Dokument: Diabetes mellitus und Vaping als Risikofaktoren einer veränderten Thrombozytenaggregation
| Titel: | Diabetes mellitus und Vaping als Risikofaktoren einer veränderten Thrombozytenaggregation | |||||||
| URL für Lesezeichen: | https://docserv.uni-duesseldorf.de/servlets/DocumentServlet?id=64869 | |||||||
| URN (NBN): | urn:nbn:de:hbz:061-20240312-141340-7 | |||||||
| Kollektion: | Dissertationen | |||||||
| Sprache: | Deutsch | |||||||
| Dokumententyp: | Wissenschaftliche Abschlussarbeiten » Dissertation | |||||||
| Medientyp: | Text | |||||||
| Autor: | Metzen, Daniel [Autor] | |||||||
| Dateien: |
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| Beitragende: | Prof. Dr. med. Polzin, Amin [Gutachter] PD Dr. med. Buchbender, Christian [Gutachter] | |||||||
| Dewey Dezimal-Klassifikation: | 600 Technik, Medizin, angewandte Wissenschaften » 610 Medizin und Gesundheit | |||||||
| Beschreibungen: | Sowohl zur Prävention thrombotischer Ereignisse als auch gefährlicher Blutungen ist es notwendig Risikofaktoren einer veränderten Thrombozytenaggregation zu identifizieren und im klinischen Kontext zu untersuchen. In der vorliegenden Dis-sertation wurde zum einen der Diabetes mellitus (DM) als Risikofaktor für Blutungs-ereignisse nach perkutaner Koronarintervention (PCI) untersucht. Zum anderen wurde der Einfluss des Vaping von E-Zigarettenliquids auf die Thrombozytenaggre-gation untersucht. Zur Bemessung des Einflusses des DM auf Blutungsereignisse wurden historische Daten von PCI-Patienten der Klinik für Kardiologie, Pneumolo-gie und Angiologie des Universitätsklinikums Düsseldorf aus den Jahren 2016 und 2017 ausgewertet. Unter Berücksichtigung von Patientenmerkmalen, Komorbiditä-ten, Komedikation und Laborwerten konnte durch die Verwendung von inverse pro-bability of treatment weighting (IPTW) und multivariater Cox Regression gezeigt werden, dass sich das Risiko für Blutungen zwischen DM und nicht DM-Patienten nicht signifikant unterscheidet. Um den Einfluss des Vapings auf die Thrombozy-tenaggregation zu untersuchen wurden die Thrombozytenaggregation bei gesun-den Vapern, Rauchern und Nichtrauchern miteinander verglichen. Unter der Ver-wendung von IPTW konnte gezeigt werden, dass Vaper eine im Vergleich zu Nicht-rauchern, aber auch im Vergleich zu Rauchern, erhöhte Thrombozytenaggregation aufwiesen. Diese Ergebnisse haben sowohl Implikationen für die Risikobewertung kardiologischer Patienten als auch für deren Therapie. Zum einen könnten DM-Patienten von einer Verlängerung einer antithrombotischen Therapie nach PCI pro-fitieren da DM in vielen Studien mit einem erhöhten Risiko für thrombotische Ereig-nisse assoziiert wurde. Da Vaping in der vorliegenden Studie mit einer erhöhten Thrombozytenaggregation assoziiert war ist es nicht unwahrscheinlich das Vaping auch zu einem erhöhten Risiko für thrombotische Ereignisse führen kann. Falls eine Assoziation zwischen Vaping und thrombotischen Ereignissen in klinischen Studien gezeigt werden kann, könnte Vaping als neuer Faktor in Scores zur Bewer-tung des kardiovaskulären Risikos aufgenommen werden.To prevent thrombotic events as well as dangerous bleeding, it is necessary to iden-tify risk factors of altered platelet aggregation and to examine them in a clinical con-text. In this dissertation, diabetes mellitus (DM) was examined as a risk factor for bleeding events after percutaneous coronary intervention (PCI). Furthermore, the effect of vaping e-cigarette liquids on platelet aggregation was examined. To meas-ure the effect of DM on bleeding events, historical data of PCI patients from the De-partment of Cardiology, Pneumology and Angiology at the University Hospital Düs-seldorf were evaluated. When controlling for patient characteristics, comorbidities, co-medication, and laboratory values with inverse probability of treatment weighting (IPTW) and multivariate Cox regression, the risk of TIMI major and minor bleedings did not differ significantly between DM and non-DM patients. To explore the effect of vaping on platelet aggregation, ADP- and Collagen-stimulated platelets of vapers, smokers and non-smokers were compared using multiplate aggregometry. When controlling for age, gender, body height, and body weight with IPTW, vapers had an increased platelet aggregation compared to non-smokers, but also compared to smokers. These results have implications for the risk assessment of cardiological patients as well as for their therapy. DM patients could benefit from an extension of antithrombotic therapy after PCI, since DM has been associated with an increased risk of thrombotic events in many studies. Since vaping was associated with in-creased platelet aggregation in the present study, it is not unlikely that vaping may also lead to an increased risk of thrombotic events. If an association between vaping and thrombotic events can be shown in clinical trials, vaping could be included as a new factor in cardiovascular risk scores. | |||||||
| Quelle: | 1. Yeh, R.W., et al., Development and Validation of a Prediction Rule for Benefit and Harm of Dual Antiplatelet Therapy Beyond 1 Year After Percutaneous Coronary Intervention. JAMA, 2016. 315(16): p. 1735-49.
2. Costa, F., et al., Derivation and validation of the predicting bleeding complications in patients undergoing stent implantation and subsequent dual antiplatelet therapy (PRECISE-DAPT) score: a pooled analysis of individual-patient datasets from clinical trials. Lancet, 2017. 389(10073): p. 1025-1034. 3. Mehran, R., et al., Cessation of dual antiplatelet treatment and cardiac events after percutaneous coronary intervention (PARIS): 2 year results from a prospective observational study. Lancet, 2013. 382(9906): p. 1714-22. 4. Nieswandt, B. and S.P. Watson, Platelet-collagen interaction: is GPVI the central receptor? Blood, 2003. 102(2): p. 449-61. 5. Ruggeri, Z.M., The role of von Willebrand factor in thrombus formation. Thromb Res, 2007. 120 Suppl 1: p. S5-9. 6. Shin, E.K., et al., Platelet Shape Changes and Cytoskeleton Dynamics as Novel Therapeutic Targets for Anti-Thrombotic Drugs. Biomol Ther (Seoul), 2017. 25(3): p. 223-230. 7. Smith, E.F., 3rd, A.M. Lefer, and K.C. Nicolaou, Mechanism of coronary vasoconstriction induced by carbocyclic thromboxane A2. Am J Physiol, 1981. 240(4): p. H493-7. 8. Bennett, J.S., et al., Interaction of fibrinogen with its platelet receptor. Differential effects of alpha and gamma chain fibrinogen peptides on the glycoprotein IIb-IIIa complex. J Biol Chem, 1988. 263(26): p. 12948-53. 9. Camerer, E., A.B. Kolsto, and H. Prydz, Cell biology of tissue factor, the principal initiator of blood coagulation. Thromb Res, 1996. 81(1): p. 1-41. 10. Kirchhofer, D. and Y. Nemerson, Initiation of blood coagulation: the tissue factor/factor VIIa complex. Curr Opin Biotechnol, 1996. 7(4): p. 386-91. 11. Narayanan, S., Multifunctional roles of thrombin. Ann Clin Lab Sci, 1999. 29(4): p. 275-80. 12. Santoro, S.A. and J.F. Cowan, Thrombin enhanced adhesion of platelets to von Willebrand factor substrates. Thromb Res, 1986. 43(1): p. 57-72. 13. Monkovic, D.D. and P.B. Tracy, Activation of human factor V by factor Xa and thrombin. Biochemistry, 1990. 29(5): p. 1118-28. 14. Mertens, K. and R.M. Bertina, Pathways in the activation of human coagulation factor X. Biochem J, 1980. 185(3): p. 647-58. 15. Boon, G.D., An overview of hemostasis. Toxicol Pathol, 1993. 21(2): p. 170-9. 16. Carrizzo, A., et al., The Main Determinants of Diabetes Mellitus Vascular Complications: Endothelial Dysfunction and Platelet Hyperaggregation. Int J Mol Sci, 2018. 19(10). 17. Mannarino, E. and M. Pirro, Molecular biology of atherosclerosis. Clin Cases Miner Bone Metab, 2008. 5(1): p. 57-62. 18. Gimbrone, M.A., Jr. and G. Garcia-Cardena, Vascular endothelium, hemodynamics, and the pathobiology of atherosclerosis. Cardiovasc Pathol, 2013. 22(1): p. 9-15. 19. Muhlestein, J.B., Bacterial infections and atherosclerosis. J Investig Med, 1998. 46(8): p. 396-402. 20. Hemmat, N., et al., Viral infection and atherosclerosis. Eur J Clin Microbiol Infect Dis, 2018. 37(12): p. 2225-2233. 21. Broos, K., et al., Platelets at work in primary hemostasis. Blood Rev, 2011. 25(4): p. 155-67. 22. Davignon, J. and P. Ganz, Role of endothelial dysfunction in atherosclerosis. Circulation, 2004. 109(23 Suppl 1): p. III27-32. 23. Gorog, D.A., Z.A. Fayad, and V. Fuster, Arterial Thrombus Stability: Does It Matter and Can We Detect It? J Am Coll Cardiol, 2017. 70(16): p. 2036-2047. 24. Patrono, C. and B. Rocca, Aspirin and Other COX-1 inhibitors. Handb Exp Pharmacol, 2012(210): p. 137-64. 25. Dorsam, R.T. and S.P. Kunapuli, Central role of the P2Y12 receptor in platelet activation. J Clin Invest, 2004. 113(3): p. 340-5. 26. Lippi, G., et al., Glycoprotein IIb/IIIa inhibitors: an update on the mechanism of action and use of functional testing methods to assess antiplatelet efficacy. Biomark Med, 2011. 5(1): p. 63-70. 27. Gresele, P., S. Momi, and E. Falcinelli, Anti-platelet therapy: phosphodiesterase inhibitors. Br J Clin Pharmacol, 2011. 72(4): p. 634-46. 28. de Leval, X., et al., New developments on thromboxane and prostacyclin modulators part II: prostacyclin modulators. Curr Med Chem, 2004. 11(10): p. 1243-52. 29. Scully, M., et al., Caplacizumab Treatment for Acquired Thrombotic Thrombocytopenic Purpura. N Engl J Med, 2019. 380(4): p. 335-346. 30. Samson, S.L. and A.J. Garber, Metabolic syndrome. Endocrinol Metab Clin North Am, 2014. 43(1): p. 1-23. 31. Tegos, T.J., et al., The genesis of atherosclerosis and risk factors: a review. Angiology, 2001. 52(2): p. 89-98. 32. Gautier, E.L., C. Jakubzick, and G.J. Randolph, Regulation of the migration and survival of monocyte subsets by chemokine receptors and its relevance to atherosclerosis. Arterioscler Thromb Vasc Biol, 2009. 29(10): p. 1412-8. 33. Schwartz, C.J., et al., The pathogenesis of atherosclerosis: an overview. Clin Cardiol, 1991. 14(2 Suppl 1): p. I1-16. 34. Boullier, A., et al., Scavenger receptors, oxidized LDL, and atherosclerosis. Ann N Y Acad Sci, 2001. 947: p. 214-22; discussion 222-3. 35. Chistiakov, D.A., et al., Mechanisms of foam cell formation in atherosclerosis. J Mol Med (Berl), 2017. 95(11): p. 1153-1165. 36. Watson, M.G., et al., A two-phase model of early fibrous cap formation in atherosclerosis. J Theor Biol, 2018. 456: p. 123-136. 37. Bentzon, J.F., et al., Mechanisms of plaque formation and rupture. Circ Res, 2014. 114(12): p. 1852-66. 38. Feron, O., et al., Hypercholesterolemia decreases nitric oxide production by promoting the interaction of caveolin and endothelial nitric oxide synthase. J Clin Invest, 1999. 103(6): p. 897-905. 39. Gries, A., et al., Inhaled nitric oxide inhibits human platelet aggregation, P-selectin expression, and fibrinogen binding in vitro and in vivo. Circulation, 1998. 97(15): p. 1481-7. 40. Ley, K. and Y. Huo, VCAM-1 is critical in atherosclerosis. J Clin Invest, 2001. 107(10): p. 1209-10. 41. Frenette, P.S., et al., Platelets roll on stimulated endothelium in vivo: an interaction mediated by endothelial P-selectin. Proc Natl Acad Sci U S A, 1995. 92(16): p. 7450-4. 42. Ruggeri, Z.M., Von Willebrand factor, platelets and endothelial cell interactions. J Thromb Haemost, 2003. 1(7): p. 1335-42. 43. Konukoglu, D. and H. Uzun, Endothelial Dysfunction and Hypertension. Adv Exp Med Biol, 2017. 956: p. 511-540. 44. Coenen, D.M., T.G. Mastenbroek, and J. Cosemans, Platelet interaction with activated endothelium: mechanistic insights from microfluidics. Blood, 2017. 130(26): p. 2819-2828. 45. Nyrop, M. and A.J. Zweifler, Platelet aggregation in hypertension and the effects of antihypertensive treatment. J Hypertens, 1988. 6(4): p. 263-9. 46. Konstantinova, E., et al., Rheological properties of blood and parameters of platelets aggregation in arterial hypertension. Clin Hemorheol Microcirc, 2006. 35(1-2): p. 135-8. 47. Fuchs, F.D. and P.K. Whelton, High Blood Pressure and Cardiovascular Disease. Hypertension, 2020. 75(2): p. 285-292. 48. Aoki, I., et al., Platelet-dependent thrombin generation in patients with hyperlipidemia. J Am Coll Cardiol, 1997. 30(1): p. 91-6. 49. Pawelczyk, M., et al., The influence of hyperlipidemia on platelet activity markers in patients after ischemic stroke. Cerebrovasc Dis, 2009. 27(2): p. 131-7. 50. Fredrickson, D.S., An international classification of hyperlipidemias and hyperlipoproteinemias. Ann Intern Med, 1971. 75(3): p. 471-2. 51. Shimasaki, Y., et al., The effects of long-term smoking on endothelial nitric oxide synthase mRNA expression in human platelets as detected with real-time quantitative RT-PCR. Clin Appl Thromb Hemost, 2007. 13(1): p. 43-51. 52. Endemann, D.H. and E.L. Schiffrin, Nitric oxide, oxidative excess, and vascular complications of diabetes mellitus. Curr Hypertens Rep, 2004. 6(2): p. 85-9. 53. Kwaan, H.C., et al., Increased platelet aggregation in diabetes mellitus. J Lab Clin Med, 1972. 80(2): p. 236-46. 54. McDonald, J.W., et al., Comparison of platelet thromboxane synthesis in diabetic patients on conventional insulin therapy and continuous insulin infusions. Thromb Res, 1982. 28(6): p. 705-12. 55. Badawi, H., et al., Platelets, coagulation and fibrinolysis in diabetic and non-diabetic patients with quiescent coronary heart disease. Angiology, 1970. 21(8): p. 511-9. 56. Mayne, E.E., J.M. Bridges, and J.A. Weaver, Platelet adhesiveness, plasma fibrinogen and factor 8 levels in diabetes mellitus. Diabetologia, 1970. 6(4): p. 436-40. 57. Keating, F.K., B.E. Sobel, and D.J. Schneider, Effects of increased concentrations of glucose on platelet reactivity in healthy subjects and in patients with and without diabetes mellitus. Am J Cardiol, 2003. 92(11): p. 1362-5. 58. Colwell, J.A. and R.W. Nesto, The platelet in diabetes: focus on prevention of ischemic events. Diabetes Care, 2003. 26(7): p. 2181-8. 59. Banerjee, C., et al., Duration of diabetes and risk of ischemic stroke: the Northern Manhattan Study. Stroke, 2012. 43(5): p. 1212-7. 60. Almdal, T., et al., The independent effect of type 2 diabetes mellitus on ischemic heart disease, stroke, and death: a population-based study of 13,000 men and women with 20 years of follow-up. Arch Intern Med, 2004. 164(13): p. 1422-6. 61. Levine, P.H., An acute effect of cigarette smoking on platelet function. A possible link between smoking and arterial thrombosis. Circulation, 1973. 48(3): p. 619-23. 62. Nair, S., et al., Changes in platelet glycoprotein receptors after smoking--a flow cytometric study. Platelets, 2001. 12(1): p. 20-6. 63. Renaud, S., et al., Platelet function after cigarette smoking in relation to nicotine and carbon monoxide. Clin Pharmacol Ther, 1984. 36(3): p. 389-95. 64. Bierenbaum, M.L., et al., Effect of cigarette smoking upon in vivo platelet function in man. Thromb Res, 1978. 12(6): p. 1051-7. 65. Blann, A.D., et al., The influence of acute smoking on leucocytes, platelets and the endothelium. Atherosclerosis, 1998. 141(1): p. 133-9. 66. Rival, J., J.M. Riddle, and P.D. Stein, Effects of chronic smoking on platelet function. Thromb Res, 1987. 45(1): p. 75-85. 67. Mehta, P. and J. Mehta, Effects of smoking on platelets and on plasma thromboxane-prostacyclin balance in man. Prostaglandins Leukot Med, 1982. 9(2): p. 141-50. 68. Barua, R.S., et al., Reactive oxygen species are involved in smoking-induced dysfunction of nitric oxide biosynthesis and upregulation of endothelial nitric oxide synthase: an in vitro demonstration in human coronary artery endothelial cells. Circulation, 2003. 107(18): p. 2342-7. 69. Padmavathi, P., et al., Chronic cigarette smoking-induced oxidative/nitrosative stress in human erythrocytes and platelets. Molecular & Cellular Toxicology, 2018. 14(1): p. 27-34. 70. Barua, R.S. and J.A. Ambrose, Mechanisms of coronary thrombosis in cigarette smoke exposure. Arterioscler Thromb Vasc Biol, 2013. 33(7): p. 1460-7. 71. Toda, N., Age-related changes in endothelial function and blood flow regulation. Pharmacol Ther, 2012. 133(2): p. 159-76. 72. Otahbachi, M., et al., Gender differences in platelet aggregation in healthy individuals. J Thromb Thrombolysis, 2010. 30(2): p. 184-91. 73. Sohal, A.S., et al., Uremic bleeding: pathophysiology and clinical risk factors. Thromb Res, 2006. 118(3): p. 417-22. 74. Gremmel, T., et al., Chronic kidney disease is associated with increased platelet activation and poor response to antiplatelet therapy. Nephrol Dial Transplant, 2013. 28(8): p. 2116-22. 75. DeEugenio, D., et al., Risk of major bleeding with concomitant dual antiplatelet therapy after percutaneous coronary intervention in patients receiving long-term warfarin therapy. Pharmacotherapy, 2007. 27(5): p. 691-6. 76. Grodzinsky, A., et al., Bleeding risk following percutaneous coronary intervention in patients with diabetes prescribed dual anti-platelet therapy. Am Heart J, 2016. 182: p. 111-118. 77. Ben-Dor, I., et al., Incidence, correlates, and clinical impact of nuisance bleeding after antiplatelet therapy for patients with drug-eluting stents. Am Heart J, 2010. 159(5): p. 871-5. 78. Doyle, B.J., et al., Major femoral bleeding complications after percutaneous coronary intervention: incidence, predictors, and impact on long-term survival among 17,901 patients treated at the Mayo Clinic from 1994 to 2005. JACC Cardiovasc Interv, 2008. 1(2): p. 202-9. 79. De Berardis, G., et al., Association of aspirin use with major bleeding in patients with and without diabetes. JAMA, 2012. 307(21): p. 2286-94. 80. Peng, Y.L., et al., Diabetes is an independent risk factor for peptic ulcer bleeding: a nationwide population-based cohort study. J Gastroenterol Hepatol, 2013. 28(8): p. 1295-9. 81. Lal, S., et al., Gingival bleeding in 6- to 13-year-old children with diabetes mellitus. Pediatr Dent, 2007. 29(5): p. 426-30. 82. Yang, C.H., et al., Diabetes mellitus is associated with gastroesophageal variceal bleeding in cirrhotic patients. Kaohsiung J Med Sci, 2014. 30(10): p. 515-20. 83. Zhang, Z., et al., Diabetes mellitus is associated with increased bleeding in pulmonary embolism receiving conventional anticoagulant therapy: findings from a "real-world" study. J Thromb Thrombolysis, 2017. 43(4): p. 540-549. 84. Kuntic, M., et al., Short-term e-cigarette vapour exposure causes vascular oxidative stress and dysfunction: evidence for a close connection to brain damage and a key role of the phagocytic NADPH oxidase (NOX-2). Eur Heart J, 2020. 41(26): p. 2472-2483. 85. Rao, P., et al., Comparable Impairment of Vascular Endothelial Function by a Wide Range of Electronic Nicotine Delivery Devices. Nicotine Tob Res, 2022. 24(7): p. 1055-1062. 86. Carnevale, R., et al., Acute Impact of Tobacco vs Electronic Cigarette Smoking on Oxidative Stress and Vascular Function. Chest, 2016. 150(3): p. 606-12. 87. Nocella, C., et al., Impact of Tobacco Versus Electronic Cigarette Smoking on Platelet Function. Am J Cardiol, 2018. 122(9): p. 1477-1481. 88. Qasim, H., et al., Short-Term E-Cigarette Exposure Increases the Risk of Thrombogenesis and Enhances Platelet Function in Mice. J Am Heart Assoc, 2018. 7(15). 89. Ramirez, J.E.M., et al., The JUUL E-Cigarette Elevates the Risk of Thrombosis and Potentiates Platelet Activation. J Cardiovasc Pharmacol Ther, 2020. 25(6): p. 578-586. 90. Ikonomidis, I., et al., Effects of electronic cigarette on platelet and vascular function after four months of use. Food Chem Toxicol, 2020. 141: p. 111389. 91. M'Pembele, R., et al., Diabetes mellitus is not associated with enhanced bleeding risk in patients after percutaneous coronary intervention. Diabet Med, 2021. 38(5): p. e14532. 92. Chesebro, J.H., et al., Thrombolysis in Myocardial Infarction (TIMI) Trial, Phase I: A comparison between intravenous tissue plasminogen activator and intravenous streptokinase. Clinical findings through hospital discharge. Circulation, 1987. 76(1): p. 142-54. 93. Morrow, D.A., et al., TIMI risk score for ST-elevation myocardial infarction: A convenient, bedside, clinical score for risk assessment at presentation: An intravenous nPA for treatment of infarcting myocardium early II trial substudy. Circulation, 2000. 102(17): p. 2031-7. 94. Austin, P.C., Balance diagnostics for comparing the distribution of baseline covariates between treatment groups in propensity-score matched samples. Stat Med, 2009. 28(25): p. 3083-107. 95. Xu, S., et al., Use of stabilized inverse propensity scores as weights to directly estimate relative risk and its confidence intervals. Value Health, 2010. 13(2): p. 273-7. 96. Metzen, D., et al., Platelet reactivity is higher in e-cigarette vaping as compared to traditional smoking. Int J Cardiol, 2021. 343: p. 146-148. 97. Valgimigli, M., The ESC DAPT Guidelines 2017. Eur Heart J, 2018. 39(3): p. 187-188. 98. Mauri, L., et al., Twelve or 30 months of dual antiplatelet therapy after drug-eluting stents. N Engl J Med, 2014. 371(23): p. 2155-66. 99. Bainey, K.R., et al., Rivaroxaban Plus Aspirin Versus Aspirin Alone in Patients With Prior Percutaneous Coronary Intervention (COMPASS-PCI). Circulation, 2020. 141(14): p. 1141-1151. 100. Bhatt, D.L., et al., Role of Combination Antiplatelet and Anticoagulation Therapy in Diabetes Mellitus and Cardiovascular Disease: Insights From the COMPASS Trial. Circulation, 2020. 141(23): p. 1841-1854. 101. Group, A.S.C., et al., Effects of Aspirin for Primary Prevention in Persons with Diabetes Mellitus. N Engl J Med, 2018. 379(16): p. 1529-1539. 102. Biondi-Zoccai, G., et al., Acute Effects of Heat-Not-Burn, Electronic Vaping, and Traditional Tobacco Combustion Cigarettes: The Sapienza University of Rome-Vascular Assessment of Proatherosclerotic Effects of Smoking ( SUR - VAPES ) 2 Randomized Trial. J Am Heart Assoc, 2019. 8(6): p. e010455. 103. Stokes, A.C., et al., Association of Cigarette and Electronic Cigarette Use Patterns With Levels of Inflammatory and Oxidative Stress Biomarkers Among US Adults: Population Assessment of Tobacco and Health Study. Circulation, 2021. 143(8): p. 869-871. 104. Fetterman, J.L., et al., Flavorings in Tobacco Products Induce Endothelial Cell Dysfunction. Arterioscler Thromb Vasc Biol, 2018. 38(7): p. 1607-1615. 105. Wolkart, G., et al., Effects of flavoring compounds used in electronic cigarette refill liquids on endothelial and vascular function. PLoS One, 2019. 14(9): p. e0222152. 106. Richardson, A., Krivokhizhina, Tatiana, Lorkiewicz, Pavel, D'Souza, Stanley, Bhatnagar, Aruni, Srivastava, Sanjay, Conklin, Daniel J., Effects of electronic cigarette flavorants on human platelet aggregation ex vivo. Toxicology Reports, 2022. 9: p. 814-820. 107. Hom, S., et al., Platelet activation, adhesion, inflammation, and aggregation potential are altered in the presence of electronic cigarette extracts of variable nicotine concentrations. Platelets, 2016. 27(7): p. 694-702. 108. Steg, P.G. and D.L. Bhatt, Is There Really a Benefit to Net Clinical Benefit in Testing Antithrombotics? Circulation, 2018. 137(14): p. 1429-1431. | |||||||
| Lizenz: |  Dieses Werk ist lizenziert unter einer Creative Commons Namensnennung 4.0 International Lizenz | |||||||
| Fachbereich / Einrichtung: | Medizinische Fakultät | |||||||
| Dokument erstellt am: | 12.03.2024 | |||||||
| Dateien geändert am: | 12.03.2024 | |||||||
| Promotionsantrag am: | 17.07.2023 | |||||||
| Datum der Promotion: | 23.01.2024 |
