informatizado de la Enfermedad TromboEmbolica venosa (RIETE) Registry. Circulation 2008; 117(13): 1711–1716.
19. Goldhaber SZ, Visani L, De Rosa M. Acute pulmonary embolism: clinical outcomes in the International Cooperative Pulmonary Embolism Registry (ICOPER). Lancet 1999;353(9162): 1386–1389.
20. Carson JL, Kelley MA, Duff A, et al. The clinical course of pulmonary embolism. N Engl J Med 1992; 326: 1240-1245.
21. Heit JA, Silverstein MD, Mohr DN, et al. Predictors of survival after deep vein thrombosis and pulmonary embolism: a population-based, cohort study. Arch Intern Med 1999; 159: 445–453.
22. Miniati M, Monti S, Bottai M, et al. Survival and restoration of pulmonary perfusion in a long-term follow-up ofpatients after acute pulmonary embolism. Medicine (Baltimore) 2006; 85(5): 253–262.
23. Heit JA. Predicting the risk of venous thromboembolism recurrence. Am J Hematol 2012; 87 Suppl 1: S63–S67.
24. Becatinni C, Agnelli G, Prandoni P, et al. Clinical research A prospective study on cardiovascular events after acute pulmonary embolism Eur Heart J 2005; 26: 77–83.
25. Schulman S, Kakkar AK, Goldhaber SZ, et al. Treatment of acute thromboembolism with dabigatran or warfarin and pooled analysis. Circulation 2014; 129(7): 764–772.
26. Bauersachs R, Berkowitz SD, Brenner B, et al. Oral rivaroxaban for symptomatic venous thromboembolism. N Engl J Med 2010; 363(26): 2499–2510.
27. Büller HR, Prins MH, Lensin AW, et al. Oral rivaroxaban for the treatment of symptomatic pulmonary embolism. N Engl J Med 2012; 366(14): 1287–1297.
28. Agnelli G, Büller HR, Cohen A, et al. Oral apixaban for the treatment of acute venous thromboembolism. N Engl J Med 2013; 369(9): 799–808.
29. Büller HR, Decousus H, Grosso MA, et al. Edoxaban versus warfarin for the treatment of symptomatic venous thromboembolism. N Engl J Med 2013; 369(15): 1406–1415.
30. Dentali F, Donadini M, Gianni M, et al. Incidence of chronic pulmonary hypertension in patients with previous pulmonary embolism. Thromb Res 2009 Jul;124(3): 256-8.
31. Pengo V, Lensing A, Prins M, et al. Incidence of Chronic Thromboembolic Pulmonary Hypertension after Pulmonary Embolism N Engl J Med 2004; 350: 2257-2264.
32. Becattini C, Agnelli G, Pesavento R, et al. Incidence of chronic thromboembolic pulmonary hypertension after a first episode of pulmonary embolism. Chest 2006; 130(1): 172–175.
33. Yang S, Yang Y Zhai Z., et al. Incidence and risk factors of chronic thromboembolic pulmonary hypertension in patients after acute pulmonary embolism. J Thorac Dis 2015; 7(11): 1927–1938.
34. Konstantinides S, Torbicki A, Agnelli G. 2014 ESC guidelines on the diagnosis and management of acute pulmonary embolism. Eur Heart J 2014; 35: 3033–3080.
35. Goldhaber SZ, Grodstein F, Stampfer MJ A, et al. Prospective Study of Risk Factors for Pulmonary Embolism in Women JAMA 1997; 277(8): 642-645.
36. Galie` N, Humbert M, Vachieryc JL, et al. 2015 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension. Eur Heart J 2016; 37: 67–119.
37. Hoeper MM, Bogaard HJ, Condliffe R et al. Definitions and diagnosis of pulmonary hypertension. J Am Coll Cardiol 2013; 62(Suppl): D42–D50.
38. Lang RM, Badano LP, Mor-Avi V, et al. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. Eur Heart J Cardiovasc Imaging 2015; 16: 233–271.
39. Simonneau G, Galie` N, Rubin LJ, et al. Clinical classification of pulmonary hypertension. J Am Coll Cardiol 2004; 43(Suppl 1): S5–S12.
40. Widimský J, Widimský P. Základy invazivní hemodynamiky, Triton, Praha, 2003.
41. Simonneau G, Torbicki A, Dorfmüller A, et al. The pathophysiology of chronic thromboembolic pulmonary hypertension. European Respiratory Review 2017; 26: 100-112.
42. Moser KM, Bloor CM. Pulmonary vascular lesions occurring in patients with chronic major vessel thromboembolic pulmonary hypertension. Chest 1993; 103: 685–692.
43. Pietra GG, Capron F, Stewart S, et al. Pathologic assessment of vasculopathies in pulmonary hypertension. J Am Coll Cardiol 2004; 43: 25S–32S.
44. Dorfmüller P, Günther S, Ghigna MR, et al. Microvascular disease in chronic thromboembolic pulmonary hypertension: a role for pulmonary veins and systemic vasculature. Eur Respir J 2014; 44: 1275–1288.
45. Tonelli AR, Haserodt S, Aytekin M, et al. Nitric oxide deficiency in pulmonary hypertension: pathobiology and implications for therapy. Pulm Circ 2013; 3: 20–30.
46. Skoro-Sajer N, Mittermayer F, Panzenboeck A et al. Asymmetric dimethylarginine is increased in chronic thromboembolic pulmonary hypertension. Am J Respir Crit Care Med 2007; 176: 1154– 1160.
47. Southwood M, MacKenzie RV, Kuc RE, et al. Endothelin ETA receptors predominate in chronic thromboembolic pulmonary hypertension. Life Sci 2016; 159: 104–110.
48. Bates DM, Fernandes TM, Chiles PG, et al. Preoperative plasma angiopoietin-2 levels may predict adverse outcomes following pulmonary thromboendarterectomy. Am J Respir Crit Care Med 2015; 191: A5411.
49. Kim NH. Group 4 pulmonary hypertension: chronic thromboembolic pulmonary hypertension: epidemiology, pathophysiology, and treatment. Cardiol Clin 2016; 34: 435–441.
50. McCabe C, White PA, Hoole SP, et al. Right ventricular dysfunction in chronic thromboembolic obstruction of the pulmonary artery: a pressure-volume study using the conductance catheter. J Appl Physiol 2014; 116: 355–363.
51. Giusca S, Popa E, Amzulescu MS, et al. Is right ventricular remodeling in pulmonary hypertension dependent on etiology? An echocardiographic study. Echocardiography 2016; 33: 546–554.
52. Delcroix M, Vonk Noordegraaf A, Fadel E, et al. Vascular and right ventricular remodelling in chronic thromboembolic pulmonary hypertension. Eur Respir J 2013; 41: 224–232.
53. van de Veerdonk MC, Bogaard HJ, Voelkel NF. The right ventricle and pulmonary hypertension. Heart Fail Rev 2016; 21: 259–271.
54. Carson JL, Kelley MA, Duff A, et al. The clinical course of pulmonary embolism. N Engl J Med 1992; 326: 1240-1245.
55. Pepke-Zaba J, Delcroix M, Lang I, et al. Chronic thromboembolic pulmonary hypertension (CTEPH): results from an international prospective registry. Circulation 2011; 124: 1973–1981.
56. Escribano-Subias P, Blanco I, López-Meseguer M, et al. Survival in pulmonary hypertension in Spain: insights from the spanish registry. Eur Respir J 2012; 40(3): 596-603.
57. Hoeper MM, Humbert M, Souza R, et al. A global view of pulmonary hypertension. Lancet Respir Med 2016; 4: 306–322.
58. Klok FA, van Kralingen KW, van Dijk AP, et al. Prospective cardiopulmonary screening program to detect chronic thromboembolic pulmonary hypertension in patients after acute pulmonary embolism. Haematologica 2010; 95: 970–975.
59. Sanchez O, Helley D, Couchon S, et al. Perfusion defects after pulmonary embolism: risk factors and clinical significance. J Thromb Haemost 2010; 8(6): 1248–1255.
60. Remy‐Jardin M, Louvegny S, et al. Acute central thromboembolic disease: post therapeutic follow‐up with spiral CT angiography. Radiology 1997; 203: 173–180
61. Bonderman D, Wilkens H, Wakounig S, et al. Risk factors for chronic thromboembolic pulmonary hypertension. Eur Respir J 2009; 33: 325–331.
62. Bonderman D, Jakowitsch J, Redwan B, et al. Role for staphylococci in misguided thrombus resolution of chronic thromboembolic pulmonary hypertension. Arterioscler Thromb Vasc Biol 2008; 28: 678–684.
63. Olman MA, Marsh JJ, Lang IM, et al. Endogenous fibrinolytic system in chronic large-vessel thromboembolic pulmonary hypertension. Circulation 1992; 86: 1241–1248.
64. Lang IM, Klepetko W, Pabinger I. No increased prevalence of the factor V Leiden mutation in chronic major vessel thromboembolic pulmonary hypertension (CTEPH). Thromb Haemost 1996; 76: 476–477.
65. Wolf M, Boyer-Neumann C, Parent F, et al. Thrombotic risk factors in pulmonary hypertension. Eur Respir J 2000; 15: 395–399.
66. Bonderman D, Turecek PL, Jakowitsch J, et al. High prevalence of elevated clotting factor VIII in chronic thromboembolic pulmonary hypertension. Thromb Haemost 2003; 90: 372–376.
67. Morris TA, Marsh JJ, Chiles PG, et al. High prevalence of dysfibrinogenemia among patients with chronic thromboembolic pulmonary hypertension. Blood 2009; 114: 1929–1936.
68. Le Gal G, Delahousse B, Lacut K et al. Fibrinogen Aα-Thr312Ala and factor XIII-A Val34Leu polymorphisms in idiopathic venous thromboembolism. Thromb Res 2007; 121: 333–338.
69. Suntharalingam J, Goldsmith K, van Marion V, et al. Fibrinogen Aα Thr312Ala polymorphism is associated with chronic thromboembolic pulmonary hypertension. Eur Respir J 2008; 31: 736–741.
70. Marsh JJ, Chiles PG, Liang NC, et al. Chronic thromboembolic pulmonary hypertension-associated dysfibrinogenemias exhibit disorganized fibrin structure. Thromb Res 2013; 132: 729–734.
71. Frey MK, Alias S, Winter MP, et al. Splenectomy is modifying the vascular remodeling of thrombosis. J Am Heart Assoc 2014; 3: e000772.
72. Remková A, Šimková I, Valkovičová T. Platelet abnormalities in chronic thromboembolic pulmonary hypertension. Int J Clin Exp Med 2015; 8: 9700–9707.
73. Alias S, Redwan B, Panzenböck A, et al. Defective angiogenesis delays thrombus resolution: a potential pathogenetic mechanism underlying chronic thromboembolic pulmonary hypertension. Arterioscler Thromb Vasc Biol 2014; 34: 810–819.
74. Bouma BN, Mosnier LO. Thrombin activatable fibrinolysis inhibitor (TAFI) at the interface between coagulation and fibrinolysis. Pathophysiol Haemost Thromb 2003; 33: 375–381.
75. Dorfmuller P, Perros F, Balabanian K, et al. Inflammation in pulmonary arterial hypertension. Eur Respir J 2003; 22: 358–363.
76. Kimura H, Okada O, Tanabe N. Plasma monocyte chemoattractant protein-1 and pulmonary vascular resistance in chronic thromboembolic pulmonary hypertension. Am J Respir Crit Care Med 2001; 164: 319–324.
77. Fartoukh M, Emilie D, Le Gall C, et al. Chemokine macrophage inflammatory protein-1alpha mRNA expression in lung biopsy specimens of primary pulmonary hypertension. Chest 1998; 114 (suppl): 50S–51S.
78. Humbert M, Monti G, Brenot F, et al. Increased interleukin-1 and interleukin-6 serum concentrations in severe primary pulmonary hypertension. Am J Respir Crit Care Med 1995; 151: 1628–1631.
79. Zabini D, Heinemann A, Foris V, et al. Comprehensive analysis of inflammatory markers in chronic thromboembolic pulmonary hypertension patients. Eur Respir J 2014; 44: 951–962.
80. Gu S, Su P, Yan J, et al. Comparison of gene expression profiles and related pathways in chronic thromboembolic pulmonary hypertension. Int J Mol Med 2014; 33: 277–300.
81. Tanabe N, Amano S, Tatsumi K, et al. Angiotensin-converting enzyme gene polymorphisms and prognosis in chronic thromboembolic pulmonary hypertension. Circ J 2006; 70: 1174–1179.
82. Chen Z, Nakajima T, Tanabe N, et al. Susceptibility to chronic thromboembolic pulmonary hypertension may be conferred by miR-759 via its targeted interaction with polymorphic fibrinogen alpha gene. Hum Genet 2010; 128: 443–452.
83. Du L, Sullivan CC, Chu D, et al. Signaling molecules in nonfamilial pulmonary hypertension. N Engl J Med 2003; 348: 500–509.
84. Meysman M, Everaert H, Buls N, et al. Comparison of ventilation perfusion single photon emission computed tomography (V/Q SPECT) versus dual energy CT perfusion and angiography (DECT) after 6 months of pulmonary embolism (PE) treatment. Eur J Radiol 2015; 84: 1816-9.
85. Cosmi B, Nijkeuter M, Valentino M, et al. Residual emboli on lung perfusion scan or multidetector computed tomography after a first episode of acute pulmonary embolism. Intern Emerg Med 2011; 6(6): 521–528.
86. Alonso-Martínez JL, Anniccherico-Sánchez FJ, Urbieta-Echezarreta MA, at al. Residual pulmonary thromboemboli after acute pulmonary embolism. Eur J Intern Med 2012; 23(4): 379-83.
87. van Es J1, Douma RA, Kamphuisen PW et al. Clot resolution after 3 weeks of anticoagulant treatment for pulmonary embolism: comparison of computed tomography and perfusion scintigraphy. J Thromb Haemost 2013; 11(4): 679-85.
88. Pesavento R, Filippi L, Pagnan A, et al. (2014) Unexpectedly high recanalization rate in patients with pulmonary embolism treated with anticoagulants alone. Am J Respir Crit Care Med; 189: 1277- 1279.
89. den Exter PL, van Es J, Kroft LJ, et al. (2015) Thromboembolic resolution assessed by CT pulmonary angiography after treatment for acute pulmonary embolism. Thromb Haemost 2015; 114(1): 26-34.
90. Choi KJ1, Cha SI, Shin KM, et al. Factors determining clot resolution in patients with acute pulmonary embolism. Blood Coagulation & Fibrinolysis 2016; 27(3): 294–300.
91. Brækkan SK, Mathiesen KV, Njølstad I, et al. Hematocrit and risk of venous thromboembolism in a general population. The Tromsø study. Haematologica. 2010; 95(2): 270–275.
92. Gagnon DR, Zhang TJ, Brand F, et al. Hematocrit and the risk of cardiovascular disease—the Framingham study: a 34-year followup. Am Heart J 1994; 127: 674–682.
93. Guilpain P, Montani D, Damaj G, et al. Pulmonary hypertension associated with myeloproliferative disorders: a retrospective study of ten cases. Respiration 2008; 76:295–302
94. Adir Y, Humbert M. Pulmonary hypertension in patients with chronic myeloproliferative disorders. Eur Respir J 2010; 35: 1396–1406.
95. IBM SPSS Statistics 24 URL:https://www-01.ibm.com/support/docview.wss?uid= swg24041224
96. R Core Team. R: A language and environment for statistical computing. R Foundation for Statistical Computing, Vienna, Austria 2018; URL:https://www.R-project.org/.
97. Therneau T. A Package for Survival Analysis in S. 2015; version 2.38, URL:https://CRAN.R-project.org/package=survival.
98. Angelo Canty and Brian Ripley (2017). boot: Bootstrap R (S-Plus) Functions. 2017; R package version 1.3-20.
99. Greenberg G, Assali A, Vaknin-Assa H, et al. Hematocrit level as a marker of outcome in ST-segment elevation myocardial infarction. Am J Cardiol 2010; 105: 435–440
100. Wu WC, Schifftner TL, Henderson WG, et al. Preoperative hematocrit levels and postoperative outcomes in older patients undergoing noncardiac surgery. JAMA 2007; 297: 2481–2488.
101. Le Gal G, Righini M, Roy PM, et al. Prediction of pulmonary embolism in the emergency department: the revised Geneva score. Ann Intern Med 2006; 144(3): 165–171.
102. Wells PS, Anderson DR, Rodger M, et al. Derivation of a simple clinical model to categorize patients probability of pulmonary embolism: increasing the models utility with the SimpliRED D-dimer. Thromb Haemost 2000; 83(3): 416–420
103. Aujesky D, Obrosky DS, Stone RA, et al. Derivation and validation of a prognostic model for pulmonary embolism. Am J Respir Crit Care Med 2005; 172(8): 1041–1046.
104. Wicki J, Perrier A, Perneger TV, et al. Predicting adverse outcome in patients with acute pulmonary embolism: a risk score. Thromb Haemost 2000; 84(4): 548–552.
105. Jime´nez D, Aujesky D, Moores L, et al. Simplification of the pulmonary embolism severity index for prognostication in patients with acute symptomatic pulmonary embolism. Arch Intern Med 2010; 170(15): 1383–1389.
106. Klok FA, Surie S, Kempf T, et al. A simple non-invasive diagnostic algorithm for ruling out chronic thromboembolic pulmonary hypertension in patients after acute pulmonary embolism. Thromb Res 2011; 128: 21–6.
Předběžná náplň práce
Porucha reperfuze, respektive porucha rezoluce tromboembolů, je klíčovým faktorem vedoucím od akutní plicní embolie (PE) k chronické tromboembolické plicní hypertenzi (CTEPH). V naší práci jsme hodnotili incidenci, rizikové faktory a klinický dopad poruchy reperfuze po plicní embolii.
Soubor a metodika: Celkem 85 pacientů po první epizodě PE bylo klinicky, scintigraficky a echokardiograficky sledováno 6, 12 a 24 měsíců po příhodě PE.
Výsledky:Perzistující defekty perfuze na perfuzním scintigramu plic byly přítomny po 6 měsících u 23,5 % pacientů, po 12 měsících u 24,9 % pacientů a po 24 měsících u 18,6 % pacientů. Pacienti s perzistujícími defekty při kontrole v 6. měsíci byli obéznější (BMI 30,8 vs 28,3, kg/m2; p 0,012) a měli vyšší hladinu hemoglobinu při iniciální plicní embolii (143,0 vs 136,0 g/l; p 0,012). Pacienti s perzistujícími defekty ve 12. měsíci byli rovněž obéznější (BMI 31,1 vs 28,5kg/m2; p 0,016) a měli vyšší hladinu hemoglobinu při iniciální plicní embolii (144,0 vs 136,0; p 0,007). Pacienti s perzistujícími defekty perfuze ve 24. měsíci po PE byli starší (67,7 vs 55,0; p 0,02), měli vyšší hemoglobin při iniciální PE (144,5 vs 136,0; p 0,031) a jejich iniciální plicní embolie byla častěji středně nebo vysoce riziková (85,7 vs 47,5 %, p 0,026), s čímž souvisel i větší rozměr pravé komory (36,5 vs 32,5 mm; p 0,044) a významnější trikuspidální regurgitace (2,0 vs 1,5; p 0,018) při vstupním echokardiografickém vyšetření. Pacienti s přetrvávajícími defekty perfuze ve 24. měsíci měli také průměrně vyšší hodnotu systolického tlaku v plicnici (30,0 vs 22,5 mmHg) při echokardiografickém vyšetření provedeném ve 24. měsíci, jinak se od skupiny pacientů bez defektů v klinických, funkčních či echokardiografických parametrech nelišili. U tří pacientů (3,5 %) byla přítomna ve 24. měsíci CTEPH.
Ze získaných dat jsme vytvořili predikční skóre, které na základě dvou parametrů – věku a hladiny hemoglobinu – rozdělilo soubor do tří skupin dle rizika přetrvávání perfuzních defektů. Ve skupině nejnižšího rizika (s hladinou hemoglobinu <140 g/l) bylo ve 24 měsíci dosaženo kompletní reperfuze v 94 % případů, ve skupině středního rizika (s hemoglobinem >140 g/l mladších 65 let) bylo dosaženo reperfuze v 75 % případů a ve skupině s nejvyšším rizikem (hemoglobin >140 g/l a věk >65 let) bylo dosaženo reperfuze jen v 66 % případů. Pacienti ve skupině s nejvyšším rizikem měli 9,4 x vyšší riziko přetrvávání perfuzních defektů než pacienti s nejnižším rizikem.
Závěr:Po 24 měsících po akutní PE byla v našem souboru přítomna nekompletní reperfuze u 18,6 % nemocných. Rizikovými faktory nekompletní reperfuze byly vyšší věk, vyšší BMI, vyšší hladina hemoglobinu a středně a více riziková plicní embolie. Pacienti s inkompletní reperfuzí ve 24. měsíci měli vyšší systolický krevní tlak v plicnici. Dle hladiny hemoglobinu a věku při vstupním vyšetření je možno určit u jednotlivých pacientů vysoké, střední a nízké riziko přetrvávání defektů perfuze.
Předběžná náplň práce v anglickém jazyce
Incomplete resolution of thromboemboli following acute pulmonary embolism (PE) is a key factor in development of chronic thromboembolic pulmonary hypertension (CTEPH). In our study, we evaluated the incidence, risk factors and clinical impact of incomplete reperfusion after acute PE.
Study population and methods: 85 patients after the first acute PE­ were assessed clinically and by pulmonary scintigraphy and echocardiography at month 6, 12 and 24 after an acute PE.
Results: Incomplete reperfusion was detected in 23.5 % of patients after 6 months, in 24.9 % of patients after 12 months and in 18.6 % of patients after 24 months. At month 6, patients with incomplete reperfusion were more obese when compared with patients with normal reperfusion BMI 30.8 vs 28.3 kg/m2; p=0.012) and their initial hemoglobin levels were higher (143.0 vs 136.0 g/l; p=0.012). Similar results were observed at month 12 – patients with residual perfusion defects were more obese (BMI 31.1 vs 28.5; p=0.016) with higher initial hemoglobin levels (144.0 vs 136.0; p=0.007). Patients with incomplete reperfusion at month 24 were significantly older (67.7 vs 55.0 years; p=0.02), their initial hemoglobin levels were higher (144.5 vs 136.0; p= 0.031) and their PE was more frequently of intermediate or high risk (85.7 vs 47.5%; p=0.026). It was associated with larger diameter of the right ventricle (36.5 vs 32.5 mm; p=0.044) and more significant tricuspid regurgitation (2.0 vs 1.5; p= 0.018) during the initial echocardiography examination. The estimated pulmonary arterial systolic pressure was elevated in patients with perfusion defects persisting at month 24 after the acute PE in comparison with remaining patients (30.0 vs 22.5 mmHg). CTEPH was diagnosed in 3 patients (3.5%) from our cohort.
From the acquired data, we created a clinical risk prediction score for persistence of perfusion defects based on two parameters – hemoglobin levels and age. This prediction score classifies our cohort into 3 groups according to the risk of persistence of perfusion defects.
In the lowest risk group (hemoglobin <140 g/l), a complete reperfusion was achieved in 94% after 24 months; in the intermediate risk group (hemoglobin level >140 g/l and age <65 years), reperfusion was achieved in 75%; and in the high risk group (hemoglobin level >140 g/l and age >65 years), reperfusion was achieved only in 66% of cases. The risk of persisting perfusion defects after 24 months was therefore 9.4 times higher in patients in the highest risk group than the in the lowest risk group.
Conclusions: During the 24 months of observation after an acute PE, incomplete reperfusion was detected in 18.6 % of patients. Higher risk of incomplete reperfusion was associated with higher age, higher BMI, higher initial hemoglobin levels and with intermediate or high risk acute PE. It is possible to predict the low, medium or high risk of persisting perfusion defects at each patient according the hemoglobin level and the age at initial examination.
 
Univerzita Karlova | Informační systém UK