Nicotine addiction and an elevated cholesterol level exhibit negative effects on platelet activation in patients with chronic Buerger’s disease
Abstract
Introduction: Buerger’s disease, or thromboangitis obliterans (TAO), is a vascoocclusive disorder of unknown etiology. Cigarette smoking is considered to be a main risk factor for the development of TAO. The aim of the study: The aim of this study was to assess the activation of platelets in patients with Buerger’s disease compared to the control group. Materials and methods: Thirty patients (24 men and 6 women, median age 51.4 years) with TAO were included in the study. In the control group there were twenty healthy adults (16 men and 4 women, median age 44.0 years). Platelets’ activation was measured by light aggregometry and flow cytometry methods with, and without, platelet activators, such as thrombin receptor agonist peptide-TRAP-6 and adenosinodiphosphate-ADP. Results: The velocity and intensity of aggregation increased in patients with TAO (p<0.05). MFI (mean fluorescence intensity) of P-selectine, CD63 (GP53-component of lysosomal membrane) and PAC-1 (platelet activation complex-1) on platelets increased in patients (p<0,05). Significantly higher aggregation velocities were noted in smoking patients in response to collagen (Coll) and to arachidonic acid (AA). Aggregation velocity in response to AA and epinephrine (EPI) was higher in smokersIn patients with an increased cholesterol level platelet aggregation and the MFI of plateletswas also higher.. Conclusion: P-selectin (CD62P), an active form of the receptor for fibrinogen (PAC-1), and the lysosomal protein (CD63) on platelets can parcipate in pathogenesis of TAO. Also smoking and lipid disturbances increases platelet activation in this group of patients.
Keywords: platelet activationP-selectinBuerger’s disease
References
- Thromboangiitis Obliterans (Buerger Disease). In: Sindawy AN, Perler BA. ed. Rutherford’s vascular surgery and endovascular therapy. Vol. 1. 9th edition. Elsevier 2019, Philadelphia, PA 2019.
- Fazeli B, Poredos P, Kozak M, et al. Diagnostic criteria for Buerger's disease: International Consensus of VAS - European Independent Foundation in Angiology/Vascular Medicine. Int Angiol. 2023; 42(5): 396–401.
- Olin JW. Thromboangiitis obliterans: 110 years old and little progress made. J Am Heart Assoc. 2018; 7(23): e011214.
- Ribieras AJ, Ortiz YY, Liu ZJ, et al. Therapeutic angiogenesis in Buerger's disease: reviewing the treatment landscape. Ther Adv Rare Dis. 2022; 3: 26330040211070295.
- Naiem N. Thromboangiitis Obliterans (Buerger Disease): Practice Essentials, Pathophysiology and Etiology, Epidemiology. https://emedicine.medscape.com/article/460027-overview?form=fpf (14 April 2024).
- Rivera-Chavarría IJ, Brenes-Gutiérrez JD. Thromboangiitis obliterans (Buerger's disease). Ann Med Surg (Lond). 2016; 7: 79–82.
- Hus I, Sokolowska B, Walter-Croneck A, et al. Assessment of plasma prothrombotic factors in patients with Buerger's disease. Blood Coagul Fibrinolysis. 2013; 24(2): 133–139.
- Brass LF. Thrombin and platelet activation. Chest. 2003; 124(3 Suppl): 18S–25S.
- Rubenstein DA, Yin W. Platelet-Activation Mechanisms and Vascular Remodeling. Compr Physiol. 2018; 8(3): 1117–1156.
- Arkkila PET. Thromboangiitis obliterans (Buerger's disease). Orphanet J Rare Dis. 2006; 1: 14.
- Seebald J, Gritters L. Thromboangiitis obliterans (Buerger disease). Radiol Case Rep. 2015; 10(3): 9–11.
- Born GV, Dearnley R, Foulks JG, et al. Aggregation of blood platelets by adenosine diphosphate and its reversal. Nature. 1962; 194: 927–929.
- Zawilska K, Komarnicki M, Mańka B, et al. [Effect of beta-blocking agents on platelet aggregation]. Pol Arch Med Wewn. 1975; 54(2): 203–208.
- Yee DL, Bergeron AL, Sun CW, et al. Platelet hyperreactivity generalizes to multiple forms of stimulation. J Thromb Haemost. 2006; 4(9): 2043–2050.
- Pietraszek MH, Choudhury NA, Koyano K, et al. Enhanced platelet response to serotonin in Buerger's Disease. Thromb Res. 1990; 60(3): 241–246.
- Yee DL, Sun CW, Bergeron AL, et al. Aggregometry detects platelet hyperreactivity in healthy individuals. Blood. 2005; 106(8): 2723–2729.
- Carr ME, Hackney MH, Hines SJ, et al. Enhanced platelet force development despite drug-induced inhibition of platelet aggregation in patients with thromboangiitis obliterans--two case reports. Vasc Endovascular Surg. 2002; 36(6): 473–480.
- Inoue T, Hayashi M, Uchida T, et al. Significance of platelet aggregability immediately after blood sampling and effect of cigarette smoking. Platelets. 2001; 12(7): 415–418.
- Nair S, Kulkarni S, Camoens HM, et al. Changes in platelet glycoprotein receptors after smoking--a flow cytometric study. Platelets. 2001; 12(1): 20–26.
- Papa M, Bass A, Adar R, et al. Autoimmune mechanisms in thromboangiitis obliterans (Buerger's Disease): the role of tobacco antigen and the major histocompatibility complex. Surgery. 1992; 111(5): 527–531.
- Rahman M, Chowdhury AS, Fukui T, et al. Association of thromboangiitis obliterans with cigarette and bidi smoking in Bangladesh: a case-control study. Int J Epidemiol. 2000; 29(2): 266–270.
- Weber AA, Liesener S, Schanz A, et al. Habitual smoking causes an abnormality in platelet thromboxane A2 metabolism and results in an altered susceptibility to aspirin effects. Platelets. 2000; 11(3): 177–182.
- Chan HC, Ke LY, Chu CS, et al. Highly electronegative LDL from patients with ST-elevation myocardial infarction triggers platelet activation and aggregation. Blood. 2013; 122(22): 3632–3641.