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CC BY 4.0 · TH Open 2022; 06(01): e26-e32
DOI: 10.1055/a-1719-6178
Original Article

Temporary Rise in Blood Thrombogenicity in Patients with Acute Myocardial Infarction

Shumpei Kosugi 
1   Cardiovascular Division, National Hospital Organization Osaka National Hospital, Osaka, Japan
,
Yasunori Ueda 
1   Cardiovascular Division, National Hospital Organization Osaka National Hospital, Osaka, Japan
,
Haruhiko Abe
1   Cardiovascular Division, National Hospital Organization Osaka National Hospital, Osaka, Japan
,
Kuniyasu Ikeoka
1   Cardiovascular Division, National Hospital Organization Osaka National Hospital, Osaka, Japan
,
Tsuyoshi Mishima
1   Cardiovascular Division, National Hospital Organization Osaka National Hospital, Osaka, Japan
,
Tatsuhisa Ozaki
1   Cardiovascular Division, National Hospital Organization Osaka National Hospital, Osaka, Japan
,
Kohtaro Takayasu
1   Cardiovascular Division, National Hospital Organization Osaka National Hospital, Osaka, Japan
,
Takuya Ohashi
1   Cardiovascular Division, National Hospital Organization Osaka National Hospital, Osaka, Japan
,
Haruya Yamane
1   Cardiovascular Division, National Hospital Organization Osaka National Hospital, Osaka, Japan
,
Masayuki Nakamura
1   Cardiovascular Division, National Hospital Organization Osaka National Hospital, Osaka, Japan
,
Takashi Fukushima
1   Cardiovascular Division, National Hospital Organization Osaka National Hospital, Osaka, Japan
,
Kohei Horiuchi
1   Cardiovascular Division, National Hospital Organization Osaka National Hospital, Osaka, Japan
,
Takashi Iehara
1   Cardiovascular Division, National Hospital Organization Osaka National Hospital, Osaka, Japan
,
Satoshi Osaki
1   Cardiovascular Division, National Hospital Organization Osaka National Hospital, Osaka, Japan
,
Kazuki Ozato
1   Cardiovascular Division, National Hospital Organization Osaka National Hospital, Osaka, Japan
,
Koichi Inoue
1   Cardiovascular Division, National Hospital Organization Osaka National Hospital, Osaka, Japan
,
Yukihiro Koretsune
1   Cardiovascular Division, National Hospital Organization Osaka National Hospital, Osaka, Japan
,
Yasushi Matsumura
1   Cardiovascular Division, National Hospital Organization Osaka National Hospital, Osaka, Japan
› Author Affiliations Funding Research grants for this study was provided by Pfizer, Bayer, Daiichi-Sankyo, Astellas, Shionogi, Nihon Kohden, Abbott, and Teijin.
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Abstract

Objective Although blood thrombogenicity seems to be one of the determinant factors for the development of acute myocardial infarction (MI), it has not been dealt with in-depth. This study aimed to investigate blood thrombogenicity and its change in acute MI patients.

Methods and Results We designed a prospective, observational study that included 51 acute MI patients and 83 stable coronary artery disease (CAD) patients who underwent cardiac catheterization, comparing thrombogenicity of the whole blood between: (1) acute MI patients and stable CAD patients; and (2) acute and chronic phase in MI patients. Blood thrombogenicity was evaluated by the Total Thrombus-Formation Analysis System (T-TAS) using the area under the flow pressure curve (AUC30) for the AR-chip. Acute MI patients had significantly higher AUC30 than stable CAD patients (median [interquartile range], 1,771 [1,585–1,884] vs. 1,677 [1,527–1,756], p = 0.010). Multivariate regression analysis identified acute MI with initial TIMI flow grade 0/1 as an independent determinant of high AUC30 (β = 0.211, p = 0.013). In acute MI patients, AUC30 decreased significantly from acute to chronic phase (1,859 [1,550–2,008] to 1,521 [1,328–1,745], p = 0.001).

Conclusion Blood thrombogenicity was significantly higher in acute MI patients than in stable CAD patients. Acute MI with initial TIMI flow grade 0/1 was significantly associated with high blood thrombogenicity by multivariate analysis. In acute MI patients, blood thrombogenicity was temporarily higher in acute phase than in chronic phase.

Keywords

blood thrombogenicity - acute myocardial infarction - coronary artery disease - T-TAS

Conflict of Interest

Y.U. received research grants from Abbott Vascular, Pfizer, Bayer, Daiichi Sankyo, Astellas, Shionogi, Sanofi, Ono, Nihon Kohden, Amgen Astellas, Actelion, Bristol-Myers Squibb, Medtronic, AstraZeneca, Otsuka, and Novartis, and lecture fees from Daiichi Sankyo, MSD, Goodman, Sanofi, Mochida, Takeda, Kowa, Teijin, Astellas, Actelion, Bristol-Myers Squibb, AstraZeneca, Boston Scientific, Sumitomo Dainippon Pharma, Eisai, and Amgen Astellas. H.A. received research grants from Daiichi Sankyo and Boehringer Ingelheim. K.I. received manuscript and lecture fees from Daiichi Sankyo, Boehringer Ingelheim, Medtronic, and Johnson & Johnson. Y.K. received lecture fees from Daiichi Sankyo, Boehringer Ingelheim, Bayer, Bristol-Meyers Squibb, and Pfizer.




Publication History

Received: 15 September 2021

Accepted: 10 December 2021

Accepted Manuscript online:
13 December 2021

Article published online:
24 January 2022

© 2022. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited. (https://creativecommons.org/licenses/by/4.0/)

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  • References

  • 1 Davies MJ, Bland JM, Hangartner JRW, Angelini A, Thomas AC. Factors influencing the presence or absence of acute coronary artery thrombi in sudden ischaemic death. Eur Heart J 1989; 10 (03) 203-208
    CrossrefPubMedGoogle Scholar
  • 2 Arbustini E, Grasso M, Diegoli M. et al. Coronary atherosclerotic plaques with and without thrombus in ischemic heart syndromes: a morphologic, immunohistochemical, and biochemical study. Am J Cardiol 1991; 68 (07) 36B-50B
    CrossrefPubMedGoogle Scholar
  • 3 Jern C, Eriksson E, Tengborn L, Risberg B, Wadenvik H, Jern S. Changes of plasma coagulation and fibrinolysis in response to mental stress. Thromb Haemost 1989; 62 (02) 767-771
    Article in Thieme ConnectPubMedGoogle Scholar
  • 4 Kawahara J, Sano H, Fukuzaki H, Saito K, Hirouchi H. Acute effects of exposure to cold on blood pressure, platelet function and sympathetic nervous activity in humans. Am J Hypertens 1989; 2 (09) 724-726
    CrossrefPubMedGoogle Scholar
  • 5 Patterson SM, Krantz DS, Gottdiener JS, Hecht G, Vargot S, Goldstein DS. Prothrombotic effects of environmental stress: changes in platelet function, hematocrit, and total plasma protein. Psychosom Med 1995; 57 (06) 592-599
    CrossrefPubMedGoogle Scholar
  • 6 Smyth A, O'Donnell M, Lamelas P, Teo K, Rangarajan S, Yusuf S. INTERHEART Investigators. Physical activity and anger or emotional upset as triggers of acute myocardial infarction: the INTERHEART study. Circulation 2016; 134 (15) 1059-1067
    CrossrefPubMedGoogle Scholar
  • 7 Caussin C, Escolano S, Mustafic H. et al; CARDIO-ARSIF Registry Investigators. Short-term exposure to environmental parameters and onset of ST elevation myocardial infarction. The CARDIO-ARSIF registry. Int J Cardiol 2015; 183: 17-23
    CrossrefPubMedGoogle Scholar
  • 8 Muller JE, Tofler GH, Stone PH. Circadian variation and triggers of onset of acute cardiovascular disease. Circulation 1989; 79 (04) 733-743
    CrossrefPubMedGoogle Scholar
  • 9 Thompson SG, Kienast J, Pyke SDM, Haverkate F, van de Loo JC. European Concerted Action on Thrombosis and Disabilities Angina Pectoris Study Group. Hemostatic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris. N Engl J Med 1995; 332 (10) 635-641
    CrossrefPubMedGoogle Scholar
  • 10 Vaziri ND, Kennedy SC, Kennedy D, Gonzales E. Coagulation, fibrinolytic, and inhibitory proteins in acute myocardial infarction and angina pectoris. Am J Med 1992; 93 (06) 651-657
    CrossrefPubMedGoogle Scholar
  • 11 Minnema MC, Peters RJG, de Winter R. et al. Activation of clotting factors XI and IX in patients with acute myocardial infarction. Arterioscler Thromb Vasc Biol 2000; 20 (11) 2489-2493
    CrossrefPubMedGoogle Scholar
  • 12 Moyssakis I, Vlahodimitris IE, Kanakis MA, Kapsimali V, Tsoucala C, Vaiopoulos GA. Behavior of coagulation factors and normal inhibitors of coagulation during the acute phase of myocardial infarction. Blood Coagul Fibrinolysis 2010; 21 (07) 670-673
    CrossrefPubMedGoogle Scholar
  • 13 Loeffen R, van Oerle R, de Groot PG. et al. Increased factor XIa levels in patients with a first acute myocardial infarction: the introduction of a new thrombin generation based factor XIa assay. Thromb Res 2014; 134 (06) 1328-1334
    CrossrefPubMedGoogle Scholar
  • 14 Merlini PA, Bauer KA, Oltrona L. et al. Persistent activation of coagulation mechanism in unstable angina and myocardial infarction. Circulation 1994; 90 (01) 61-68
    CrossrefPubMedGoogle Scholar
  • 15 Hosokawa K, Ohnishi T, Kondo T. et al. A novel automated microchip flow-chamber system to quantitatively evaluate thrombus formation and antithrombotic agents under blood flow conditions. J Thromb Haemost 2011; 9 (10) 2029-2037
    CrossrefPubMedGoogle Scholar
  • 16 Thygesen K. ‘Ten Commandments’ for the Fourth Universal Definition of Myocardial Infarction 2018. Eur Heart J 2019; 40 (03) 226
    CrossrefPubMedGoogle Scholar
  • 17 Al Ghaithi R, Mori J, Nagy Z. et al. Evaluation of the Total Thrombus-Formation System (T-TAS): application to human and mouse blood analysis. Platelets 2019; 30 (07) 893-900
    CrossrefPubMedGoogle Scholar
  • 18 Yamamoto K, Ito T, Nagasato T. et al. Effects of glycemic control and hypoglycemia on thrombus formation assessed using automated microchip flow chamber system: an exploratory observational study. Thromb J 2019; 17: 17
    CrossrefPubMedGoogle Scholar
  • 19 Mitsuse T, Kaikita K, Ishii M. et al. Total thrombus-formation analysis system can predict 1-year bleeding events in patients with coronary artery disease. J Atheroscler Thromb 2020; 27 (03) 215-225
    CrossrefPubMedGoogle Scholar
  • 20 Idemoto Y, Miura SI, Norimatsu K. et al. Evaluation of the antithrombotic abilities of non-vitamin K antagonist oral anticoagulants using the Total Thrombus-formation Analysis System® . Heart Vessels 2017; 32 (03) 309-316
    CrossrefPubMedGoogle Scholar
  • 21 Thaulow E, Erikssen J, Sandvik L, Stormorken H, Cohn PF. Blood platelet count and function are related to total and cardiovascular death in apparently healthy men. Circulation 1991; 84 (02) 613-617
    CrossrefPubMedGoogle Scholar
  • 22 Vinholt PJ, Hvas AM, Frederiksen H, Bathum L, Jørgensen MK, Nybo M. Platelet count is associated with cardiovascular disease, cancer and mortality: a population-based cohort study. Thromb Res 2016; 148: 136-142
    CrossrefPubMedGoogle Scholar
  • 23 Folsom AR, Wu KK, Rosamond WD, Sharrett AR, Chambless LE. Prospective study of hemostatic factors and incidence of coronary heart disease: the Atherosclerosis Risk in Communities (ARIC) Study. Circulation 1997; 96 (04) 1102-1108
    CrossrefPubMedGoogle Scholar
  • 24 Klovaite J, Benn M, Yazdanyar S, Nordestgaard BG. High platelet volume and increased risk of myocardial infarction: 39,531 participants from the general population. J Thromb Haemost 2011; 9 (01) 49-56
    CrossrefPubMedGoogle Scholar
  • 25 Arima Y, Kaikita K, Ishii M. et al. Assessment of platelet-derived thrombogenicity with the total thrombus-formation analysis system in coronary artery disease patients receiving antiplatelet therapy. J Thromb Haemost 2016; 14 (04) 850-859
    CrossrefPubMedGoogle Scholar
  • 26 Clifford CR, Jung RG, Hibbert B. et al. Dual antiplatelet therapy (PEGASUS) vs. dual pathway (COMPASS): a head-to-head in vitro comparison. Platelets 2021; 00: 1-6
    CrossrefPubMedGoogle Scholar
  • 27 Brass LF, Zhu L, Stalker TJ. Minding the gaps to promote thrombus growth and stability. J Clin Invest 2005; 115 (12) 3385-3392
    CrossrefPubMedGoogle Scholar
  • 28 Sato Y, Hatakeyama K, Yamashita A, Marutsuka K, Sumiyoshi A, Asada Y. Proportion of fibrin and platelets differs in thrombi on ruptured and eroded coronary atherosclerotic plaques in humans. Heart 2005; 91 (04) 526-530
    CrossrefPubMedGoogle Scholar
  • 29 Yamashita A, Sumi T, Goto S. et al. Detection of von Willebrand factor and tissue factor in platelets-fibrin rich coronary thrombi in acute myocardial infarction. Am J Cardiol 2006; 97 (01) 26-28
    CrossrefPubMedGoogle Scholar
  • 30 Ueda Y, Kosugi S, Abe H. et al. Transient increase in blood thrombogenicity may be a critical mechanism for the occurrence of acute myocardial infarction. J Cardiol 2021; 77 (03) 224-230
    CrossrefPubMedGoogle Scholar